Atko ViruTABLE OF CONTENTS Chapter 1 * General Outlines of Adaptation Processes and the Biological Nature of Exercise Training Adaptation and Trai Homeostatic Regulai Mechanism of Ge I Adaptation Mobilization of Metabolic Reso Ss Acute and Long-Term Adaptation The Nature of Exercise Training Model of the Top Athlete References, * Chapter 2 «Hormones in Adaptation to Physical Exercises (Hormonal Responses Exercise) Blood Hormonal Ensemble During Exer Stabili ability in Hormonal Responses to Exercise The Rate nonal Responses . Determi Significance of Exercise Int nificance of Exercise Du nts of Hormonal Responses Training Effects The Interplay Betwe Fitness of Persons ignificance of Exercise Duration and the Homeostatic Needs tors Mod fer nonal Responses to Exercise Chapter 3 ~ Significance of Hormones in Regulation of Metabolism During Exercise the Hormone Ef me Privaie and Attending Regulatio Exercise-Induced Effects at the Level of Modulating Regulation Factors Determini Training Effects at the Level of Modulating Regulation Mobilization of Energy Reserves Activation of Glycogenolysis in Skeletal Muscles ilycogenolysis in the Myocardium .. Regula Giucone Utilization of Blood Glucose Blood Glucos Mobilization of Lipid Resources Mobilization of Pre atic Regulal Glycogenolysis in th Homeostasis During Exercise ein Resources : n of Water-Electrolyt alance During Exercise enc Chapter 4 Post-Exercise Recovery Period Ouilines of the Post-Exercise Recovery Restoration of Normal Functional Activities .. Oxygen Transport Syster Lactate Dynamics and pH Values in Post-Exercise Recovery Endocrine System 49 84 4 88 90Glucocorticoids Pancreatic Hormones ‘Thyroid Homiones .. Responses to Test Exercis Water-Electrolyte Homeostasis . z : ‘Central Nervous Sy: Repletion of Energy Stores Sequence of the Repletion of Various Substrates ...... Supercompensation . Control of Glycogen Resynthesis ‘Substrates for Muscle Glycogen Repketion .. Lactate Glucose Glaconcogenesis and Lipid Metabolism - Hepatic Gluconcogemesis ene ‘Lipid metabotism Protein Synthesis in Skeletal Muscles... Degradation and Turnover of Protein: ‘Conclusions. ReFCTENCES ener rne . - Chapter 5 Specific Nature of Training on Skeletal Muscles Hypertrophy of Myofibrils Hypertrophy vs. Hyperplasia. ‘Contractile Mechani Sarcolemma Sarcoplasmic Reticulum (SR) wens Actomyosin ATPase Activit Characteristics of Contraction... ochondria and Oxidative Enzymes ... Enzymes of Anaerobic Pathways of ATP Resy Buffer Capacity . Anaerobic Working Capacity Intramuscular Energy Stores and Myoglobin. ATP a Phosphocreatine . Glycogen. Triglycerides Myoglobin Musele Capillarization.. Fiber Type Transformation Problem ‘Conclusion .... References... . Chapter 6 Specificity of Training Effects on Aerobic Working Capacity and the Cardiovascular System Training Effects on Anaerobic Threshold and Maximal Oxy; Anaerobic Threshold — = en Uptake160 160 169 172 174 15 7 Ww Exercise Economy .enenernennese Maximal Oxygen Uptake .o.o-e- Specificity of Training Effects on the Cardiovascular System: Heart Hypertrophy ‘Cardiac Performance ‘Contractile Mechanism of the Myocardium Energeties of the Myocardium ive Changes in the Oxygen Transport System . . Chapter 7 Specificity of Training Effects on Control Functions and the Connective Tissue Endocrine Functions... Neural Adaptation Changes in the Central Nervous System Cross-Effects of Training on Untrained Muscles ... Training Effects on the Connective Tissue References... : « Chapter 6 Molecular Mechanisms of Training Effects Protein Synthesis in Trainin; Evidences of Augaiented Protein Synthesis in Training Metabolic Control of Protein Synthesi Control of Transcription ce - Protein Degradation Products. Creatine Amino Acids... Specific RNA .. Energy Balance. Muscle Stretch Calcium . Prostaglandins. Tissue Growth Factors... Muscle Satellite Cells «0. ‘Control of Synthesis of ‘Translation ComtrOl nomen Hormonal Action on Adaptive Protein Syathesis in Training . Adaptive Protein Synthesis in the Myocardium, Other Theories of Training, Mechani ‘Conclusion References. Chapter 9 Gender Differences in Training Effects Metabolic Capacitics in Male and Female Athletes ‘Endocrine Systems in Exercise in Women Hormonal Responses to Exercise in Wom ‘Ovarian-Menstrual Cycle and Hormonal Responses to Exercise ‘Training Influence on the Female Reproductive System... ‘Training Effects on Muscle Strength and Hypertrophy .. Training Effects on Aerobic Working Capacity ‘Summary. References:Chapter 10 Physiological Aspects of Selected Problems of Training Methodology (Training Tactics) Choice of Training Exercises... Exercise and Training Method .. Manifestations of Training Specificity in Exercises for Improvement of the Mai 241 Qualities of the Human Physical Working Capacity .. 24S Training Session ..... : 247 Criteria of the Trainable Effect of Training Sessions 249 Metabolites... 249 Hormones 256 Simplified Criteria .. 257 Heart Rate Studies ... 257 Inter and Volume. of Training ‘Loads .. 261 Significance of Exercise Schedule . Endurance and Strength Exercises... Necessity for Increased Load (Saturation Phenomenan) .. Microcycle of Training... Vaniants of Training Microcyel Summation of Influences of Subsequent Sessions Microcyeles with Variable Training Loads... Two or More Daily Training Sessions .. ‘The Main Principles of Training Tacties .... Referenc 262 263 264 265 263 267 wie 212 273 275 216 Chapter 11 _ Physiological Aspects of Selected Problems of Training Methodology (Training Strategy) ‘Training Design for a Period of Many Years ‘Ontogenetic ASPECTS Year-Round Training Interrelations Between Various Training-Induced Changes ‘The Steady Training Effect pt as Detraining Effect ‘The Concentrated Unidirectional Training Adaptivity of the Organism eee een cr ‘Conclusion, Reference: ‘Concluding Remarks . Index .......Chapter 1 GENERAL OUTLINES OF ADAPTATION PROCESSES AND THE BIOLOGICAL NATURE OF EXERCISE TRAINING ADAPTATION AND TRAINING Musculas tivity belongs to the group of factors closely related to: adaptation processes in the organism. exercise triggers acute adaptation processes mecessary to adjust body functions to the corresponding level of elevated energy metabolism. Adjustments are also necessary to avoid harmful alterations in the internal milieu of the organism. In turn, all these adjustments enable exercise performance and to & great extent determine the performance level. Systematic repetitions of exercises induce long-term stable adaptation that is founded on structural and metabolic changes, making possible increased functional capacitics HOMEOSTATIC REGULATION Sinee the publications of C, Bernard! and W.B. Cannon,” well recognized that adaptation to life conditions and to any kind of bodily activity is always directed towards maintaining or restoring the constancy of the body's internal milicu, For this purpose certain specific reactions are introduced. The integrated sum of these reactions was defined by W.B. Cannon*? as homeostatic regulation. However, only some of the param. eters of the body's internal milieu are kept at a constant level, while others vary to a great extent. Accordingly, the rigid and plastic constants of the internal environment were discriminated The rigid constants have a very narrow range of fluctations between the resting and activity levels, deviations from which cannot be associated with maintenance of life. The plastic constants can change to a great extent, Often their changes are necessary to compensate for the influences on the rigid constants or to restore their activity (Figure 1-1). The changes of plastic constants may also reflect the mobilization ‘of bodily resources for certain activities, However, there are also special mechanisms responsible for the limitation of alterations of plastic constants and for restoration of the resting levels. he main rigid constants are temperature, pH, osmotic pressure, and contents of ions, water, and pO;, It is simple to notice that there are conditions which determine the optimal activity of enzymes enables us to understand the importance of the constancy of rigid constants. out the necessary conditions which ensure the optimal activity of enzymes, metabolic processes will be disturbed and possibilities of maintain- ing life will be reduced. Homeostatic regulation is affected through controlling factors at the level of cellular autonomic, hormonal, and neural regulation. According to comemporary knowledge, the homeostatic function may be extended to many hormones and other bioactive substances in cooperation with processes triggered by direct nervous influences. In various cases, behavioral responses are included into homeostatic regulation as well.‘Adaptation in Sports Training Homeostac Regulation] eae Dynamic Constants of Internal Miliews a Changes to maintain or restore the level of rigi ‘constants FIGURE LI. Homeostatic regulation (se text) MECHANISM OF GENERAL ADAPTATION Adaptive processes cannot be limited by specific homeostatic reactions. In many cases nonspecific alterations, independent of the specific nature of the activity, are observable. ‘The nonspecific character of adaptation is expressed by the theory of W.B. Cannon? about the emergency function of the sympatho-adrenal system. L.A. Orbeli® discussed the adaptive trophic function of sympathic innervation. Originally, nonspecific adaptation processes were conceptualized by H. Selye.’ An extensive study of nonspecific adaptation responses enabled. him to establish the stress reaction as a sum of nonspecific responses of the body to any strong: demands made upon it, ‘The nonspecific adaptation responses constitute the mechanism of general adapta- tion’? (Figure 1-2). The major components of the mechanism of general adpatation are: (1) mobilization of the body's energy reserve, (2) mobilization of the protein resources, and (3) activation of the body's defense faculties (immunoactivities etc.). As a result, ncreased possibilities will be provided om the one hand, for homeostatic regulation, and ‘on the other hand, for actualization of any necessary bodily activities, including muscu lar exercises. MOBILIZATION OF METABOLIC RESOURCES The main principle of metabolic control is that the substrate/product ratio determines the activity of enzymes catalyzing respectively the conversing of a substrate (S) into a certain product (P) and the reaction in the opposite direction: The increase of the substrate as well as the decrease of the product stimulate enzyme activity (catalyzes the conversion of the substrate S into the product P) and inhibit enzyme e, (catalyzes the opposite process) activity. The substrate can be converted into the product if the activity of enzyme e, surpasses the activity of enzyme €,, The opposite situation will emerge in the decrease of the substrate and the increase of the product. Then an inhibition of enzynGeneral Outlines of Adaptation Processes and the Biological Nature of Exercise Training 3 FIGURE 1-2. Ascheme of adapeationto ses. srossor sor, In response to stressor both specific homo- static mechanisms andthe mechanism of geezal ‘adoption are sctivate. The hater consists in rnoblizationleacray eset, poten S046, and defense faculties. ‘The mobilization of the _ CNS ‘body's enerpy reserve increases the possibilities Pe foc energy altaining of homecstatic responses. ea et eee lization, in resources us o Pesaran eae ee enables us He ic ‘General additional energy reserve as well so yomonslatic scene indoce rapid syhesis of enzyme protcins. which arnecessary for actualizng the specific homeo- ¥ static mechanism, mobilization of energy reserve, ‘Mobilisation: and activation of immunologic responses and aie y™ ‘ther defense facutes Increased functional 3¢- Aca ASation Protein Defense ‘expressed in adaptive synthesis of stmctare and — Basco test (decrease of power output from the fist tothe fourth 15-5 period)" Phosphocreatine machanss Negligible Relative Integral indices “Margria staircase test™ Masui power output measurement Detailed indices ' Phosphocreatine kinase acti muscles (tiopsy) [Dynamics of muscle phosphocreatine i exercise of high intensity" Most simple indices Macgaria staircase test Bosco test (power output daring the frst 15 5) igh High Relative yin16 Adaptation in Sports Training Table 1-4. A Generalized Scheme of Determinants of the Main Qualities of the Human Physical Working Capacity: Significance of Energy Stores and Functional Stability Endura Aerobic Anacrobic Speed Power Strength Energy stores Direct measurement Muscle glycogen content (biopsy) High High Relative Negligible Negligible Muscle phosphocreatine content (biopsy) Negligible High High Relative Relative Indirect assessment Blood glucose dynamics during prolonged Mobilization of extramuscular energy stores High High Negligible Negligible Negligible Detailed indices Blood glucose dynamics during. competitive exercise Blood free fatly acids and glycerol dynamics during conapetition exercise compared to lactate change Blood alanine dynamics daring ‘competition exercise Muscle tissue sensitivity to enemy ‘mobilizing bormones (biopsy) ‘Adipose tissue scasitivty to lipolytic hormones (biopsy Interrelation of adrenaline, somatotropin, ‘glocagon, cortisol and insulin changes, during competition exercise Functional stability High High Relative Negligible Negligible Ttegral indices Indices of capacity of ATP resynthesis mechanicms (see Table 1-1) Dynamics of VO, during competition exercise! Detailed indices Dynamics of eardiovespiratory functions, hormone levels, EMG indices etc Most simple index Dynamics of working capacity (Force or power autput or speed) duringGeneral Outlines of Adaptation Processes and the Biological Nature of Exercise Training 17 Table 1-5. A Generalized Scheme of Determinants of the Main Qualities of the Human Physical Working Capacity: Significance of Determinants. of Muscle Function Endurance Aerobie Anaerobic Speed Power Strength Muscle composition “Measurement of ratio of muscle fibers of various types (biopsy) & slow twiteh onidative fibers High Negligible Negligible Negligible Negligible % fast twitch oxidative glycolytic fibers Relative High Relative Relative Nepligble S% fast slyeolytie fibers Neplipible Relative High High High Muscle strength Totegral indices Volotey strencth of various muscle ‘roups and steagih afer sopranaxinal tectical timation Assessment of strength deficit Detailed indies Ultrasonic assessment of muscle hypertrophy ‘Micasurement of cross-section arca of Tach fibers of Yacous lppee (oper) Foece ooipet percrous-setion of mescle ‘Concentration of contrctle proteins (biopsy) Myosin ATPase activity (biopsy) Maximal value of integral EMG during conti Most simple indices Streagth test according to competion acti Calculation of kan body mass oa basis ‘of measurement of specific gravity of the body* Ratio of a sum of various strength tests to the lean maa”13 Adaptation in Sports Training Table 1-6. A Generalized Scheme of Determinants of the Main Qualities of the Human Physical Working Capacity: Significance of Determinants of Motor Unit Coordination and Homeostatic Regulation Endurance Aerobie Amacrobie Motor enit coordination Relative Relative icpral index EMG characicistics of various Detailed indives Interrelation of EMG of antagonist muscles in various movements Force-velocity curve in dynamic FForce-time curve in static efforts Integral EMG ratio to force output and velocity of movement Assessment of spinal motor reflexes ‘Most simple index Force-velocity and force-time relations in performing competition exercise Homeostatic regulation of water-electrolyte High Relative balance Integral index Dynamics of water, sodium and potassium contents in muscles (biopsy) ‘and blood during competion exercise [Detailed iedices Dynamics of water, sodium and potassium ‘excretion by urine and sweat during competition exercise Matimal perspiration rate Dynamics of blood concentration of hormones, regulating water and sovfium-potassium balance ‘Most simple index. Dynamics of body weight in various ‘exercises Pomer of rmuscle contraction Relative Relative Integral indices Maximal power output measurement aaa sairease lest Detailed indices “Time needed to produce various levels f force output Force-velocity curves of various muscles Force time curves in maximally rapid Maximal intcgral EMG at contraction with varloas velocities oc forces Maximal rate of Ca* sequestering by SR Most simple indices ‘Various power tests according to competition exercise Speed of mavements Negligible Relative Tegal indices ‘Speed of various movements Detailed indices ‘Speed of movements at various levels of ‘Time of initiation of the contraction “Time for initiation of relaxation Time needed to achieve the highest integral EMG. Time of single movesneats Time of maximal relaxation Indices of nerventuscular lability and excitability Negligible Negtigible High High High High Strength High Negligible Relative Relative aGeneral Outlines of Adaptation Processes and the Biological Nature of Exercise Training 19 Table 1-6 (continued). A Generalized Scheme of Determinants of the Main Qualities of the Human Physical Working Capacity: { Significance of Determinants of Motor Unit Coordina- tion and Homeostatic Regulation A _ Power teenth: Maximal rte of calcium uptake by SR Maximal rte of Na,K-pump Most simple indices Assessment of the highest frequency of variows movements Agility test according to competition exercise REFERENCES |. Bernard, C., Lecons sur les Phénontdnes de la Vie Communs aux Animaucx eraux Végéraue, Vol.1, Libera, J-B., Ba, Baillites et Fils, Paris, 1873. ‘Cannon, W-B., Organization of physiological homeastasis, Physiol. Rew., 9, 399, 1929. The Wisdom of the Body, Kogan, P., Ed., Trench, Trubner, London, 1952, ’ General principles of the formation of the body's defense adaptations, Vesinit Akad, USSR, 17(2), 16, 1962 (in Russian) ‘ 5, Cannon, W.P., Bodily Changes in Pain, Hunger, Fear and Rage, Appelton-Century, Crofts, New York, 1929. 6. Orbeli, L-A., Review of the theory about the sympathetic innervation of skeIctal muscles, organs of sense, and central nervous system, Sechenov Physiol. J. USSR, 13, 1, 1932 (in Russian) ‘Selye, HL, The physiology and pathology of exposure to stress, Med. Publ, Montreal, 1950. ‘Viru, A., Hormonal Mechanisess of Adaptation and Training, Nauka, Leningrad, 1981, 9. Viru, A., Mechanism of general adaptation, Med. Hypothesis, 33, 296, 1992. 10. Conlee, R.K McLane, J.A., Rennie, M.J., Winder, W.W., and Holloszy, J.0., Reversal of phosphory lase activation in muscle despite continued contractile activity, Am J. Physiol. 237, R291, 1979. 11, Richtes Ruderman, N.B., Gavras, HL, Belur, E.R, and Galbo, H., Muscle plycogenolysis during ‘exercise: dual contral by epinephrine and contractions, Am. J. Physiol, 242, E2S, 1982 12 Chasiotis, D. Regulation of glycogenolysisin human mascle at rest and daring -encrcise, J. Appl. Physiol, $3, 708, 1982. 13, Arnall, DLA. Marker, J.C-,Comlee, RIK. and Winder, W.W. Effet of infusing epinepbine en liver and muscle glycopenolysis hring exercise in rats, Am. J. Physiol, 250, E41, 1986. 14, Spritt, Libs Rew, J.M, and Holtman, E., Epineplzine infusion enhances wscle plycogenclysis daring prolonged electrical stimulation, J. Appl Physiol, 64, 1439, 1988. 15. Ijin, V.S., and Protasava, ‘T.N., Biochemical foundations of homeostatic mechanisms, in Monscastasis, Gorizoctov, P.D., Ed, Medicina, Moscow, 1976, 93 (in Russian. 16 Mader, A. A transciptioe-trnslation activation feedback circuit 48 a function of protein degradation, quality of protein mass adaptation related to the average functional load, J. Theor: Biol, 134, 3S, 1988 17. Viru, Ag How to understand the training. Modeen Athlete and Caach, 32(2) 1994, 18, Virw, A.jand Viru, M., The specific ature of waining on muscle: a review, Sport Med. Training Rehab, 4 79, 1993, 19. Hollmana, W., and Hettinger, T...Sporimedizin — Arbeits and Trainingsgewndlagen, Sehattaucr, Stuttysc 1976. 20, Jakowlew, N.N., Sportbiochemie, Barth, Leipzig, 1977. ? 21, For, E.L., and Mathews, D-K., Physiological Basis of Physical Education and Athletics, 3nd ed, WB. Saunders, Philadelphia, 1981 itn, By and Gollaick, PD., Skeletal muscle adaptbiiy: significance for metabolism and performance, in Handbook of Physitogy, Skeletal Muscle, Peachy. LD, Adrian, RHL, and Geiger, SR Bids Amerivan Physiological Saciety, Bethesda, 1983, 555. 23, Shephard, JR, and Astrand, P.-O., Eds,, Endurance in Spor, Blackwell Ssienifie Publications, Oxford, 1992, 24, Costill, D-L., Ms Oxford, 1992. 25. Komi, PX, Stcength and Power in Sport, Blackwell Scienific Publications, Oxford, 1992 lischo, E:W., and Richardson, A.B., Swimming, Blackwell Scientific Publications,20 Adapiation in Sports Training 26. Poortmans, J.R., Effects of long lasting physical exercises and training on protein metabolism. in Metabolic Adaptations to Prolonged Physical Exercise. Howald, H. and Poontnans, J... Birthaucr, Base, 1975, 212 27, Viru, As, The mechanism of training effects: an hypotbesis int J. Sports Med, 5. 219, 1984, 28. Peortmans, JLR., Protein metabolism, in Principles of Exercise Biochemistry, Voortmas, LR, EA. Karger, Basel, 1998, 164 29. Booth, F-W., Pespectives on meclecular and cellular excrciso physiology, J. Appt Physio 65, 1261. 1988: 30. Booth, F.W., and Thomason, .B., Molecular and cellar adaptation of muscle in response 1 exetcse pempectives of varioas models, Payot. Rev, 71, S41, 1991. 31. Bouchard, C., and Malina, R.M., Genetics and olyrupic athletes, Med. Sci. Sports Exercise, 18, 28, 1984. 532 Bouchard, €., Boulay, MLR, Simoneau, J.A., Lorti, G., and Pérusse, L., Heredity and wainablity of aerobic and anaerobic performance. An update, Sports Med. 5. 69, 1988. 33, Viru, A. A bigh performance model, Modern Athicte and Coach, 25(3), 27. 1987 34. Volkov, NLL Haman Bioenergetic in Strenwous Muscular Activity and Pathways for improved Performance Capacity in Sportomen, Amokhin’s Inst. Normal Physiol. Moscow, 1990 35. Volkay, NL, Testr and Criteria for Evaluation of Endurance ix Sportsmen. Cental Inst. Phys. Cult, Moscow, 1989 Gn Russian) 36, Belyayey, ALN. studyof raining and competition loads in volleyball. Thesis of aca. diss. Centra Ins of Physical Culture, Moscow, 1974 tin Russian) 37. Koryagin, VM, study of competition and training loads in bastetbothplayers of high qualification, Thesis of acad, diss, Cental Institue of Physical Culture, Moscow, 1973 (in Russian) Godiky M.A.. Control of Training and Competition Loads, FS, Moscow. 1980 (in Russian). Guminsky, A.A., Tarasov, ALV., Ellzarova, O.S.,and Samsonov, 0.A., A stdy of aerobic and anaerobic indices in ice-hockey players, Teor. Prat. Fi. Rule, 11,39, 1971 (in Russian), 40, Urhausen, A Coen, B Weile, B., and Kindermann, W., Sportmedirinische Leistungsdingnostik and Teaininge-sicacrung in Ruckschlagspiciea, Lecrangsporr, 20, 29, 1990. 41, Astrand, P-O., and Redahl, K.. Texzbook af Work Physioleey, McGraw Hil, New York, 1977 42, Brouha, L. The step fest A simple method of measuring physical fitness for muscular work in young nen, Res. Quart, 14, 31, 1983 43, Wahlund, H., Determination ofthe physical working capicity. Acta Med. Scand., 132 (Suppl 215), 1948, 44. Cooper, K.H.. A means of assessing maximal oxygen uptake, JAMA, 203, 135, 1968. (43, Mader, A. and Heck, HL, A theory of the metabolic origin of “anaerobic threshald”, fr. J. Sports Med. 7 (Suppl 1), 45. 1986 446. Mader, A., Evaluation of the endurance pesformance of marathon runners and theoretical analysis af test results, J. Sports Med. Phys. Fitness, 31, 1, 1991, 47. Concont, F., Ferrari, M., Ziglio, P.G., Droghetti, P., and Codeca, L., Determination of the anaerobic thveshold by a noninvasive field tet in runners,” Appl Physiol, $2, 869, 1982 48, Bar-Or, O, Dotan, Re, Jubar, O., Retstem, A. Karlson, J, and Tesch, P.. Anierobic capacity and auicle ber type distibution. ht J. Sports Med. 1, $9, 1980 4, Jacobs, I, Blood fatate implications for training and sports performance, Sports Med, 3, 10, 1986: ‘30, Volkov, NuL, Shirkovets, EA. and Barilkevich, V.E., Assessment of acrobic and anaerobic capacity of athltes ia. tread cunning tests, Eur. J Appl. Physiol, 34. 121. 1975. 51, Vandewalle, HL, Pérts, G., Heller, J, and Monod, H., All out anaerobic capacity tests on eycle ergometer, Eur. J, Appl. Physiol, 54. 222, 1985. 52, Bosco, C. Lathtanen, P., and Komi, P.V., Simple method for measorcmcal of mechanical power in jumping. Eur. J. Appt. Physiol, 0, 273, 1983 ‘33. Margaria, K., Aghemo, P., and Rovelli, B.. Measurement of muscular power (anaerobic) in man, J. Appl. Physiol, 21, 1662, 1968 54. Hirvonen, J, Rehunen, ., Rasko, Hand Hiirkinen, M.,Bieakdowen of high-energy phosiate compounds and lactate accumulation during short supramarimal exercte, Eur. J. App Piso. 56,253. 1987 55. Kots, JM. Methods of investigation of muscular apparses, Teor. Pratt. Fiz Kule,9, 31,1972 Gn Russian) 456, Sir, WE. The gross composition ofthe body, Adv. iol Med. Phys, 4,239, 1956 a. 4 Viru, A., Human special strenath snd its ontopenctic dynamics, Teor Pratt, Fi Kult. 9. Rassian. 58, Bigland-Ritchie, Ik, EMGHforce relation and fatigue of human voluntary contraction, Etereite Sport Set Ker.. 9,75, 1981. 59. Sale, D., Neural adsplation in strcgth and powcr traning. in Haman Mascle Power, Jones, N.. McCanacy, N.. and McComas, A, Eds, Haman Kinetics Publ, Champaign, 1986, 241 0, Komi, P.V.. Training of muscle strength and power: interaction of pearometoric, hypertrophic and mechani- tal factors, Ind J Sports Med. 7 (Soppl) 10. 1986. te —— SSSRe et nt RM a, Chapter 2 HORMONES IN ADAPTATION TO PHYSICAL EXERCISES (HORMONAL RESPONSES TO EXERCISE) BLOOD HORMONAL ENSEMBLE DURING EXERCISE The task of hormonal regulation is to interfere with cellular autoregulation in order to achieve a pronounced mobilization of bodily resources and functions and to warrant an effective homeostatic regulation (see Chapter 1, p. 4). Thus, hormonal responses are essential both for specific homeostatic regulation and for activation of the mechanism of general adaptation (Figure 2-1). During performance of exercises, hormones have an important fonction in mobilization of energy and protein resources and homeostatic control (see Chapter | 3). They are also essential in regulation of recovery processes after exercise (see Chapter 4). ; ‘Training effects depend on hormonal influences both on transcription and translation, in the adaptive protein synthesis (see Chapter 8). ‘A great amount of data is concerned with hormonal changes in the blood during exercise.'* Figure 2-2 sums up the main effects of various exercises on the endocrine system. If in the case of some hormone responses there is a good accordance between the results of various authors, in regard to other responses there exists a pronounced discrepancy. These discrepancies were not excluded by the general use of radioimmunological methods possessing a high level of both accuracy and specific nature. Consequently, in order to evaluate the actual hormonal changes one must take into account the possibility that there exists a mumber of factors that } determine the response as well as a number of conditions that modulate the response. They ‘both can be connected with the individuality of persons, the parameters of performed exercise, ‘and the conditions in which exercise is performed { STABILITY AND VARIABILITY IN HORMONAL RESPONSES TO EXERCISE In order to determine the stability and variability of hormonal responses to exercise, a number of hormones were repeatedly determined in $2 male persons during a2-h exercise on the bicycle ergometer at the level of 60% VO;max.” Results show that some hormone responses are common and stable (Figure 2-3) while others arc connected with great interindividual differences. According to individual analysis of the obtained data, a rise was common in the concentration of aldosterone and somatotropin both in trained and untrained persons and of corticotropin in trained persons. Common and stable responses were also ‘decreases in insulin and C-peptide. In most of the previous studies a pronounced increase in } aldosterone! and somatotropin,"*™ and decrease in insulin®% and C-peptide levels #27 were commonly detected. Only during short-term anaerobic exercise a drop in insulin may be absent,!25* as well as after exercises of extreme duration a rise in the somatotropin level has not always been observed." In these cases the stable and common responses of insulin and somatotropin are altered to variable ones. A common corticotropin rise has been sug- gested" However, a number of persons were found who did not reveal corticotropin response during prolonged exercise. An exercise-induced response is the increased secretion of corticoliberin by hypothalamic neurosecretory cells.™ an Adaptation in Sports Training eis = — Homeostatic regulation Mobilization of the mecha— To avoid ‘exaggerated ‘fa in the parameters Mobilization Mobilization of internal miliew of energy ‘of protein determining the optimal resgrve® source activity of enzyme: ~~ Hormonal regulation of metabolism FIGURE 2-1. Tasks of hormonal regulation in exercise. ‘There is no doubt that catecholamine responses?! and probably also glucagon,7*S4¥4*45 vasopressin, >" renin, "234644 angiotensin Il,!®" and atrial natriuretic peptide! re~ sponses belong to the group of common endocrine changes during exercise. A pronounced increase was found in the melatonin level during protonged exercise ** The magnitude of this response varies in dependence of lighting as well as of body mass and age.** “The changes in hormone levels that arc common to all persons exhibit an inter-individual variability, but only in the magnitude of changes and in some minor characteristics of the dynamics, e.g. in the dynamics of somatotropin level either a rise throughout a 2-h exercise was observed, or a rise up to @ constant niveau that was maintained until the exercise was stopped; or there was an initial rise, then a constant niveau, and during the final stage of exercise a moderate diminution? ‘A great intraindividual variability” as well as various changes in the group's mean values have been observed in cortisol 22°25 and testosterone** 537404 levels, Five variants have been found in the dynamics of cortisol concentration (Figure 2-4)’: (1) an initial increase that was changed after 20 to 30 min of exercise by a decrease down to the basal level or below it, (2) biphasic increases (peak values during the first 30 min and at the end of exercise, with a decrease after the first peak), (3) a monophasic increase during the whole period of exercise, (4) a lack of alterations or a moderate decrease during the first 20: to 60 min of exer e and pronounced increase during the second hour of exercise, and (5) adecrease during the whole period of exercise. As alterations in the corticotropin level were characterized mainly by a biphasic increase, the dynamics of corticotropin and cortisol coimeided only in the second variant. In the first variant the adrenal cortex did not respond to the second corticotropin peak, in the fourth variant to the first peak and in the fifth variant to either peaks. Nevertheless, there are two eases when the cortisol response to exercise is stable and common. First, a pronounced rise in the cortisol level is commonly observed during and/or after short-term exercise, the intensity of which is above the anaerobic threshold"? The other case is exercise lasting more than 2 to 3 h.'S"!2667! These-facts together suggest that the typical cortisol dynamics is a biphasic increase during exercise whereas the first increase depends on exercise intensity and the second one on its duration. If the first peak is of short duration, the second rise in the cortisol concentration seems to be characterized by maintaining the high level for a long time. ‘An increase in the [-endorphin level is common during short-term high-intensity exer- cise27 However, during prolonged exercise the situation is analogous to changes in the cortisol concentration. A pronounced variability is evident’ due to which some authors ETHormones in Adaptation to Physical Exercises (Hormonal Responses to Exercise) swopsun} 2au20pu> wy sa8urey> paonpurastasox9 Jo si2o4y> onogeIOM: MIE “+E THOT vonteaD 7 hs etecteussdskto —_syaevoboeussn te era (\f vorger30" svouS18007% SW nneou0LeHOs: sisted peweascu] | ~sesuousy eel Srkisc, seas2urg4 Adaptation in Sports Training coms © mem +33 we tore FIGURE 2-3, Stable hormonal responses to 2-h eycling exercise. Solid lines — endurance athletes, interrupted lines — unirained persons. (From Viru, A.. Karclson, K..and Smimova, T. Inc J. Sports Med. 13,230, 1992. With permission ) obtained an elevated i-endorphin level" but the others did not find a significant change”™75 ¢ end of prolonged exercise, During a 2-h exercise at 60% VO,max approximately the same variants of B-endorphin level dynamics were observed in regard to the cortisol pattern: (1) an increase during the first 30 min followed by a decrease below the initial values, (2) a biphasic increase (peak values at the 30th and 120th min), (3) an increase only during the 2nd hour of exercise, and (-#) a decrease during the whole period of exercise (Figure 2-5)."° ‘The results obtained during the 2-h exercise did not allow us to establish any common variants in either testoterone nor progesterone dynamics. However, there are also data atHormones in Adapiation to Physical Exercises (Hormonal Responses to Exercise) 25 FIGURE 24. Five variants of costsol dynamics during 2-h cycling exercise. Solid lines — coetisol dynamics, ‘terropted lines — corticotropin dynannics.(Hrom Wiru, A, Karelson, K.,and Smirnova, TInt J. Sportr Med. 13 230, 1992. With pesmission ) suggesting that during short-term exercise the testosterone level increases while during prolonged exercise it decreases."**! Cumming et al.S observed a significant elevation of the testosterone level in man with a short-term progressive cycling exercise up to the maximal intensity. The same group of investigators found a decreased testosterone concentration in cases of maximal intensity swimming in male and female swimmers. A constant rise in the progesterone level has also been reported.* A common increase-in the estradiol concentration has been noted in women in some papers or in some groups" but in others no exercise-induced elevation has been found. In ‘women, exercise seems to raise progesterone™**” and prolactin *? levels too. The marathon race resulted in a common rise in the testosterone level, but various changes in the progest- erone and estradiol levels. In men, the prolactin response to exercise seems 10 be quite variable” despite some reports indicating a common and stable increase." Exercise- induced responses in the blood level of lutropin and follitropin are variable both men'®2249! and women.**“? There exist data about an increase in some persons and a decrease in others.“ In a recent study the decline in the Iutropin level was preceded by an increase in the corticoliberine concentration in the blood. Ik was suggested that the lutropin decrease was caused by the gonadotropin-depressant property of corticoliberine.™*Adaptation in Sports Training | eo. 807 88 20 304 a 105 2 SigOnameeT oO, oT 20- 205 10- ro 30 60 120 24 04 1 a Spates a 0 30 ‘60 1Hormones in Adaptation to Physical Exercises (Hormonal Responses to Exercise) 2 ‘The exercise-induced responses of thyroid hormones? as well as those of thyrotropin°"* are rather variable. Do the s variants of hormone responses to exercise indicate a different quality of adaptation? Theoretical analysis of various experimental data allowed us to suggest that the functional systems in whose activity the endocrine functions participate, contain not only alterations in the production of related hormones for ‘private regulation’, but also a compli- cated cooperation of actions by the ‘attending regulation’. The latter is actualized by (1) modulating regulation influencing the number and state of cellular receptors, (2) metaboli regulation influencing through other receptors cellular metabolism and thus changing the realization of private regulation, and (3) regulation of the synthesis of proteins participating in the actualization of private regulation. The existence of the regulation of hormonal signal on two levels — on the level of cells producing the signal molecules, and on the level of receptors receiving the signal — makes variability of tactics of adaptive responses possible?” ‘Therefore, the Variability of responses seems to be completely natural. Nevertheless, this seems to happen if there are no strong demands on hormonal regulation. In cases where a decisive role belongs to hormonal regulation, the hormone response is common and stable. THE RATE OF HORMONAL RESPONSES Tn exercise-induced hormonal changes fast responses, responses of a modest rate, and responses with a lag-period can be discriminated (Figure 2-6). Fast response is characterized by a rapid increase in the concentration of hormones in the blood plasma within the first few ninutes of exercise. Typical examples of these responses are rapid rises in catecholamine,”®*”” corticotropin," and cortisol" concentration. A 6-s exercise at the highest possible power output level was sufficient to result in increases in adrenaline and noradrenaline concentrations.!® Significant increases in plasma adrenaline were observed immediately after exercises causing exhaustion within 3.31 or 0.78 min and 15 min after exercises causing exhaustion within 0.1 min, In all cases significant increases in plasma noradrenaline were observed immediately after exercise." Immediately after a I-min anaerobic test adrenaline: and noradrenaline concentrations were increased by 7.1 and 7.4 times the starting valuc.'* Corticotropin and endorphin response was detected 5 min after the I-min test.! While catecholamine response is elicited by direct action of sympathetic nerves to the adrenal medulla and by liberation of noradrenaline from the sympathetic nerve endings for increased release of pituitary trophic hormones, an increased secretion of corresponding liberins is necessary. A 13-min incremental exercise induced a rise in the serum corticoliberine level, associated with an increase in the corticotropin concentration.™* ‘Responses of modest rate are characterized by a gradual increase in the hormone concen- tration which may continue up to the end of exercise or even fora longer time. In other cases the gradual increase during the first period of exercise is followed by a leveling-off to a constant niveau, Examples are increases in aldosterone ™!5 renin,!®" and angiotensin II.'@1 ‘An initial lag period preceding the onset of changes has been described in regard to somatotro- pin,'“° insulin. glucagon“ and calcitonine'™ response. Determination of hormone concentration by 10-min intervals during the first 30 min of exercise (at 60% VO,max) confirmed the lag period in regard to somatotropin and insulin responses. However, it was only revealed as a possibility but not as a common characteristic of the response. Most frequently the lag period was found in the somatotropin response, In the insulin response the lag period was observed only in 25% of untrained persons and in 15% of athletes. FIGURE 2-5. Foucvasianis off endorphin dynamics during 2-h cycling exercise. Each variants characterized by two represcatative cases. (Prom Viru, A, Tendzegoskis, 2, and Smimova.T., Endocrin, Exp. 24,63, 1990 With permission)28 Adaptation in Sports Training FIGURE2-6. Individual dynamics of conicetroin (solid Hine), aldter ne (interrpted line) and somata. Pin (interrupted line with dots) in an 2 untrained person. The alterations of — “dosterone —_coricuopn level belong totter of fat responses, of aldosterone {he group of responses of a modest fie and of tomatotopin — to the 00P of tespomes witha log period, Ceo 180 min 15.201, 1992, wit permesson) Results were also obiained indicating that the response of the same hormone may have Various lanetics depending on exercise intensity, For instance, short-term anaerobic exercises Of Righ intensity cause a somatotropin response of a rather fast rate.° Even the glucagon Fesponse may be quite rapid in these exercises.* Ithas been suggested that there are two types of mechat function at the beginning of excteise. One of them is responsible for a rapid activation, the other for a delayed activations The mechanism of rapid a n has to be connected with the functions of nervous centers and a high rate transfer of nervous influences to endocrine lands. The result of stating the mechanism of rapid activation is fast hormone responses. The mechanism of delayed activation is dependent on some effects of exercises which are cum lative, This mechanism determines the final hormone levels in the blood. If the rate of hormone changes in the first minutes of exercise depends on the degree af activity of the ‘mechanism of rapid activation, the magnitude of hormone change depends on the mechanisin of delayed activation. The response which occurs after the lag period is probably due to the lack of activity of the mechanism of rapid activation According to Galbo's’ interpretation, at the onset of exercise, impulses from working muscles and motor centers modulate the activity. in higher centers of the central nervous system in accordance with the relative work load. In turn, these centers el increased secretion of some pituitary hormones and increased sympatho-adrenal activity, controlling the changes in the secretion of subordinate endocrine cells (Figure 2-7), During continued cxercise, hormone responses are modulated by impulses from receptors sensing temperature, intravascular volume, oxygen tension, and glucose availability. In this way the mechanisms of rapid activation (fast nervous component) and of delayed activation (slow internal milieu component) can be discriminated and their nature understood. Sn ms for activating the endocrineHormones in Adaptation to Physical Exercises (Hormonal Responses to Exercise) 29 “Central motor command’ Hypothalamus, Sm ee: a ; J Adeno— ie hac res | i pe maker prea oe FIGURE 2-7. Control of endocrine Proprio= moter command and impulses from ‘Various ee eee aes ‘The importance of the function of cerebral motor centers has been evidenced by the results of experiments using tubocurarine, which weakens the skeletal muscle and increases the ‘voluntary effort necessary to produce a certain work output. In partially curarized men a higher central command has been associated with exaggerated catecholamine, somatotropin, and. conicotropin responses ata given submaximal work lad and oxygen uptake.7-" The role of the slow internal milieu component has been stressed by the theory of glucostatic control ‘of hormonal responses to exercise (see p. 36). It has been suggested that at least in intensive exercise a significant stimulus for activating the endocrine function may arise from. metaboreceptors of skeletal muscles sensitive to the accumulation of anacrobic products,*7 DETERMINANTS OF HORMONAL RESPONSES ‘SIGNIFICANCE OF EXERCISE INTENSITY Most hormone responses are dependent on exercise intensity. First of all, this has been ceonvineingly demonstrated in regard to catecholamine responses. A curve-linear relation: between exercise intensity and both adrenaline and noradrenaline levels (Figure 2-8) has been established in a number of studies.*°5'%17 Up to the relative intensity of 50 to 70% VOmax, catecholamine changes are only modest or are not detectable. A pronounced. crease in adrenaline and nordrenaline concentrations is followed by a further increase ‘exercise intensity.2%7* *!!0" Thus, there exists a certain level of exercise intensity that triggers the catecholamine response. This exercise level may be termed threshold intensity for hormonal response. Simultaneous determination of lactate levels suggests that threshold intensity for the catecholamine response is closely related to the aerobic threshold.®."™ Most data show that an increase in the blood cortisol concentration is displayed if the intensity of exercise exceeds 60 to 70% VO,max.!577-15811!° Almost the same is revealed in regard to alterations of corticotropin’ and B-endorphin.”'"' Threshold intensity of the activation of the pituitary-adrenocortical system is also closely relaied to the anaerobic threshold. A. close relationship has been found between lactate levels on the one hand and cortisol," corticotropin, and B-endorphin'" levels on the other hand. However, differently from the catecholamine response, in several cases the investigators have failed to obtain results showing any further dependence of adrenocortical activation on the intensity of exercise beyond the threshold load.°*!!""!? The data of Barwich et al.'"? suggest that a high level of hydrogenic ions may suppress cortisol secretion. However, during over-threshold ‘exercises the activation of the pituitary-adrenocortical system is determined by the amount ofa Adaptation in Sports Training RIGURE 2-8. Blood catecholamine levels during exercise with gradually increased inteosity (expressed as W on the Itt side and 25% VO,max on the righ ide) in trained (VO,ax 6544.) ci 1 closed circles) and Serine persons (VO,max 49.2 £98 mi-mier'kg! pen ctces). Consructe from reals of Lehmann et a. tulized possibilities for anaerobic glycogenclysis rather than by the actual imensities of ‘exercise: less intensive but more prolonged acrobic-anacrol ahigher I Sccumulation than a brief intensive anaerobic exercise, A pronounced sctivaten of this endocrine system was established only in the first exercise.!" During tunder threshold exercises a decline in the blood cortisbl level was noticed!3* that ve Trnanably, related to the augmented rate of cortisol elimidation from the blood." A linear relationship has been found between renin activity and exercise in tensity" that was interpreted by the dependence of renin production on the function of the sympatho-adrenal System. The renin response was found at exercise intensities of 60 and 80% ‘VO.max, but not at 25 and 40% VO.max.'5 {here are data about the dependence of other hormone responses on exercise tensity, but a clear-cut dependence has not been demonstrated. When the Intensity of exercise corre- Sponded to 20% VO,max, a drop in the plasma insulin level was noted only with a fat-rich diet, but not with a standard or high-carbohydrate diet. When the load was SO or 70% VO,max, a lenificant reduction in the insulin concentration was detected with all diets wither any further dependence on the intensity of exereise.® Exercise intensities of 40% VO.max” and 47% VO,max!"® seemed to be enough to cause a decline in the insulin concentration. _The existence of a threshold intensity for somatotropin response and ste dependence on exercise intensities has been evidenced in several studies, !"* This threshold tensity has been ‘eported to be about 33% VO.max"” or between 40 and 70% VOmax.” During intermittentHormones in Adaptation to Physical Exercises (Hormonal Responses to Exercise) 31 exercise causing a rise in blood lactate over 4 mmol, the somatotropin concentration increased more than during continuous exercise associated only with the initial elevation of the lactate level up to 2 mmol. It has also been suggested that work intensity is a factor determining testosterone re sponse: work intensity was found to be, positively correlated with increases in the plasma testosterone concentrations." According to Jezova™ plasma testosterone level was elevated at the exercise intensity of 4 W/1 kg of body weight but not at 1.5, 2.0, of 2.5 Wikg. During prolonged exercise at 45% VO,max the aldosterone concentration rose less than during exercise at 60% VO,max;# 20-min cyclic exercises elicited an aldosterone response when the exercise intensity was at least 40% VO,max.'"* During incremental exercise an increase in aldosterone concentration was found at lower exercise intensitites than the cortisol response. However, there are a number of factors that influence aldosterone production. ‘Comparison of the effects of various exercises for improved endurance showed that if there were thresholds by exercise intensity to elicit an aldosterone and somatotropin rise as well as an insulin drop in the blood, they had to be substantially lower than the anacrobic threshold." “The vasopressin response was found at exercise intensities of 60 and 80% VO;max but not at 25 and 40%. The plasma level of atrial natriuretic peptide increased at all four exercise intensities." ‘An elevation in the estradiol level was found after 20 min of rather moderate exercise (30 to 35% VO,max) but only in the post-ovulatory phase. SIGNIFICANCE OF EXERCISE DURATION ‘A considerable amount of results demonstrate the dependence of the magnitude of hormone responses on exercise duration. Of course, if the dynamics of hormone responses is charac- terized by a continuous rise, the increase in the hormone concentration has to reach a higher level with the prolongation of exercise. The situation changes in the following cases: (1) if the dynamics of hormone response is characterized by leveling off to a stable level or by a change in the hormone rise with a decline and (2) if exercises of various intensities are compared. In more intensive exercises an enhanced hormone response is possible when it develops more quickly. At the same time the maximal possible duration of exercise decreases with a rise in ity. Therefore, when exercise. duration is sufficient for a hormone response to reach the peak values, the magnitude of hormone responses is determined by exercise intensity. However, when the time until peak values of the hormone level exceeds exercise duration, the actual hormone level during brief highly intensive exercise is lower than during less intensive but more prolonged exercise, despite the less rapid development of hormone response. In several studies it has been found that in exercises of various intensity and duration the latter might mask the significance of intensity; the hormone responses were more pro- nounced in more prolonged but less intensive exercises,*! At the onset of exercise, impulses from working muscles and motor centers elicit am increased sympatho-adrenal activity and enhanced secretion of hypothalamic liberine, fol- Jowed by the release of pituitary tropic hormones and increased activity of comesponding ‘peripheral endocrine cells. These changes depend on the intensity of muscular activity. These changes in their turn determine the rate of the hormone response.*?” During continuous ‘exercise the slow internal milieu component is added to the’ fast nervous component in the activation of endocrine systems. Hormone responses are modulated by the impulses from receptors sensing temperature, intravascular volume, oxygen tension, and glucose availabil- ity.}4? The role of the slow internal milieu component is stressed by the theory of glucost control of hormonal responses to exercise."™ In exercises with intensity over the anaerobic threshold, a significant stimulus for activation of the endocrine function may arise from metaboreceptors of skeletal muscles sensitive to the accumulation of anaerobic metabolism products «740610622 Adaptation in Sports Training FIGURE 2-9. A scheme of thneshotd intensity and threshold duration of enercise for activation of endocrine responses. (From Viru, A. Int. J. Sports Med.. 13, 201, 1992. With permission ) Consequently, during prolonged exercises the hormone response is determined both by the rate of the hormone response depending on exercise intensity and by changes in the organism. Decreasing availability of carbohydrates, dehydration, or changes in the electrolyte balance are examples of factors additionally influencing endocrine activities. ‘The significance of these factors increases with exercise duration and, accordingly, the need for changes in the hormone ensemble rises with the duration of muscular activity. In some cases the need for hormone responses is revealed only after a certain amount of muscular work has heen done. In this ‘connection it is reasonable to establish a threshold duration of exereise to elicit the hormonal responses (Figure 2-9). In exercises of under-threshold intensities the threshold duration is expressed by the onset of the hormone response. In this connection a long duration of the lag period of glucagon and calcitonin % responses, as well as in some cases the appearance of a rise in the corticotropin and cortisol levels only during the second hour of exercise” can be interpreted. In exercise the intensity of which is over the threshold, the achieved second threshold (threshold duration of exercise) is expressed by changes in the rate of the hormone response or in the appearance Of a secondary activation of the endocrine function (Figure 2-10). In a 2-h exercise the most frequently observed variant of corticotropin and cortisol dynamics was a biphasic increase in their concentrations with peak values during the first 10 to 20 min and again at the end of exercise.” In regard to these two hormones it was established that the first rise in the levels is a short-term one and soon changes by a drop toward the initial values or below them. The secondary activation of the pituitary-adrenocomtical system is characterized by stable cortisol level that may be maintained for a very long time. An expression of this is the cortisol levels after a marathon race,***°*7! triathlon," 2-h skiing,?® and 100 km running, =! However, during a 1000-km run, the daily portion of 60 to 100 km did not elevate the cortisol level! Only a very low running speed enabled this performance, Consequently, there exist minimal exercise intensity levels which will not lead to the activation of the pituitary. adrenocortical system even in an extreme duration of exerci TRAINING EFFECTS ‘The increase of cellular resources duc to training reduces the necessity for overall mobi- lization of resources during vigorous exercise. Inthis connection the necessity for homeostatic reactions may also diminish to some extent. Together, both give a possibility for decreasing the exercise-induced hormonal responses or avoiding them altogether. A great amount of data has been published indicating that adrenocortical, adrenomedullary, and pancreatic a-cells secretion as well as somatotropin production is reduced during moderate exercise due toHormones in Adaptation to Physical Exercises (Hormonal Responses to Exercise) 33 FIGURE 2-10, Donn disor iges Buran, eee ‘excrcisc of oveathreshold intensity is indicated crrermangsnokd nnenety _— by solid lines, im exercises of undertveshld bass ee intensity by interrupted line, When threshold uration is reached, thea in case of oventveshold intensities, ether further increase in horrnonal response fellows, or anew rise in hormone con= centration appearsin addition to the initial short tem increase. In case of undenthreshold inten sity, the bormane response may appear only afer the threshold duration is reached. Hormone Level in Blood Exercise Duration training. The decrease in the blood insulin level becomes less pronounced (see References 2, 3,5, and 128). First of all, these alterations are related to the change in the threshold intensity of exercise for the activation of endocrine responses. After training, the threshold intensity of exercise, neasured in units of power output, is shifted to a higher level.!*™! Thereby exercises that used to be beyond the threshold, were under the threshold after training (Figure 2-11). More intensive exercises that exceed the new threshold level induce a pronounced hormonal response after the training period." Pronounced hormonal responses to exercises of high intensity (in most cases to those exceeding the level of individual anaerobic threshold) are usual findings in highly qualified sportsmen.!°4"!"" When after training, the load of test exercise corresponded to approximately the same relative level (% WO,max) as before the training period, the blood noradrenaline response proved to be approximately the same.‘ However, in one investigation a decrease in the responses of blood glucagon and adrenaline to exercise of the same relative intensity (62% VO,max) was found after trai 2 There- fore, one must not exclude the alteration of threshold intensity in relation to VO.max or a general reduction of activation of endocrine systems. In trained rats the increment in the blood corticosterone concentration was: than in untrained rats after injection of histamine, inhalation of ether, or surgery." A ng-ml 12 1 call kgm- min 1483483 1.483483 7a 0 % 11% before training after training 08 0.4 FIGURE 2.11, The effect of S-min exercise on blood level of adrenaline before and after 7 weeks of training resulting in an increase of VO,max from 3.46 £021 10 423-4 0.13 Imi, The relative VO.eas) and absolve (ke min) imteascy of exercise i indicated on top of colurans. Constructed by WLW. Wier tal °°4 Adaptation in Sports Training In regard to threshold by exercise duration, the training effect has not been established. In a study after a training period a delayed onset of corticotropin and cortisol responses was found during the 3-h exercise at 50% VO;max. After training a delayed decrease in the blood glucose concentration was also observed.!™ When exercise intensity is below the threshold, 4 reasonably greater amount of exercise has to be performed to achieve the threshold by duration in a trained organism. However, some data suggest that in case of a biphasic increase in the hormone concentration (c.g. responses of corticotropin, cortisal, and B-endorphin to prolonged exercise), training promotes the appearance of a secondary activation of endoct systems.» For explanation one must bear in mind that transition from the initial activation of hormone secretion to its inhibition may be connected with the need for time to speed up hormone biosynthesis. If this is so, the functional potential for hormone synthesis will determine the possible time for a secondary activation. ‘Training-induced adrenal hypertrophy is associated with an increased number of mitochon= dria, their vesicular cristae, elements of endoplasmic reticulum, and polysomes in adrenocorticocytes of the fascicular zone as well as with an elevated content of cytochrome a-a; in the adrenal cortex.'"* Mitochondria and endoplasmic reticulum are the main sites of biosynthesis of glucocorticoids. Consequently, the training-induced morphofunctional im- Provement has to be reflected in the augmented potential for hormone synthesis. Adrenal hypertrophy is founded not only on the increase of the adrenal cortex but also the adrenal medulla,'™ Thus, a sports adrenal medulla develops.* The increased capacity of the adrenal medulla for hormone secretion is also founded on the augmented storage of adrenaline and noradrenaline," as well as on the increased activity of tyrosine-hydroxylase and dopamine-B-hydroxylase!” and improved noradrenaline methylation." The taining-induced increase in the capacity to secrete adrenaline. was confirmed by the results about the effects of glucagon, acute hypobaric hypoxia and acute hypercapnia on the adrenaline concentration in the blood of endurance-trained athletes in comparison with sedentary males.!*At the end of a prolonged exercise the adrenaline concentration in the plasma and the estimated adrena- line secretion were higher in athletes than in untrained subjects.'® An expression of the improved capacities of endocrine systems is the increased magnitude of blood catecholamine;*!-*" somatotropin,*="- corticotropin, cortisol" and B-en- dorphin’* responses to supramaximal exercise, and the enhanced plausibility for increase in the thyroxine level during exercise”? in the trained organism. Consequently, in cases of sximal demand on the endocrine system, the hormonal responses are not reduced but magnified in athletes. Some data indicate that the differences in hormone responses may be partly connected with the various rates of responses in athletes and sedentary persons, After maximal cycling exercises until exhaustion the highest cortisol level occurred in endurance athletes just after exercise, but in untrained persons it occurred 15 min" or 1 fi later,'“@ In Junior paddlers a 4-month training period augmented the cortisol response, but decreased the somatotropin, corticotropin and aldosterone response to all-out exercise of 4 min. Obviously, the actual training-induced changes in the hormone response to exercise depend on a combination of various alterations in the organism, including (a) an increase in the working capacity, resulting in a decrease in threshold intensities, (b) a specific adaptation to the training exercises, reducing the need for hormone responses, (e) an augmented lability of endocrine systems reflected in more rapid changes, and (d) an increased functional capacity of endocrine systems, allowing to achieve extremely pronounced and stable changes. In addition, a certain significance may belong to alteration in hormone metabolism. Data were obtained indicating that physical training increases the catecholamine turnover rate in rats." In man this difference was not found in the resting state, but during exercise the adrenaline clearance seemed to be higher in trained persons.!*” Training-induced changes may also occur on show alternated lutropin responses following stimulHormones in Adaptation to Physical Exercises (Hormonal Responses to Exercise) ‘The training-induced alteration in responses of hormones that regulate the water and electrolyte balance (vasopressin, aldosterone) is not evident.!*"*!"© There are only some results lower levels of plasma renin-angiotensin and vasopressin during exercises at equal intensities in trained individuals. In this study a greater absolute amount of fluid efflux to the interstitial space was formed in tained persons." It is reasonable to suggest that these hormone responses depend more on homeostatic needs than on the improvement of physical working capacity and adaptation to exercises. THE INTERPLAY BETWEEN SIGNIFICANCE OF EXERCISE DURATION AND THE FITNESS OF PERSONS To evaluate the relative importance of exercise intensity and duration in hormone re- sponses, the effects of two types of strenuous exercises were compared in qualified male rowers.'" Both tests were performed on a rowing apparatus. One of them consisted of 7-min rowing at the highest possible rate. The other was 40-min rowing at the anaerobic threshold level, determined by lactate 4 mmol-I'. The results indicated that with exercise duration an additional stimulus for cortisol and somatotropin responses arose, resulting in increases in t ‘concentrations of these hormones to higher levels than those in 7-min very intensive exercise (igure 2-12). This experiment was repeated after a year of training. The increased performance capacity was associated with increases in somatotropin and cortisol concentrations to a higher level in the 7-min test and of cortisol in the 40-min test, Thus, training would appear to increase the capacity to secrete hormones. The functional capacity of the pituitary-adrenocortical system was capable of increasing the cortisol level even more, when rowers of national class repeated 2000 m rowing 8 times. Consequently, in strenuous exercise cortisol and somatotropin concentration responses were determined by an integration of exercise intensity and duration, as well as the perfor- mance capacity of the subject, Responses were triggered, obviously, by exercise intensity. An additional stimulus arose from exercise duration. The actual magnitude of the response would seem to depend an the functional capacities of the endocrine systems. HOMEOSTATIC NEEDS The dependence of hormonal responses to exercise on homeostatic needs is obvious in regard to changes of hormones regulating water and electrolyte balances. Vasopressin and the renin-angiotensin-aldosterone complex contribute to renal and sweat gland retention of fluids and electrolytes as well as to regulation of the peripheral vascular tone. Therefore, naturally, the responses of those hormones depend on water and salt supply and environmental t®. These conditions are the main determinants of water and electrolyte regulating hormone responses, rather than the modulating factors. A hyperhydration reduced vasopressin response to 15-min exercise at 70% VO;max.' After salt loading, virtually no increase in plasma renin activity" and aldasterone concentration was observed. During prolonged exercises in the heat, renin and angi creases were significantly diminished by administration of sodium-potassium electrolyte solution, in amounts equivalent to the subjects’ sweat loss.'™ Afler salt depletion the plasma renin activity roughly doubled during exercise. The plasma volume loss and subsequent increase in the vasopressin and renin- angiotensin levels during 4 h of exercise were prevented by progressive rehydration.’ ‘Hormonal control of euglycemia during exercise will be discussed in Chapter 3. FACTORS MODULATING HORMONAL RESPONSES TO EXERCISE During exercise the activity of endocrine systems is determined by the intensity and duration of muscular activity on the one hand, and by the adaptation of the organism to36 Adaptation in Sports Training Sate eee T-min 40-min 8x 2000 min FIGURE 2-12. Somatouopin and cortisol concentrations before, immediately and 30 min after three rowing exercise tests: 7-mnin exercise on rowing appratus performed af supramaximal intensity, 40-min exercise on arowing ‘apparatus performed at the: intensity of anacrobic threshold, 8 x 2000 m rowing at 75 to 85% of the competition velocity (4smin rest periods between exercise periods). Mean and SEM are indicated. Open cicles, interrupeed lines firs experiment on promising junior rowers, Closed circles, solid lines —a year lages, when the rowers had reached 1a performance level of national class. Astesisks denote significant difference (P-<.(5) from the initial values of the group. (Prom Snegovskaya, V., and Vira, A., Eur. J. Appl. Physiol, 67, $9, 1993. With permission.) muscular activity, expressed in physical fitness indices, on the other hand. Besides these three main determinants there exist factors modulating the hormonal response to exercise (Figure 2-13). One of them is emotional strain. Ini a highly emotional situation the adrenocortical response was obtained in exercises of under-threshold intensily.'™ During a more intensive exercise the competitive situation caused a more pronounced increase in the noradrenaline! and 17-hydrocorticoid'® concentration. The dependence of somatotropin response to exercise on emotional strain has also been suggested.* Subjects with high trait-anxiety exhibited both ahigher pre-cxercise adrenaline level and a higher noradrenaline response to exercise (cycling at the heart rate of 170 BPM) in comparison with subjects characterized by low trait-anxicty.'" In another study of subjects with pronounced emotivity, the adrenaline but not the noradrena- line response to exercise at 80% VO,max was exaggerated.™ In persons with high trait- anxiety, serum testosterone and Dy-androstenedione levels were suppressed. An 80-min37 Hormones in Adaptation to Physical Exercises (Hormonal Responses to Exercise) (Cuotssraured tah “2661 “TO ads 'pmmy “y-"tat wos) ‘eAuera8 CAsoua yo uoHeRI| GoM 0} sououNoY Jo sosuodsay uo SIO}>H) sHOLAE yo SUDNYUT JO SUD! “EE DAADL sanper OWRRSIIUIpe 134 pOuseRs Btu ui esconiS wow pic? euequediy pesrecep qe25 0 estes 1 + L bob tot L + + wsaysks 0.035 ep ‘9uuD9pue: abBcoti6 yOUpadi 19 Ayoedeo: mot mo] BURSE) HOMO! oy BIxodKy pesee:cut ler ureas —_s]>@ye voneuiuie jenuy one} Aiédns © ABave = wouuoNAUe §=—feuoqowe = GuIe38 Adaptation in Sports Training eyeling at 80% VO,max caused a pronounced increase in the blood androgens concentrations, but this response was less pronounced in high trait-anxiety persons than in low trait-anxi Persons. Lartropin was higher before, as well as during and after exercise in high trait-anxiety persons. ‘Trained persons performed a 5-min supramaximal exercise twice: once alone in the laboratory, the other time in a competition situation, being stimulated to exhibit the best Performance. In the competition situation the total amount of work was increased by 12 to 21%. The blood lactate level increased to 15.1 0.8 mmol" instead of the 8.6+ 0.6 mmol of exercising alone. Catecholamine excretion was twice as high asafter the exercise performed alone. Before competition exercise the blood insulin concentration was doubled, but the exercise-induced drop was significant only in the competition situatian. In both situations the blood cortisol concentration increased by 18% immediately after exercise and by 20% 15 min after exercise.!® Hypoxic conditions enhance the hormone response to exercise “#4! and induce the Tesponse in exercises of under-threshold intensity.! However, in hypoxic conditions the same absolute work level corresponds to an elevated relative exercise intensity. At the same relative intensities, noradrenaline, somatotropin, corticotropin, and cortisol responses were similar in hypoxic and normoxic conditions. Only the adrenaline response was exaggerated in trained ‘but not in untrained men when they exercised in hypoxic conditions." Hyperbaric conditions? ‘as well as O; breathing" reduced the noradrenaline concentration during exercise During exercise the concentrations of noradrenaline, cortisol, somatotropin, and glucagon are higher when the environment is hor.' Fluid supplement abolished the exaggerated blood Cortisol’ and somatotropin' response to exercise in the hot environment. At 4 to 10°C catecholamine!” and somatotropin '”""”? responses were inhibited ‘The modulatory effect of prior dies on the hormone responses to exercise has been established in numerous studies. Toa large extent, these modulations scem to be related to the differences in carbohydrate supply. A carbohydrate-rich diet!™ ' as well as glucose admin istration**“4°+"" reduce the responses of hormones related to the mobilization of energy reserves (catecholamines, *-!?5!7605177 elucagon,2#41" somatotropin,!™? and cortisol"). In these cases an increase in the insulin level accurs instead of a drop*4*!™ The opposite effects were elicited by low carbohydrate and lipid-rich diets“! fasting -™ and cases of decreased glycogen stores.'™™ The results are in accordance with the view that the glucostatic mechanism plays an important role in determining the hormonal response to exercise.! Probably the main role belongs to the glucose-sensitive centers located in the brain.” It been suggested that the responsiveness of these centers depends on insulin availability during the time preceding exercise. The exaggerated catecholamine and other hormone responses to exercise in states of insulin deficiency such as fasting, intake of a fat diet, and diabetes are considered to be proof of this view.’ ‘There is some evidence that both circadian and sessional rhythms alter the hormone responses to exercise, In most cases when the pre-exercise level is high, the post-cxercise level is also higher, but the magnitude of the response is lower than in cases of low pre-exercise evel due to circadian and sessional rhythms.*""* Hormone responses to exercise are varied to some extent in various phases of the ovarian-menstrual cycle ™"-™ However, this influ= ence is not reflected in all hormone responses." ‘The activity of endocrine systems is controlled by feedback inhibition. It has been found that corticotropin-induced peaks, af the bload cortisol level depressed the subsequent meal- related peaks, the exercise-induced peaks, and augmented secretory episodes at the end of the nnight.""* Intravenous administration of 10 mg dexamethasone 30 min prior to exercise elimi- nated the cortisol response at the 20th minute of exercise at 900 kpm.min-!. In dogs, in the absence of blood cortisol due to treatment with chladitan, the activation of the corticotropin function proceeded more intensively while: standing with a load on the back; the reduction ofHormones in Adaptation to Physical Exercises (Hormonal Responses to Exercise} 9 the corticotropin concentration after its initial increment was less demonstrable as compared to that seen in the normal adrenal function."* According to these data, from the augmented pre-exercise level the blood cortisol concentration usually drops or does not elicit any change during exercise."* "™ There are also results suggesting that a high corticotropin level may suppress the activation of the pituitary function during exercise.” In hormone responses of modest intensity the amplitude or even the direction of changes the blood plasmna hormone concentration depends to a considerable extent on the alteration of plasma volume,"®"! or on hormone elimination rate.''* It has been suggested that the elevated testosterone and estradiol concentrations in short-term exercises are mainly due to the decreased hormone elimination rate!” or due to the decreased plasma volume!!? without actual changes in hormone secretion. Special reviews have refered to many facts indicating the simultaneous occurrence of pronounced fatigve and of decreased activity symptoms of the sympatho-adrenal!”®"*!** and pituitary adrenocortical!**""1% systems both in men and test animals. Differently from other marathon runners, one subject who collapsed after running 15 km had very low testosterone and lutropin values. Instead of an increase in the cortisol level observed in other sportsmen, his cortisol concentration was unchanged.” In a group of middle- and long-distance runners a daily strenuous training regime caused first a pronqunced elevation in the cortisol resting level in conjunction with unusually high responses of cortisol and somatotropin to training exercises. Afterwards a high resting level of blood cortisol was accompanied by a reversed cortisol response and a low somatotropin level after exercise." In conclusion, it must be stressed that hormone responses to exercise are determined and modulated by numerous factors. In regard to hormones controlling energy and protein metabo lism, the main determinants of hormone responses to exercise are the intensity and duration of exercise and the organism’s adaptation to exercise, The modulating factors are the emotivity of a person and the situation in which the exercise is performed, environmental conditions, previous diet, fatigue state, endogenous rhythms, initial level of hormones in the blood, and changes in the plasma volume and hormone elimination rate. The main determinants of hormones controlling the water and electrolyte balance are the shifts in the corresponding homeostatic parameters. Besides the above mentioned factors, pathological conditions as well as age differences may alter the endocrine functions during exercise. When the exercise causes only moderate demands on endocrine systems, there is a pronounced inter-individual variability in hormone responses, and their dynamics express differences in individual tactics of adaptation: adjustments at the level of production of regulative molecules or adjustments at the level of reception of these molecules. REFERENCES 1. Derevenco, P., Ejoryit! st Sistemul Endocrin., Editora Dacia, Cla} Napoca, 1976. 2, Terjung, R.. Endoctine responses to exercise, Exerc, Sports Sei, Rev , 7, 184, 1979. 3. Galbo, H., Hormonal and Metabolic Adaptation to Exercise, G, Thietoe Verlag, Stuttgart, 1983. 4 Fortherby, K., and Pal, S.B., Eds., Exercise Endocrinology, De Gruyter, Beslin-New York, 1985. s Hormones in Muscular Activity, Vol. 1, Hormonal Ensemble in Exercise, CRC Press, Boca Ratoa, 1985, 6. Galbo, I, Exescise physiology: humoral functions, Sports Set. Rev. 1,65, 1992. 7. Kjaer, ML, Regulation of hormonal and) metaholi responses during exercise in humans, Buere. Sport Sei Rev. 20, 161, 1992 ‘8. Viru, A, Plasma hormones and physical exercise, In. J Sports Med, 13, 201, 1992 9. Virw, A Karelson, Kz and Smirnova, T., Sisbilty and variability in hormose responses to prolonged cexercise, Int J Sports Med, 13,230, 199240 Adaptation in Sports Training 10, Adlercreutz, H., Hlirkénen, M., Kuoppasalmi, K., Niveri, H., and Rehunen, 8, Physical activity and hormones, Adv, Cardial., 18, 144, 1976, 11, Castill,D.L., Branam, G., Fink, W., and Nelson, R., Exercise-induced sodium conservation: changes in plasma renin and aldosterone, Med. Se. Spars, 8,208, 1976. 12, Geyssant, A., Geelen, G., Denis, C., Allevard, A.M. Vincent, M., Jarsaillor, E., Bizollon, 1 Laceury, IP. and Charib, C. Plasma vasopressin, renin activity, and aldosterone: effect of exercise and training. Eur J Appl. Physiat, 46,21, 1981 13, Kesunen, K., Pakarinen, A., Kuoppasalmi, K., Naveri, HL, Rehunen, 8. CC, Hiirkinen, M., and Adlercreutz, H., Cardiovascular function and the renin-angioten: system in long-distance runner: during vasious taining periods, Scand J. Clin, Lab, Invest, 40, 429, 1980. 14, Melin, B., Eclache, J.B. Geelen, G., Annat, G., Allevard, A.M., Jarsaillon, Ex Zebid, Ay Legras, JJ. and Charab, C., Plasoa AVP, neurophysin, renin activity, and aldosterone during submatimal exercise performed uatil exhaustion in trained and untrained man, Eur. J. Appl Physiol., 44, 141, 1980. 1S, Sundsfjord, J.A..Strimme, S.E., and Aakvaag, A., Plasma aldosterone (PAA), plasma renin activity (PRA and cortisol during exercise, in Metabolic Adspiasion 1 Prolonged Physical Exercise, Howald, H., Poomtmans, J.P, Eds. Bidkhluser Verlag, Basel, 1975, 208. 15. Buckler, IM. Exercise asa srcening test for growth hoemone release, ctr Endocrin, 8, 219, 1972 17, Hartog, M., Havel, R.J., Capinsehi, G., Earli,J.M., and Ritchie, B.C., The relationship Between changes in sum levels of growth hormone and mobilization of fat during excrcste ia man, Quart J. Exp. Physiol. 52.86, 1967, 1k, Hunter, WM. Fonsenka, C.C., and Passmore, R., Growth hormone: important role in muscular exercise ‘i adlts, Seience, 150, 1051, 1965. 19, Sutton, JAR., and Lazarus, L. Growth hormone in exercise: comparisoa of physilogic and pharmacologi stimuli, J. Appl. Physiol, £1, $24, 1976, 20, View, A Smirnova, T., Tomson, K., and Matsin, T, Dynamics of blood levels of pituitary trophic hormones during prolonged exercise, in Biachemisiry of Exercire IV-B, Poortmans, J, Nist, G., Eds. University Park Press, Bakimore, 1981, 100 - Hartley, Lally Mason, JLWon Hogan, BLP. Jones, LG Katchen, Tubs Mougey, EH, Wherry; PE. Pennington, LL, and Ricketts, PT, Moltiple honnonal respoascs to prolonged exercise i relation to physical training, J. Appl. Physiol,, 33, 607, 1972. sted, J, Galbo, He, Somme, B., Schwartz, Tx Fahrenkrogs J Schaffalitzky de Muskadell, OLB Lauristien, KB, and Trammer, 1, Gactoenteropancreatic hormonal changes during exercise, Am J Physiol , 299, GIR6, 1980, 23, Hunter, W.M., and Sukkar, M.Y., Changes in plasma insulin levels during muscular exercise, J. Physiol. 136, HOP, 1968 24, Layeks, AS. Pirnay, Fa Krzentowski, Gu and Lefebyre, Pa Issulin and glicagon during muscular ‘exercise in normal men, in Biochemisiy of Exercise 1V-A, Poortmans J. Niet J, Eds, University Park Press. Baltimore, 1981, 131 25, Pruett, E.D.R., Glucose and insulin during prolonged work stress in men living on differeat dicts, J. Appl. Physiol, 28, 199, 1970. 26, Pruett, E.D.R., Plasma insulin. concentration during prolonged work at near maximal axyren uptake, J: App Preysol.29, 195, 1970. 27. Wirth, A, Diehm, C, Mayer, I, Micl, HL, Voge, 1, Bjdentrop, P., and Schlicrf,G., Plas C-peptide and insulin in rained and untrained eubjects, 1 Appl. Physiol, $0, 71, 1981 28, Hermansen, Ing Pruett, E.D.R., Osnes, J.B and Giere, F.A., Blood glucose and plasma insulin response to maximal exercise and glucese infusion, J. Appl. Physiol, 29, 13, 1970. 29. Wecker, H., Rettenmeier, A. Ritthaler, Fy Frank, H., Bieger, W.P., and Klett, G.,lafluence of anabolic ‘and catabolic hormones of substrate conceniration dering: various running distances, in Biachemisiry of Exercise 1V-A, Poonmans, J, Nise, G., Eds, University Park Press, Baltimore, 1981, 208 20, Dufaus, By Assman, G., Order, U., Holderath, A, and Hollmann, W., Plast lipoproteins, hormones aod cencrgy substrates during the first days after prolonged exercise, Int J. Sports Med, 2. 256, 1981 31. Dulac, S., Quicion, A, De Carnfel, D., LeBlanc, J, Jobin, M. Cite, J, Brisson, G.R., Lavoie, JM. and Diamand, P., Metabolic and hormonal responses to long-distance swimming in cold water, dat. J. Sports Med. 8,352, 1987 32. Dessypris, A., Wagar. G., Fyrquist, F, Makiren, T., Welim, M.G., and Lamber, B.A., Marathon cua: effects on blood cortisol, ACTH, iodothyronines-TSH and vasopressin, Acta Endvcrin., 98, 191, 1980. 433, Farrell,P.A., Adrcoocortivotropin hocone and exercise, in Exercise Enadocrinofogy. Potherbyy, K..Pal.S.B.. Buds, De Gruyter, Berlin, New York, 1985, 139. as, A.N, Wilson, A. Pandin, MLR, Chane, Utsum), 2, IKayaleth, R.,and Stone,S.C.,Comicotropin ‘releasing hormone and gonadotropin secretion in physically active males after acute exercise, Eur. J. Appl Physiol, 62, 171, 1991Hormones in Adaptation to Physical Exercises (Hormonal Responses to Exercise) 4a 35. ho, H., Richter, Ean Hilsted, J, Holst, J Christensen, NJ, and Henrikson, J., Hoconal regulation during prolonged exercise, Ann. N.Y. Acad. Sci. 301, 72, 1977. 36, Higgendal, L., Hartley, LHL, and Satin, B., Arteria! noradrenaline concentration during exercise ia relation to the relative work levels, Scand. J. Clin. Lab. Dnvest, 26, 337, 1970 37. Hartley, LLH., Mason, J.W., Hogan, RLP., Jones, L.G., Kotches, T-A.. Mougey, EAH, Whetty, F.Ex Penning, L-L and Ricketts, P.T., Multiple boanonal responses to graded excrcise in relation to physical training. J Appl. Physiol 33, 602, 1972 38, Kindermann, W..‘Schnabel, A., Schmitt, WM, Biro. G., Gassens, J, and Weber, F., Catecholamines, roar hormene, cortiso, insulin and sex hormones in aerobic and anacrobie exercise, Eur. J Appl Physiol 49, 389, 1982 39. Kjaer, ML, Epinephuine and some other hormonal responses to exereise in mam: With special reference to pysical training, Int J Sports Med. 10, 1, 1989. 40. Lehmann, M., Keol, J, and DaPrada, M., Plasma catecholamines in rained and untrained volunteers during graduated exercises, int. J. Sports Med. 2. L43, 1981 41, Niveri, H., Keoppasalmi, K., and Hirkdoen, M., Plasma glucagon apd catecholamines during exhaustive short-term exercise, Eur J. Appl. Piysial. 53. 308, 1985: 42. Péronmet, F., Blier, P., Brisson, G., Diamond, P., Ledoux, M., and Valle, M., Repcoducibilty of plasma FIGURE 3-5, Liver glocose outpat during 4-h exercise in man. (From Wabren, J, and Bjéekman, O., Blochemisiry of Exercise IV-A, Poortmans, J, and Niset, G., Es., University Park Press, Baltimore, 1981, 149. With permission.) controls; addition of insulin increased the glucose uptake." When prior swimming increased the glucose uptake by the perfused rat hindquarter, the addition of insulin inte the perfusate did not further increase the glucose uptake.'" There are also data indicating that muscular contractions caused a seven-fold increase in glucose uptake by the perfused muscle from a diabetic rat despite the lack of insulin in the perfusate," Insulin increases glucose clearance in exercising dogs." In pancreatectomized dogs exer cise did not increase the elimination rate of glucose from the blood plasma. In these dogs infusion of minimal amounts of insulin (necessary for maintaining the glucose level in the blood during exercise) did increase the glucose elimination rate during a strenuous but not a moderate exercise." In the cxercising human forearm the glucese uptake was augmented due to administration of insulin.” In normal subjects the use of glucose during exercise can be elevated by hyperinsu after glucose administration." However, the peripheral glucose utili increases in exercise, although there is a reduction in the: circulating insulin lev. (On the basis of all these results taken together, the following conclusions were drawn: (1) insulin is an essential hormone for regulating the flux of gl tional insulin availability does not significantly change the icrement in glucose uptakeSignificance of Hormones in Regulation of Metabolism During Exercise 6 Pg-100 ml h FIGURE 4.6. Blood corticosterone (412/100 ml plasma) and liver glycogen (mg/g of wettissue) in normal rats. aftex swimming for 4, 8, 12 and 16 b. Solid line — blood corticosterone, interraped line — liver glycogen. (From Viru, M, Litvinova, L., Smimova, T., and Viru, A., J. Sports Med. Pipes. Fimess, 1994, With permission.) caused by exercise;"”" (3) the presence of a low concentration of insulin exerts a permissive effect om the glucose uptake by the contracting muscle." ‘Asa general conclusion it was suggested that the presence of insulin is not essential for a small exercise-induced increase in the muscle glucose uptake, but an amount of insulin is required for the full response.'”” "Adrenaline inhibits glucose uptake by the skeletal muscle.!™ Adrenaline suppresses the insulin-stimulated level of glucose uptake as well.! In this connection one may explain the hypoglycemia in:man™ and dogs! during exercise after B-adrenergic blockade. The same result was obtained in rats after adrenaldemedullation.'"° M. Berger et al.17 suggested that the increased glucose utilization is balanced by the combined action of adecreased level af inst and increased levels of adrenaline, cortisol, and glucagon in the blood. However, the dimin- ished hyperglycemic effect of adrenaline during exercise™ suggests that the inhibitory effect of adrenaline on glucose uptake by muscles is completely counteracted by the stimulatory effect of the contractions and insulin. In dogs adrenaline infusion substantially decreased the metabolism of labeled glucose and amplified peripheral glycogenolysis during exercise.!® Adrenaldemedullation abolished the exercise-induced hyperglycemia seen in sham-operated animals." This fact has to be ex- plained by the lack of decrease in blood glucase clearance due to the increased level of adrenaline seen in the normal organism. “The inhibitory effect may be exerted also by somatotropin. In patients with hypopituitarism a moderate exercise of 30 min did not clevate the somatotropin level in the blood as was ‘observed in normal subjects. The blood glucose and pyruvate levels were higher in patients during this exercise and also after 90 min of running." In rats the development of hypoglycemia ‘during exhaustive running was avoided by ganglionic blockade but not by adrenaldemedullation, B-adrenergic blockade, and hypophysectomy. ‘Thus, among factors controlling blood glucose belongs to an essential, critical level of insulin. ization during exercise, the main role BLOOD GLUCOSE HOMEOSTASIS DURING EXERCISE During the first 60 min of light exereise (30 to 40% VO,max) the normal glucose level in the blood plasma is maintained by an increase in the hepatic glucose output that balances the62 Adaptation in Sports Training increase in glucose utilization by working muscles and other tissues. The regulative role sulin and glucagon in these changes was considered to be minimal, since no change in their levels was detected over the first 60 min of light exercise." In another study these changes were also detected in 60-min exercises at 40% VO,max.' During a more strenuous ‘r more prolonged exercise these changes are pronounced. Even in these circumstances, the precise role of the mentioned hormonal changes in glucose homeostasis is not clear. A study Of pancreatectomized dogs led to the suggestion that changes in insulin and glucagon concentraions were not necessary for the regulation of blood glucose concentration in exer- cise." In contrast, the use of various combinations of somatostatin and glucagon infusion during exercise indicated that the ratio of glucagon to insulin was directly correlated with glucose production.'* The importance of the glucagon response in stimulating glucose pro- duction in exercising dogs has been confirmed in a more recent study.*® When changes in insulin and glucagon were prevented with the aid of simultaneous infusion of somatostatin, insulin, and glucagon, the plasma glucose concentration fell during Uh of exercise at 40% VO;max. The fall was particularly pronounced if high level of insulin (approximately 20 pmol-ml-!) was maintained during exercise. In this ease the glucose uptake increased to a greater extent than in the normal situation, and glucose production did not increase sufficiently to compensate for the increase in glucose uptake associated with an elevated rate of glucose oxidation. It was concluded that during prolonged exercise there must be a reduction in insulin concentration and/or an increase in glucagon concentration if euglycemia is to be maintained. If such changes do not occur, hypoglycemia follows.” During the experiment of somatostatin, insulin, and glucagon infusion, adrenaline and nora- drenaline levels were elevated more than in normal conditions. Despite that, hypoglycemia occurred.” MOBILIZATION OF LIPID RESOURCES ‘The main link in the mobilization of lipid resources is the activation of lipases. Hormone- ‘sensitive lipase is the rate-limiting enzyme in the lipolytic process. For its activation human adipocytes possess stimulatory B-adrenoreceptors besides inhibitory c-reccptors. The activa- tion of the enzyme is effected through reversible phosphorylation catalyzed by cAMP (see Reference 201). In the activation of lipases, a number of hormones participate (Figure 3-7). Their role during exercise was well demonstrated by P.D. Gollnick and co-workers." They found that ‘exercise-induced lipolysis was depressed by hypophysectomy or by -adrenergic blockade in rats. The combin: of hypophysectomy and B-blockade completely abolished the exercise- induced rise in the adipose and plasma levels of free fatty acids. The B-adrenergic blockade excluded the lipolytic action of catecholamines and impaired the increased secretion of glucagon. Hypophysectomy aggravated the activation of the pituitary-thyroid and pituitary- adrenocortical systems and climinated the direct actions of somatotropin, thyrotropin, and corticotropin. In another experiment the increase in the plasma level of free fatty acids induced by a I-h swim was abolished by adrenalectomy, hypophysectomy, or thyroidectomy; B-adrenergic blockade or adrenaldcmedullation did not prevent free fatty acid release.” A large body of experimental data has been collected about the significance of the lipolytic action of catecholamines during exercisc. In rats the exercise-induced release of free fatty acids was impaired after adrenaldemedullation™ as well as after chemical sympathectomy." In adrenaldemedullated rats the free fatlty acid response to exercise was normalized by adrenaline administration. In untrained rats the B-blockade was effective, but not in trained ones.* Effective B-blockade was shown in exercising dogs" and men" in regard to the release of free fatty acids. The results of a study suggest that the catecholamine-induced increase of lipolysis is mainly mediated via beta-I-adrenoreceptors.™ Total blockade of B-receptors by propranolol fully prevented the reduction of the triglyceride level both in theSignificance of Hormones in Regulation of Metabolism During Exercise 63 sulin Suppcession Glucose Adrenaline ae jucagan Sgmateiopin —_ Sir meen: “Thyroxine oeaeealors zh ive cca Pani erat cwoseicaton Cortisol Free Fi bee ae > Glycerol ae alease into boed stream FIGURE 3-7, Hormomal conirol of lipolysis during exereise. red muscle and in the myocardium" during swimming for 3 h with an additional load of 1% body weight ‘no convincing evidence as to the special role of glucagon in exercise-induced lipolysis. H. Galbo'! suggests that the role of glucagon in this process is not indispensable. During exercise the increase in the blood level of somatotropin is usually accompanied by an elevated concentration of free fatty acids. Both responses are eliminated by glucose administration.» The role of pituitary hormones in exercise-induced lipolysis is emphasized by data about the depression of a risc in the free fatty acid level due to hypophysectomy.!°522 Nevertheless, in patients with hypopituitarism, a moderate exercise for 30 min did not elevate the somatotropin level in the blood, as was observed in normal subjects, but the increase in the bleod concentration of glycerol, free fatty acids, and Ketone bodies was even more pronounced.” When patients with Cushing’s disease were both adrenalectomized and hypophysectomized, the rise in free fatty acids and glycerol persisted during exercise.” In normal men a prior somatotropin administration clevated its level but not the free fatty acids response during exercise. The lipolytic effect of somatotropin, unlike:that of other lipolytic hormones, requited a lag period of at least 1 h.'!* Hence, the presence or absence of simul- taneous and comparable changes in the blood levels of somatotropin and free fatty acids does not have any physiolagical meaning. Thus, no coavincing evidence of the decisive role of pituitary hormones in lipolysis in humans during exercise is as yet available. ‘There is some evidence of the participation of thyroid hormones in the mobilization of lipid resources during exercise, In dogs, administration of thyroxine or triiodothyronine enhanced the rise in the free fay acids level during runs of 15, 30, and 60 min.?” In hyperthyroid patients, exercise-induced increase in the free falty acids concentration Was more pronounced than in normal persons.2!° In exercising thyroidectomized dogs, the plasma free fatty acids level !!212 and free fatty acids tumover rate?!" were far below those found in normal dogs during exercise. Accordingly, both at rest and during exercise, normal rats maintained higher plasma levels of glycerol and free fatty acids than thyroid-deficient animals.*!' Thyroid hormones have also been implicated in the lipoprotein changes induced by phy’ cise ‘Adrenalectomy decreased the rise in the free fatty acids level in the blood plasma during prolonged exercise.'™52 Cortisone treatment reversed this change.'" However, ina Adaptation in Sports Training adrenalectomized patients with Cushing’s disease the exercise-induced rise in the plasma levels of free fatty acids and glycerol were more pronounced than in normal persons, in spite of the higher level of insulin” This can be altributed to the effect of the higher levels of corticotropin, noradrenaline, and glucagon in those patients. The glucocorticoid aetion on lipolysis is not a direct effect, but rather a permissive influence on adrenaline and other hormone actions.?!* sulin possesses a direct antilipolytic action.*!* This effect is related to the decrease in the cAMP content?! and increased cAMP-phosphodiesterase activity?” as well as to conversion ‘of the hormone-sensitive lipase from the phosphorylated to the dephosphorylated state.2* It ‘was suggested that during prolonged exercise the decrease in the blood insulin level was a tool for the transition from utilization of carbohydrates to lipid oxidation.™*!" This standpoint was confirmed by reciprocal changes in insulin and free fatty acids concentrations during pro- longed exercise, as well as by the exaggerated free fatty acids and glycerol responses andl fatty acids oxidations to exercise both in diabetic animals*"'2! and diabetic patients.2# Insulin treatment tended to normalize these responses to exercise?” In insulin-deficient diabetics fat oxidation accounts for a selectively larger portion of total fuel utilization by the exercising muscle than is observed in healthy persons.” Lipolysis was also higher during exercise when the subjects were made hypoinsulinemic by prolonged fasting." Furthermore, enhancement of the exercise-induced depression of the plasma insulin concentration by infusion of soma- iin was accompanied by accelerated lipolysis The exercise-induced decrease in the muscle triglyceride content and their oxidation is higher in pancreatectomized than in normal dogs. Ta conclusion, adrenaline is the main hormonal factor inducing intensive glycogenolysis in exercising muscles as well as lipolysis in the adipose tissue. These effects of adrenaline. are supported by the permissive action of glucocorticoids, Besides adrenaline, the lipolytic action also belongs to glucagon, somatotropin, thyroxine, and some other hormones. One cannot exclude their participation. However, there is no convincing evidence of their decisive role. inc is not responsible for the increase in hepatic glucose output. In this process the main significance belongs to hypoinsulinemia and probably also to direct nervous influences. Hypoinsulinemia docs not exclude: glucose transport to muscle cells. Some results suggest the participation of somatotropin in the control of glucose utilization during exercise Hypoinsulinemia is a decisive factor in the mobilization of lipid resources. The lipolytic action of various hormones can be actualized only after the decrease in the insulin level in the blood. tos MOBILIZATION OF PROTEIN RESOURCES “Typical responses to acute exercise are suppressed protein synthesis and elevated protein degradation%2% Comparison of these responses in muscles containing various types of fibers indicated that the rate of protein synthesis was suppressed and the rate of protein degradation «was elevated mainly in muscles less active during exercise” Thus, the less active muscles, but not those that fulfill the main task during exercise performance, are used as a reservoir for mobilization of protein resources. The exercise-induced catabolism is not extended (o contrac tile proteins.2 During exercise the catabolic response is extended to the smooth muscle of the gastrointestinal tract, lymphoid tissue, liver, and kidney (see Reference 226), Both the antianabolic and catabolic effects have to be considered as tools for mobilization of protein resources during a stressful situation (Figure 3-8). As.a result, an increased pool of available free amino acids is created. Due to the suppressed protein synthesis, the free amino ‘acids pool is used for supplying the necessary protein synthesis by ‘building materials’ only toa minor extent. The amino acids are mainly used for additional energy supply to contracting muscles. There are at least three pathways connecting. free amino acids with cnergy processes. One of these consists in the oxidation of branched-chain amino acids. The main site of this i... reSignificance of Hormones in Regulation of Metabolism During Exercise 65 Inductor Effect a ae of Protein Metabolites = FIGURE 3-8. Cisation and utilization of the pool of free amino acids daring exercise. pathway is the contracting muscle, An increased oxidation of leucine during exercise was established in human?" as well as in animal="!2" studies, The metabolism of several amino acids Ieads to the formation of metabolites of the citric cycle, which also has a beneficial effect ‘on muscle metabolism by increasing the capacity of the citric eycle for oxidizing the ace CoA units generated from pyruvate and free fatty acids * A pathway goes through alanine (and glutamine) formation in the muscles from pyruvate and amino groups reversed in the oxidation of branched-chain amino acids (Figure 3-8). Alanine is transported by the blood to the liver where the nitrogen-free products of its deamination are used im gluconeogenesis.'** A by-product of amino acid use is urea formation al the expense of the released amino groups. ‘Many of the alterations in the hormonal ensemble during exercise favor (or even constitute the main cause of) protein and amino acid mobilization. First, attention must be paid to the action of glucocorticoids. The general catabolic action of glucocorticoids has long ago been documented by the negative nitrogen balance. Regarding muscular tissue, it has been shown that glucocorticoids cause a suppression of protein synthesis, augmented release of amino acids, clevated protein degradation rate, enhanced activity of myofibrillar proteases, and increased excretion of 3-methylhistidine 2" Alll these changes are undoubtedly subjected to many control factors and the similarity of responses caused both by glucocorticoids and exercise does not prove the single role of glucocorticoids. For example, in adrenalectomized rats the dynamics of 3-methylhistidine excretion during and after daily moderate exercise was found to be the same as in normal animals ‘The many factors involved in the control of protein and amino acid mobilization during exercise (Figure 3-9) are emphasized by studies that indicate that muscular activity exerts a protective effect against the catabolic action of glucocorticoids on the muscular tissue.!%!? ‘This effect probably rules out the possible harmful action of a high level of glucocorticoids. Muscular activity inhibits the stimulating effect of glucocorticoids on myofibrillar alkaline proteases." Here a substantial role may be played by the opposite action of testosterone.66 Adaptation in Sports Training cane - bene thesis mutation Cetmnnanon es aaa FIGURE 3.9. Hormonal contol of amino acid metabolism during exercise ‘Systematic muscular activity did not stimulate the alkaline proteolytic activity of the skeletal muscle if testosterone was administered simultaneously.” Accordingly, G.L. Dohm and T.M. Louis" found that decreased testosterone concentrations during muscular activity might promote the apparently increased protein catabolism evidenced by elevated urea excretion. Besides testosterone, the inhibitory action of adrenaline and cAMP on muscle protein degra- dation may have some significance as well.2?* However, in rats after administration of sympatholyte the increase in the urea concentrations in the blood, muscle, and liver was less pronounced than in the control experiment.*” The significance of the inhibitory action of sulin on proteolysis? is questionable because of its decrease during exercise It was mentioned above that the site of the catabolic response to exercise is within the inactive but not the active muscles. Therefore, at least during acute exercise, the protective effects against the general catabolic action of glucocorticoids may contracting muscles. This question still waits for an answer. Calcium (Ca") is a factor stimulating proteolysis in the skeletal muscle (see also p. 206) ‘Therefore, the influence on protein degradation may begin with the release of calcium ions from the sarcoplasmic reticulum during the excitation of the muscle cell. The action of amplifies or modulates the response primarily induced by Ca"* itis not impossible that the in vive accumulation of calcium ions up to the level of ing proteolysis is related to the alterations in the function of the calcium pump. vel of glucocorticoids in the blood and hypoinsulinemia common to vigorous exercise provide a stimulus forincreased alanine production. Thyroxine may provide an additional stimulus here. The significance of glucocorticoids during exercise has been confirmed in adrenalectomized patients with Cushing’s disease. Exercise caused a less pro- nounced increase in the blood plasma alanine concentration in these patients than it did in normal persons.” J.B. Critz and TJ. Withrow! established an increased transaminase activity in the skeletal and heart muscles after swimming. In rats, after‘adrenalectomy or pharmacological blockade of adrenocortical activity, no increase in transaminase activity was found. Hence, the process of enhanced transamination of amino acids, including. alanine formation, is dependent on the adrenocortical activity. Studies in vitro have shown that adrenaline or CAMP application inhibits alanine release from the skeletal muscle. Adrenaline also reduces alanine formation in the muscles obtained e directly from the‘ance of Hormones in Regulation of Metabolism During Exercise oT Blood plasma Activity of Na-K-ATPase corticosterone content in microsomal fraction of Hg 100 mr" myocardium cells (iM of P per img of protein during 30 min.) 40 10 shrs ‘Swimming O1tSmin 90min ' FIGURE 3-10. Dynamics of blood corticosterone level (solid fine) and activity of Na,K-ATPase in myocardiom during prolonged swimming at 3310 34°C, From Kérge, P. Roosson, $..and Oks, M., Acta Cardiol. 29, 303, 1974. With permission.) from diabetic tats or animals treated with thyroxine or cortisone. However, alanine and glutamine formation from precursor amino acids is unaffected by adrenaline or cAMP application It scems reasonable to assume that in the exercising normal organism these effects of adrenaline are negligible, as alanine production still rises despite hyperadrenalinemis. ‘Hypertestosteronemia duc to testosterone infusion caused a diminished alanine level during exercise? Therefore, changes in the blood testosterone level may modify the alanine re~ sponse toexercise. Glucagon or prostaglandin E, application did not interfere with alanine and glutamine release by the isolated skeletal muscles. Besides gluconeogenesis, amino acids may also be used for protein synthesis in the liver during exercise, A decreased incorporation of labeled amino acids into liver proteins was observed in rats sacrificed immediately after swimming for 90 min, while the level of free amino acids in the liver decreased by 43%. Such a combination suggests that the main use of amino acids is probably for gluconeogenesis. Immediately after swimming for 12 h protein synthesis continued to be depressed in the muscle, but returned to normal in the liver tissue. ‘The level of free amino acids remained below normal (by 57%). In this situation the hepatic free amino acid pool was, obviously, also used for protein synthesis to a remarkable extent. In this series in female rats an increased blood corticosterone level was observed only after swimming for 12 h. Tt was suggested that the augmented adrenocortical activity might be of yportance for the restoration of the protein synthesis rate in the liver in conditions of enhanced energy demands. The stimulation of protein synthesis. in the liver, amino acid transport into hepatocytes, and gluconeogenesis by glucocorticoids are well established phe~ nomena. ‘The role of glucocorticoids in the use of free amino acids by the liver during exercise was demonstrated in studies after swimming for 3 h. This exercise caused an increase in the blood68 ‘Adaptation in Sports Training corticosterone level, accompanied by a decreased free amino acid level and an augmented alanine aminotransferase activity in the liver of sham-operated rats, In adrenalectomized rats these changes were not observed, but they appeared again when corticosterone was adminis- tered to adrenalectomized rats before swimming, While swimming induced a trend to a decreased amino acid level in the muscles of sham-operated rats, in adrenalectomized rats the opposite trend was observed. Differently from normal rats, adrenal insufficiency excluded the exercise-induced rise im the alanine levels of blood plasma, oxidative muscle, and liver. While in normal rats elevated alanine contents were associated with an increased activity of alanine-aminotransferase in oxidative fibers, in adrenalectomized rats the enzyme activity did not change in muscles and decreased in the hepatic tissue during exercise. The dependence of exercise-induced changes ‘on corticosteroids was confirmed by the increase of the enzyme activity after exercise in adrenalectomized rats treated with 125 jig of corticosterone, In normal rats, training excluded both the rise of blood corticosterone and activation of hepatic alanine-aminotransferase during exercise. Thus, the stimulation of the glucose-alanine cycle by glucocorticoids promotes the alanine supply and utilization in the liver during exercise. In adrenalectomized rats, arginase activity decreased during exercise in conjunction with a lack of further elevation of urea levels in the blood, liver, and skeletal muscles. Consequently, the use of alanine and other amino ids for urea formation depends on glucocorticoids.“ Evidence of the dependence of tryptophan oxygenase activity on the induction of enzyme synthesis by glucocorticoids was obtained in experiments with adrenalectomized rats. Hepatic tryptophan oxygenase activity in rats after prolonged swimming was suppressed by adrenalectomy and elevated by administration of cortisol for 5 days prior to adrenalectomized rats, When the RNA synthesis was blocked by treatment with actinomycin D, cortisol did not elevate the enzyme activity.2** Thus, the change in tryptophan oxygenase activity was founded ‘on the enzyme induction by glucocorticoids. Despite the general suppression of protein synthesis in skeletal muscles during exercise, the intensified synthesis of some particular proteins during exercise cannot be excluded. For ‘example, during exercise the “C-leucine incorporation into both myosin heavy chain and actin decreased, but increased into the myosin light chain.*” Reasonably, there may be an increased synthesis of some regulatory proteins as well Swimming caused an elevation of the activity of Na’,K*-ATPase. A period of swimming for 90 min was required to detect a statistically significant increase in the enzyme activity in the microsomal fraction of the myocardial cells of untrained rats (Figure 3-10). Further ‘continuation of exercise up to 6 to 10h was accompanied by the return of the enzyme y to the initial level. After an extreme duration of exercise (more than 16 h) the Na’,K*-ATPase activity decreased significantly. The dynamics of plasma corticosterone concentrations and the activity of myocardial Na*,K*-ATPase were: approximately parallel during these exer- cises.* In the skeletal muscle with predominantly white fibers the Na’,K*-ATPase activity was increased immediately after swimming for 90 min and dropped to the initial level after swimming until exhaustion. In the muscle with predominantly red fibers no significant changes were found. In previously trained rats swimming for 1.5 hdid not increase cither the plasma level of corticosterone or the myocardial NaK*-ATPase activity. After an extreme duration of swimming (18 to 20 h) corticosterone in the blood of trained rats remained at an elevated level and the Na’K*-ATPase activity did not differ from the initial levels.” Rats exhausted by a I-week hard training regimen, exibited a decreased level of corticosterone in the blood and a diminished Na*,K’-ATPase activity in the skeletal muscle.“? ‘Swimming with an additional load of 3% body weight until exhaustion (mean duration 201 niin) caused a substantial increase in the Na‘,K'-A'TPase activity in the myocardial cells of normal rats. In adrenalectomized rats the lowered enzyme activity persisted after the exercise *!I EE a | Significance of Hormones int Regulation of Metabolism During Exercise ro) “These studies led to the suggestion that during prolonged exercises an additional synthesis ‘of Na’,K,*-ATPase is necessary for maintaining an adequate function of the Na’,K*-pump. } “The induction of this synthesis obviously required a sufficient supply of glucocorticoids. In conclusion, mobilization of protein resources is the function of the pituitary-adrenocor- tical system. However, as everywhere in the organism, this function is actualized in compli- cated cooperation with other regulatory factors. The co-action of various hormones obviously ‘excludes a dangerous exaggeration of the glucocorticoid catabolic action. HOMEOSTATIC REGULATION OF WATER-ELECTROLYTE ;ALANCE DURING EXERCISE | During exercise perspiration is called forth to avoid overheating of the body. Water losses by perspiration make it necessary 10 inhibit diuresis with the aim of preventing dehydration. When total body water declines during work, the level of plasma water is relatively well ‘maintained because there is a rapid exchange of water between the plasma and extravascular sources.5®"Thus, water losses are, in great part, made up from intracellular water. The result is intracellular dehydration, which may impair cellular metabolism. A loss of water of more than 2 to 4% of body mass disturbs the cardiovascular function and causes a decrease in the ‘working capacity in humans.*" The inhibition of diuresis by stinmulating water resorption in the tubulus of nephrons is the function of vasopressin. However, the antidiuretic action of the clevated level of vasopressin can be opposed by the influences of other factors. The main result of vasopressin at the kidney level — the increased tubular resorption of water — is not always revealed during exercise, B. Melin et al found that during all-out exercise at 80% ‘YO.max the vasopressin concentration in the plasma increased 4.8 times but the decrease in } the urine flow was not statistically significant. "The water content of body fluid compartments depends on osmolality. To check water resis independent of plasma and urine osmolality, the free water clearance is calculated. During exercise the free water clearance tended to become positive in humans, ‘This change was in combination with the increased vasopressin concentration in the plasma2™ During repeated exercises the increases in the vasopressin level and plasma osmolality were sim taneous.25 Prostaglandins may block the action of vasopressin. Nevertheless, in men an inhibition of prostaglandin synthesis was evoked by aspirin administration for 3 days prior to exercise. This procedure, however, did not influence the alterations in creatine clearance, urine volume, osmolar clearance, and electrolyte excretion.” During exercise the water balance is influenced not only by water losses due to perspira- | diuresis, and exhaled water vapor, but also by the production of water in glycogen breakdown and oxidation processes." It is calculated that during endurance exercises the combustion of glycogen leads to a release of intracellular water that can amount to 1.5 | or nore in a well-trained 65-kg athlete2** Nevertheless, in humans water losses usually exceed | the intracellular water output. ‘The sweat excreted by humans during exercise is hypotonic, thereby preserving the salt stores 2" Of all the chemicals lost with sweat, sodium and chlorine make up by far the most ‘At the same time, these ions are primarily responsible for maintaining the water content of the extracellular compartment2” In spite of the faet that in sweat the concentration of sodium and chlorine are roughly one third of that found in the plasma,*” the total loss of 4.1 1 (5.8% reduction in body weight) resulted in Na* and Clr losses of 155 and 137 mM, respectively, in comparison with K* and Mg** losses of 16 and 13 mM. These sweat losses produced a defeit in the body sodium and chlorine of S and 7%, respectively. At the same time the total body K* and Mg" decreased less than 1.2%.4@70 Adaptation in Sports Training ‘Therefore, prolonged exercises cause, above all, the loss of ions that are mainly extracel- lular. In connection with the loss of Na’ the question arises as how does it act on the transmembrane ion shift that initiates the process of excitation with the cell type-specific physiological response, including the contraction act in the muscle cell? It must be noted that a more pronounced water loss helps fo maintain an adequate sodium concentration in the exctracellular compartment and, thereby, avoids the decrease in the ionic gradient for sodium, ‘Usually, during prolonged exercise the sodium concentration in the plasma does not decrease, ‘or it may even increase a little? B. Melin et al‘ found a significant increase in plasma ‘osmolality during exercise at $0% VO.max in well-trained sportsmen. In less-trained sports- ‘men and untrained persons plasma osmolality did not change. However, a critieal decrease in the sodium concentration in the extracellular compartment is possible if during exercise sweat losses are replaced by water without any addition of salt The renin-angiotensin-aldosterone system controls the sodium level in the extracellular compartment. The main effect of this system is an ingreased Na* resorption with the aim of conserving sodium in the organism. The occurrence of this effect of aldosterone during prolonged exercise has been demonstrated by DL. Costill et al." This is evidenced also by the decreased sodium concentration and Na/K ratio in the urine as well as by the increased potassium excretion during exercise” The latter is some compensation for the release of potassium from the muscles as a result of glycogen and protein breakdown?! V.A. Convertino et al. found a pronounced increase in the plasma volume together with elevated plasma osmolality and albumin content during 8 days of repetitive 2-h cycling at 65% ‘VO,max. They associate-the plasma hypervolaemia with the rise in plasma vasopressin as well as renin concentration that stimulate aldosterone production through conversion of angio- tensin I to angiotensin II. Additionally, the rise in albumin concentration provided increased water-binding capacity for the blood. During a $00-kin road race that extended over 20-days, ordinary flow rates, creatinine clearance, osmotic clearance, and free water clearance as well ‘as urinary excretion of vasopressin showed no significant change in the runners. Plasma, ‘osmolality and urinary aldosterone excretion increased. As a result of aldosterone: action, the urinary sodium concentration and the percentage of filtered sodium excreted were signifi cantly lowered on the days of running. “The distribution of water and electrolytes between the extra- and intracellular compart- ments and the rate of related transmembrane shifts depends on the Na,K-pump function. The ‘energy for the Na,K-pump activity is provided by hydrolysis of ATP. The activity of Na,K- ATPase catalyzing this process depends on shifts in sodium and potassium concentrations between the extra-and intracellular compartments. At the same time, hormonesalso exert their action on the enzyme. - Studies of the Na,K-pump function in exereise gave two main results. First, after a very prolonged period of exercise the efficiency of the Na,K-pump decreased in the myocardial and skeletomuscular cells in association with the reduced Na,K-ATPase activity. As a conse- quence, sodium ions are not eliminated from the muscle cells and their concentration in- creases.” The resultant increase in the osmotic pressure of the intracellular compartment causes the accumulation of water inside the cells. The second main result was the relat these changes to the decreased adrenocortical activity (see above). Later the activation of the Na,K-pump function by exercise was confirmed. Under resting conditions i vitro less than 10% of the total population of Na,K-pumps in skeletal muscles is utilized. Hence, there is a considerable spare capacity for active Na,K-transport to be used during exercise. Neverthe~ less, the muscle contains too few Na,K-pumps to maintain its K* content when assuming full activation of all the available Na,K-pumps. These estimates are in keeping with the obserya- tion that during contractile activity, muscles undergo a net loss of K*. Therefore, the concentration of Na,K-pumps in skeletal musele is rate limiting for the K* homeostasis during exercise. A wide variety of studies have shown that adrenaline and noradrenaline atSignificance of Hormones in Regulation of Metabolism During Exercise 1 Adrenaiine Na, K-pump =< Conisot Thyroxine Plasma Momorane Extracellular Intracetular Compartnent Compartment Loss by. Naa— Ana sweat _— k« |" ok Aalyeoen nee a Brea fo a fon = ioe om Stimusaton of Na ss resorption in renal tubules, ALDOSTERONE (Na conservaton)| water resorption in ———— renal tubles by VASOPRESIN: Ua eaten ~N Loss by Inhibition of K rime resorption in renal tubles by ALDOSTERONE (& elimination) FIGURE 3-11. Hormonal control of water, sodium, and potassium shifts during exercise, physiological concentrations stimulate active Na*,K*-transport in muscle fibers by up to 100% within a few minutes." The regulative significance of the exercise-induced increase in catecholamine levels is indicated by the fact that hyperkalemia caused by exercise is exaggerated when the B-adrenoreceptors are blocked Activation of the Na,K-pump is induced also by insulin. However, the drop of insulin secretion during exercise makes this regulatory influence doubtful during acute exercise. “Training produces an increase in the Na,K-ATPase activity in the sarcolemma as well as the total concentration of [*H]-ouabain binding sites (Na,K-pumps) in muscle biopsies ‘This effect may be related to the thyroid hormone-induced up-regulation of Na,K-pump concentration.*2"! Figure 3-11 sums up the role of hormones in control of the water- electrolyte balance. a 28 i 2d Eo] > =e 30] ©‘ e 8p 2% FIGURE 3612, Dynamics of caciom (mer |B rupted line) and calcitonin (solid line) vets 884 & in blood plasma during profonged exercise. Sg 1 (From Dracvetskaya, | A, and Limanskii, NS N.,Sechenoy Pitysiol. J. USSR, 64, 1498, 1978, o 0. With permission ) o 0s & Shes.n Adaptation in Sports Training Powerful regulators of calcium metabolism are calcitonin and parathormone. 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JL» and Hollosay, J0., Persistent increase in glacose uptake by eat skeletal muscle Following exercise, ‘Am. J, Physiol, 241, C300, 1981 189, Wallberg-Henriksson, H, and Hollosay, J.0., sein s not necessary forthe stimulation of muscle glucose uptake by contractile activity, Acta Endocrinol, 106 (Suppl. 263), 264, 1984, 190, Issekutz,B., Paul B., and Miller, HL, Metabolism in normal and pancreatomized dogs during steady-state exercise, Am J, Physiol, 213, 857, 1967 191. Trap-Fensen, J; Dahl-Hansen, A.B. Kil, C., and Moer, J. Effect of sulin on glucose uptake in the exercising human foreacm, seta Endocrinol, 8 (Soppl. 203). 2, 1976 192, Ablhorg, G.,and Felig P. Substrate utilization during prolonged exercise preceded by ingestion of glucose, Am J. Physiol, 233, E188, 1977 193, Wranic, M., Kawamori, R., Pek, S, Kevaccvic, N.,and Wrenshall, G.A., The esseniality of inal and the role af glucagon in regulating elucose wilization and production during strenuous exercise in dogs, J.Clin = Invert, 57, 248, 1976, 194, Hinanas-Hagen, J., Sympathetic regulation of metabolism, Phurraseot Rev. 19, 367, 1961 rats given cootinuous injections 188.19s. 196. 197. 198, 199, 200, 201 203. 204, 208, g g 215, 216, 217, 218, 219, 20, zi. 2 ficance of Hormones in Regulation of Metabolism During Exercise 9 (Chiasson, J.L., Shikama, H., Chu, D.T-W,, and Exton, HL, tobibitory effect of epinephuine o stimulated glucose uptake by rat skeletal muscle, J: Cin. davest. 68. 706, 1981 Issekutz, B., Effect of epinephrine on carbohydrate metabotism in exercising dogs. Metabolism, 34, 457, 198s. Johnson, R.A., Rennie, MJ», Walton, J.Land Webster, M.H.C., The effect of mnderate exercise on blood metabolites in paticats with hypopituitarism, Clin. Sci 40, 127, 1971. Ahibors, G., Feliz, P., Hagenfeltt, L, Hendler, R., and Waren, J, Substiate remover dering prolonged exercise in man, Splancnic and leg metabolism of glucose, fee fatty acids and amina acids. J. Clim. Invest, 53, 1080, 1974 Wolle, RAR, Nadel, EAR., Show, JLHLF. Steplrenson, L.A. and Wolfe, M.EL, Role of changes in insu and glucagon in glucese homeostasis in exeecise, Clin Invest, 77, 900, 1986, Wasserman, D.H., Lichley, HLL.A., and Vranic, M., Interactions between glocagon and other counterregulatory hormones during normoglycemia and hypoglycemia exercise in dogs, J. Clin, Tavest, 74, 1404, 1984. Kilov, J., Lipid mobilization and utilization, in Principles of Exercire Biochemistry, 1 Poortmans, Ed., Kanger, Basel, 1988, 140. Faderspil, G., Lefebvre, P, Luyckx, A., and DePale, A.. Endocrine wechanisms of exercise induced fatty acids mobilization in rats, in Metabolic Adaptation to Prolonged Physical Exercise, Howald, H., and Poortmans, J. Eds, Birkhauser Verlag. Basel, 1975, 301 Gollnick, PD. Exercise, adrenergic blockade and free fatty acid mobilization, Am J. Physiol, 213, 734, 1967, Franz, J.W., Lohinan, F.W., Koch, G and Quable, HLJ., Aspects of hormonal regulation of lipolysis during exercise: effects of chronic [preceptor blockade, Int J. Sports Med, 14, 1983, ‘Stankiewicz-Choraszuchs, B., and Gérski J, Bifect of beta ndrenerpie blockade on intramuscular triglyc- ceide mobilization daring exercise, Experimentia, 34, 357, 1978 Hanter, WML, Foncenka, C.C., and Passmore, R., Growth hormone: important role in muscular exercise in adults, Science, 150, 1051, 1965, Barwich, D., Hagel EL, Weiss, M., and Weicker, HL, Homional and metabolic adjustinent in patients with ‘central Cushing's diseace after adrenalectomy, Int. J. Sports Med. 2, 720, 1981, “Toode, K., Smirnova, T., Tendzegolskis, Z.,and Vir, A., Growth hormone action on blood glucose, lipids and insulin during exercise Biol. Sport, 10, 99, 1993. ‘Kaciuba-Uséilko, H., Greenleaf, JE., Kazlowski,S., Braesineka, #..Narar, K,and Piersba, A..Thysoid hormone-induced changes in boxy temperature and metabolism during exercise in dogs, Am. J. Physic. 222, 260, 1975, ‘Nana, K., Chorabinsks-Moneta, J, Machalla, J, and Kaciuba-Ustilko, H., Metabolic and bod) temperae ture changes during exercise in hyperthyroid patients, Clin. Sei. Mol. Med., $4, 323, 1978, Paul, P, Fffects of long lasting physical exercise and training on lipid metabolism, in Metabwlic Adaptation 410 Prolonged Exercise, Howald, H., and Poontmans, J, Eds., Bitkhauser Veriag, Basel, 1975, 156. Kaciuba-Uséilko, H., Breerinsks, Z., and Kobryn, A. Metabolic and temperature responses to physical exercise in thyroideetomized dog, Bur J. Appl Physiol, 40, 219, 1979 ‘Story, J.A., and Griffith, D.R., Effects of thyroxine and exercise on serum and hepatic cholesterol in mature rats, Horm Meiab. Rex. 4, 380, 1972. Fain, J.N,, Inhibition of glucose trancpost in fat cells and activation of lipolysis by glucocorticoids. in Glucocorticoid Hormone Action, Baxter, .D., and Rousseau, G.G., Eds., Springer-Verlag, Berlin, 1979, 547 Fain, JLN., Kovacey, V.P., and Seow, R.O., Aatilipolytic effect on insulin in isolated fat cells of the rat Endocrinotogy, 78, 773, 1966. Butcher, RW, Sneyd, LG-T., Park, CR, and Sutherland, IW. Effect of insulin on adenosine ¥5'- rmoaophasphatc in the rat epididymal fat pad, J. Biol Chem. 24, 1651, 1966 ‘Senft, G., Schultz, G., Munske, K.,and Hoffman, ML, Influence of insulin on cyclic ¥.SAMP phosphoi- ‘esterase activity in liver, skebetal muscle, adipose tissue, and kidney, Diabetologia, 4, 322, 1988. Nilson, N.O., Strolfors, P., Fredrikson, G., and Belfrage, P.. Regulation of adipose tsswe lipolysis: effects ‘of noradrenaline and insulin on phosphorylation of hormone-scasitive lipase and on lipolysis in intact rat adipocyte, FEBS Lett, 111, 125, 1980, Hunter, WM. and Sukkar, M.Y., Changes in plasma insolin levels during muscular exercise, J: Physiol, 196, 110P, 1968. Wahren, J. Felig, P, Hagenfelat, I, Hendler, R., and Ahtborg, G., Splanchnic and leg metabolism of glucose, free fatty acids and amino acids during proloaged exercise in man, in Metabolic Adaptation 10 Prolonged Exercise, Howald, H., and Poortmans, J. Ede, Biskhiuscr Verlag. Basel, 1975, 144. Issckutz, B. Miller, HJ, and Redabl, K., Effect of exercise on FFA metabolism of pancreatomized dogs, ‘Am. J. Physiot, 205, 645, 1963. Wahren, J., Felig, P, and Hagenfeldt, L., Physical exercise and fuel homeostasis in diabetes mellitus, Diabetologia, 14, 213, 1978,80 Adaptation in Sports Training 223, Brockman, RLP.,Ffect of somatostatin on plasma glucagen and insulin and plicose tumoverin exercising sheep, J. Appl Physick, 47,273, 1979, 224, Isselute, Band Pant, P. Intramuscular cnergy sources in exercising normal and pancreatomized dog, Am J. Physiol, 215, 197, 1968. 225. Dahm, G.L., Kasperek, G.J., Tapscott, E.B., and Barakat, HLA. Protein metabolisen, during endurance exercise, Fed. Prac, 44, 348, 1875. 226, Viru, A.. Mobilization of structural proteins during exercise, Sports Med. 4, 95, 1987. 227, Varrik, E, Viru, A. Oiipik, Vi. and Viru, ML, Exercise-induced catabotic responses in various muscle fibess, Can. Sports Sci, 17, 125, 1992, 228. Dob, L.G., Tapscott, FX, and Kasperek, Gl, Protcin degradation during endurance exercise and recovery, Med. Sci. Sports Exerc, 19 (Suppl). S166, 1987 229, Millward, D.J., Davies, C:T-M., Halliday, D., Wolman, 51. Matihews, D.ML, and Rennie, ML, Effect of excrete on protcia metabolism in humans as explored with stable botopes, Fed Proc. 4, 2686, 198? 230, Wolfe, R.R., Goodenough, R.D:, Wolfe, M.H., Royl, G.T., and Nadel, E-R., Isotopic analysis of leucine stad wea metabolism in exercising humans, /- App. Physiol, 52. 458, 1982, 231, White, T.P., and Brooks, G.A., U-'C-glucose, -alanine, and -lewcine oxidation in rats at rest and two ‘intensities of running, Am. J. Physiol, 240, E155, 1981 232, Lemon, P.W.R., Nagle, FJ, Mullin, J.P., and Benevenga, N. vo intasitics of exercise, J. Appl Phystol, 56.947, 1982. 253, Mayer, M. and Rosen, F. Interaction of glucocorticoids and androgens with skeletal muscle, Metabolism, 26, 937. 1977. 234. Varrik, ESeene, T.,and Viru, A, 3-Methyihistidine excretion dari training exercises inadrenalectomized animals, Acta Comment. Univ. Tarraenss, 610, 83, 1984 (in Russian) 235. Dublmann, B., Widjoja, A., and Reinauer, H Antagonistic effects of endurance teaining and testosterone on alkaline proteolytic activity in rat skeletal muscle, Eur. J. Appl. Physiol 46, 229, 1981. 236, Dol, Gales and Louis, TM. Changesin androstenedione, testosterone and protein metabolisth as result of exercise, Proc. Soc, Exp. Biol. Med., 158, 622, 1978. 237, LA JLB. and JefTerson, LS. Effect of isoproterenol on amino acid levels and protein tumover in skeletal rauscle, Am. J. Phys, 232, E243, 1997. 238. Ettinger, JLD., and Matsumata, K., Interaction of calcium, cyclic AMP. and tension in the regulation of rote degradation in muscle, ia Metabolismand Functional Changes daring Exercize, Seruiginovsky, B. and Tucek, S., Eds, Charies University, Prague, 1982, $7. 239. Lenkova, P.., Usik. .V. and Yakovlev, N.N.. Chaages of urea content in blood and tissues in mascular activity in dependence of the adaptation of the organism, Sechenov Piysiol. J USSR, $9, 1097, 1973 (ia Russian) 240, Futks, RM Li, 1.B., and Goldberg, AL, Effect of iasolin, glacose and amino acids on protein turnover in cat disphrapin, J. Biol. Cher, 250, 290. 1975 241. Critz,1..,and Withrow, T.J., Adrenocortical blockade and the transaminase response lo exercise, Steroids, 5,719, 1965, 242. Garber, AJ.. Karl, J.B. and Kipnis, DM. Alanine and glutamine synthesis and release from skeletal muscle, LV. f-Adrenergic inhibition of amino acid release, J, Biol. Chem., 251, 851, 1976. 243, Gucrennec, G.1., Ferre, P, Sermuricr, B., Merino, D., Amonad, Mand Pesquires, PxC., Metabolic effects of testosterone daring proloaged physical exercice and fasting, Eur. J. Appl. Physio, $2, 300, 1984 244. Viru, A.,and Eller, A., Adrenocortical reg ulation of protein metabolism during proloaged physical exertions, Bull Blsp, Biol Med., 82, 1436, 1976 (in Russian). 245. Viru, A. Litvinovay L~ Viru, Ms and Smirnova, Glucoconticolds in metabolic contol during exercise alanine metabolism, J- Appl. Physiol, 76, $01, 1994, 246. Vieu, A, and Smirnova, T., lavolvement of protein synibesis ia action of glucocorticoids on working capacity of adrenalectomized rats, Int J. Sports Med. 6, 225, 1985 247, Seene,‘., lev, K., and Pehine, A, Effect of muscular activity on the tamover rate of actin and myosin beavy and light chains in different types of skeletal muscle, fat J. Sports Med, 7, 287, 1986. 248. Korge, P., Roassor and Oks, M., Heart adaptation to physical exertion in relation to work duration, Acta Cardiol, 29, 303, 1974 249. Kérge, P., Masso, R., and Reasson, S., The effect of physical conditioning on cardiac response to acute exercise, Can. J, Physiol Pharmacol, $2,745, 1974 250. Korge, P, Viru, A.,and Roosson, ., The effect of chronic physical overload on skletal muscle metabotism and adrenacontcal activity, Acta Physiol. Acad Sct Hung. 5,41, 197A. 251. Kérge,?. and Rowson, S.The importance of adrenal glands inthe improved adaptation of trained animals to physical excrtion, Endotrinologi, 64, 232, 1975. » [in vtro leucine oxidation at rest and during 252. Kodlowskt, S., and Saltin, I. Elfect of sweat loss on body Muids, Appl. Physiol, 19. 1119, 1964 253, Saltin, Band Custll,D, Fluid andelectrolytehalance during prolonged exercise, in Exercise, Nutrition and Energy Metabolism, Hora, ES. nd Texjung, RL, Eds., Macmillan, New York. 1988, 150.Significance of Hormones in Regulation of Metabolism During Exercise 81 254. Mein, B., Eclache, J.B., Geelen, G. Annert, G., Allevard, AM. Jersaillon, E, Zelid, A, Legras, J, ‘and Charab, C., Plasma AVP. neurophysin, renin activity and aldosterone during submaximal eacscise Performed until exhaustion in wained and untrained min, Eur. J. Appl Physiol, 44. 141, 1980, 255, Harwich, D., Keilholz, U., Merkt, Jy and Weicker, H., Serum kinetic des antidivretischen Hormons (ADH) and Saure-Basea Henshalts bei fahnradenergometrischer Aucbelastung, in Sport: Leistang and Gcsondtaty, Heck, H.. Hollmann, W.. Liegea, H., and Rost, R. Eds.. Deutsch Arztc Verlag, Koln, 1983, 221. 256, Zambraski, E, Rofrane, T., and Ciccone, C., Effect of aspirin ueatmest on kidney fonction in exercising man, Med, Sct. Sports Exerc. 14, 419, 1982 257. Olson, KE, and Satin, B., Variations in total body water with muscle glycopen changes in man, Acta Physiol. Seand., 80, 11, 1970, 258, Saltin, B.. Aerobic work capacity and circulation st exercise in man. With special reference tothe effect of Prolonged exercise and Jor heat expasute, Acta Physi. Scand. 62 (Suppl, 230), 1964 259, Cost D.L.and Miller, 19M Nutstion for endurance som: caxbohiydrate and Tid eslance, In. J. Sports Med... 1980, 260, Costill, DAL. Branam, G., Fink, W., and Nelson, R., Exercise-induced sodium concentration changes in plasma renin and aldosterone, Med. Sci Sports. 8, 209, 1976. 261. Fenm, W.O. Electrolytes in muscle, Physot. fe., 16,450, 1936. 262. Bergstrém, J, Gaurnteri,G., and Hultmann, F., Changes in muscle water and electolytes ding execs in Limiting Factors of Physical Performance, Kevl,J.,Ed,, Georg Thicese Verlag, Stata 1973. 17% 263. Converting, V.A.. Kei, LC, and Greenleaf, JE. Plstha volume, renin, and vasopressin responses to graded exercive after training, J. Appl. Physil., $4, 508, 1983 268, Clausen, T... Regulation of active Na’-K*transpoet in skeletal muscle, Physiol. Rev., 66, 542, 1986. 268. Sisgaard, G., Adams, R-P., and Saltin, B., Watce and ion shifs in skeletal muscle of humans with intense: dynamic knee extension, Ant J. Physiol, 248, RI%, 1985, 266, Clausen, T., and Flatman, J.A., The effect of catecholamines on Na.K transport and messbane potential in fal soleus muscle, J. Physiol, 270, 383, 1977, 267. Claucen, T. and Fatman, J.A.. Effects of insulin and cpinepbrine on Na'-K*and glucose transport in soleus muscle. Am. J. Physiol 252. E492, 1987 268 Knochel, J, Blachley, J.D., Joheson, J.HL, and Carter, N.W., Muscle cell electrical hyperpolazation and reduced exercise hyperkalaemia in physically conditioned dogs, J. Clin, Javest, 75, 740, 1988 269. Kjeldsen, K., Richter, E.A., Galbo, IL, Lertie, G., and Clausen, 7. Training increases the coaccatration ‘oF PH) oubain-binding sites in rat skeletal use, Biochem. Biophys, Acta, 860, 708, 1986 ard, HL, and Clausen, T., Increased total concentration of Na.K pumps in vastus lateralis muscle of ld tained human subjects, J. Appl Physiol, 67, 2491, 1989, 271. Kjeldsen, K., Norgaard, A. Getsche, C.0,, Thamassen, A., and Clausen, T,, Effect of thyroid function (om number of Na-K-pumip in human skeletal mascle, Lancet, 2, 8, 1984, 272. Draevetskaya, 1 yy and calcium level in plasma during muscular activity, Sechenov Physio. J. USSR, 64, 1498, 1978 (in Russian), 273. Aloia, JF. Rasolo, P., Deflas, LJ. Voswani, A., and Yeh, J.K., Exercise-induced hypercalcemia and caleiotropic hormones, J Lab. Clin. Afed., 106, 229, 1985.Chapter 4 POST-EXERCISE RECOVERY PERIOD OUTLINES OF THE POST-EXERCISE RECOVERY ‘The end of exercise means the cessation of muscle contractions, but not the cessation of increased functional and metabolic activities. More or less prolonged time is necessary to normalize the functions of various organs. For a comparatively prolonged period the me bolic activities remain far from the resting state. In 1919 it was indicated that during the first 5 to 15 min after exercise, oxygen uptake remains above the basal metabolic rates. This excess oxygen uptake matched the oxygen deficit contracted at the beginning of exercise. After imensive or exhaustive exercise the amount of consumed oxygen is larger than the oxygen deficit. Some years later, the accordance between excess oxygen uptake after exercise (oxygen debt) and lactate accumulation was established? Accordingly, abolishment of oxygen debt was considered the main reason for increased functional activities after exercise.* Ik was also considered that the oxygen debt means a consumption of ‘extra oxygen’ necessary to supply energy for various restitution processes and particularly for the resynthesis of phospho- creatine and for the oxidative elimination of lactate. However, the problem is more comp! cated: the oxygen uptake after exercise does not exactly correspond to the amount of energy released during exercise on account of anacrobic processes.*® In regard to metabolism, the recovery period means not only transition from high to low energy demands, but also restoration of energy reserves, abolishment of the accumulated tabolic intermediants, as: well 8s normalization of water and ionic composition in body compartments. In the course of repletion of energy reserves the phenomenon of supercompensation has been found. This gives a peculiar feature to the delayed stage of the recovery period.’ Recovery period means also a change in protein metabolism opposite to that happening during exercise. The altered balance between anabolic and catabolic processes has to warrant an effective renewal of exhausted cellular structures and enzyme molecules as well 1s the opportunity for the increase in active structures and in the number of enzyme molecules. In this meaning as well as in regard to the supercompensation of energy reserves we have to consider the reconstructive function of the recovery period. ‘Consequently, the main functions of the recovery period are mel 1. Normalization of functions (their transition from the exercise level to the resting level) Replenishment of cnergy resources together with temporary supercompensation for them 3. Normalization of homeostatic equilibriums 4. Reconstructive function, particularly in regard to cellular structures and enzyme systems n minutes ‘The first and third functions are actualized with or, in particular cases, within some hours. The corresponding processes constitute the first stage of recovery (Figure 4-1). This stage may be called the stage of rapid recovery. The actualization of other tasks consumes far more time. Therefore, they can be considered to constitute the stage of delayed restitution of bodily resources and working capacity. Howevcr, it would be wrong to think that this stage begins only after the cessation of the first stage. Indeed, it begins with the end of asEo Adaptation in Sports Training EXERCISE RECOVERY Rapid recovery | Delayed recovery 1. Normalization of functions 2. Normalization of homeostatic balances 3. Restitution of ‘working capacity 4. Restitution and supereompensation of energy stores 6. Reconstructive function FIGURE 4-1. A generalized scheme of the post-cxercise recovery period ise. In regard to some enet possible already during exercise. a delayed realization of tasks. stores, the onset of their replenishment is assumed 10 be hus the term ‘delayed” does not mean a delayed onset but RESTORATION OF NORMAL FUNCTIONAL ACTIVITIES OXYGEN TRANSPORT SYSTEM Cessation of muscular contractions at the end of exercise or various kinds of physical work causes a change in regulatory influences. The regulatory actions of central command and proprioceptive impulses drop out. Ax a result, rapid changes occur in the functions of organs responsible for oxygen transport, despite the persisting high demand for oxygen supply of skeletal muscles having only just acted. These transitory changes are opposite to the. initial adjustment at the beginning of exercise in the direction of change, but similar to the general pattern: first there is a rapid and then a gradual decrement of functional activity. While the rapid changes within the first 1 to 2 min express the cessation of the actions of entral nand and proprioceptive influences, the second gradual and often undulated decrease may be explained by the reduction of influences from metaboreceptors and of hormonal fluences. Exercise intensity is a factor that retards the rate of post-exercise changes. After highly intensive exercise during the first 510 10s the heart rate may not change and then the following decrease is not characterized by so steep a slope as afler less intensive exercise."* A possibility of a regulatory inertia seems to exist as well, The duration of exercise may be idden by the persisting excitement of the cardiac center, stimulating a sino-atrial node through sympathetic discharge. A further increase in the heart rate was noticed during the first Sto 8 s in 65% of persons after 15 s of cycling at maximal possible rates.* “The post-exercise dynamics of heart activity are characterized by enhanced respiratory arrhythmia as well as by pronounced waves in the duration of the cardiac cycle corresponding to the third waves in blood pressure (Figure 4-2). This picture is revealed in association with ‘a steep slope of heart rate decrement and mainly in well-trained persons. An increased rate ‘of recovery of heart frequency was found in trained persons also after exercise with increasing, ity up to the individual maximum. *Itis likely that the steep slope of heart rate expresses not only the decrement of metabolic influences but also the high activity of parasympath nerves. Mostly in well-trained persons the heart rate decreases for 20 to 40 s to the initial* (Figure 4-3). This can be considered an expression of ‘ on85 Post-Exercise Recovery Period ‘ert | rues tia cis a EAT 586 Adaptation in Sports Training FIGURE 4-3, Dynamics of cardiac cycle duration after exercise: 1—undulated process (a rapid decrease to values of cardise eyele duration above initial ones), 2 — aperiodic process with restitution of worm heart rate within 1 to 2 min, 3 — aperiodic process with stabilization of candiac cycle duration om a level below the initial, 4 — torpid process without aay stabilization during the first 5 min. Constructed as in the academic dissertation of E. Saoroskaya (Harte University). autonomic nervous influences. According to E, Gellhorn,"" autonomic imbalance due to the: prevalence of sympathetic or parasympathetic actions causes the increased sensitivity to change in the opposite direction. The previous prevalence of sympathetic influence during exercise sensitizes the parasympathetic effects. As a result the heart rate decreases below the initial values. However, this change does not appear after very strenuous exercise: Instead of that, after strenuous exercise and in most cases in untrained persons, the heart rate may stabilize to a level of 5 to 20 beats/min higher than the initial.* ‘The significance of the increased vagal tone was emphasized by results indicating that the heart rate decreased exponentially to the initial level during the fi cercise minute despite the maximal noradrenaline level in the blood at the same time.!? By using various methods it was found that a rapid decrease in cardiac output and stroke ‘volume occurs within the first 1 to 2 min post-exercise. Then a less abrupt decrease follows.'*"* ‘The transition from exercise to rest is connected with a short-term drop in the intra-arterial pressure, often to values below the initial.'™* After only 5 to 10 s a new increase in blood pressure takes place, The latter lasts approximately 20 to 40's." After that a gradual decrease in arterial pressure follows. The same dynamics were established in the mean arterial pressure using a noninvasive method for its continuous recording.” A secondary increase in stroke volume was found during 1 to 2 min postexercise, During this time period the peripheral resistance remained low and only later did it gradually increase.!* By using special equipment, auscultatory recording of blood pressure was obtained after every 8 to 12's. A comparison of the pattern of auscultatory blood pressure during and after various exercises showed that after exercise the maximal arterial pressure rises tolevels higher than those recorded during excreise when the exerci: ‘ation was 30 to 60 s and therefore, not enough for blood pressure to increase to the adequate-level. After cessation of exercises lasting for 3 to S min, maximal arterial pressure decreases without any secondary rise.” When the person was in a standing position, the blood pressure drop was common immediately after the end of a I-min cyclic exercise. The subsequent rise in maximal pressure as well as the decrease in heart rate were less pronounced than in a sitting position. When the blood flow to the legs was prevented by a bandage on the thighs, there was no immediate decrease in blood pressure and the post-exercise increase was the same a8 in a sitting position.” Thus the ____ liePost-Exercise Recovery Period 87 immediate post-exercise drop in arterial pressure is related to the aggravated venous return due to the cessation of the muscle pump function. As early as the 1930s it was demonstrated that a circulatory collapse called “gravity shock" is revealed during prolonged standing after intensive exercise. The phenomenon can be avoided by a pressure bandage on the thighs.” Differently from this mechanism, a late mild hypotension may follow within a period from 0.5 to 3h after the end of exercise.**" An increased sensitivity of vagal baroreflex was found persisting through 24 h of recovery **** Prostaglandins produced by skeletal muscles and kidney as a result of exercise may contribute to prolonged post-exercise vasodilatation as well. The transition of lung ventilation and oxygen uptake from exercise level to resting level is usually described by a simple exponent: during the first 1 to 2 min the changes are faster than later on.° Immediately after the end of a 5-min cycling al moderate intensity the respiratory frequency and depth decreased in association with reduced bioelectric a of intercostal muscles.*! However, the exponential curve may not be found after short-term highly intensive exercises or after static efforts. After a 15-8 cycling exercise performed at the highest possible rate, the VO, increased during the first 20 to 30s. Only then did an exponential decline follow. After a 2-min exercise at the highest possible rate the level obtained at the end of exercise persisted for 15 to 20 s before the exponential decline followed. When the exercise duration Was enough to obtain the maximal oxygen uptake level (more than 3 min), the recovery period began with a steep decline transferring later to a more gradual decrease" In 1920 Lindhard* reported that after static efforts the VO, and cardiac output increased to higher levels compared to the values obtained during effort. The lung ventilation remained ‘on the exercise level and respiratory frequency decreased, but tidal volume as well as alveolar ‘ventilation increased. Similarly, after brief tetanic contractions the oxygen consumption by muscle tissue increases and thereafter declines exponentially. ‘The exponential pattern of post-exercise VO, was described with the aid of two straight lines in order to discriminate the fast and slow components of oxygen debt, called alactatic and lactatic debts, respectively." (Figure 4-4) However, there is no direct evidence that the replenishment of ATP and phosphocreatine stores occurs during the time of repayment of the fast component of the oxygen debt, A study of the rat leg musele by phosphorus nuclear magnetic resonance demonstrated that phosphocreatine concentration rises to the initial level during a rather long-lasting period in accordance with the normalization of VO, by muscle issue.“ Thus, the restitution of muscle macroergic phosphates lasted not only during the fast component of oxygen debt, but also during the whole period of ©, debt repayment. Serious doubis arose also in regard to the exact correspondence between the slow compo- nent of O, debt and lactate elimination as well as between the total O, debt and the amount of energy released in anaerobic processes. The main counterarguments are 1. Elevated body temperature decreases phosphorylative coupling and, consequently, more , is required for a given amount of ATP to be synthesized.” The temperature effect is calculated to amount to 1.21 of , during the first hour of recovery after submaximal and to 0.6 1 after supramaximal exercises when the persons exercised in comfortable temperature.” The elevated temperature was considered to be the most important factor influencing the mitochondrial O, consumption and thereby, excess VO, after exercise.*! 2, Changes in the blood level of adrenaline, thyroxine, and some other hormones may alter the rate of oxygen uptake and the ratio between oxidative phosphorylation and free oxidation, including free radical oxidation. In the canine gastrocnemius-plantaris muscle group the VO, increased significantly by noradrenaline infusion during post-contraction recovery." The blockade of adrenoreceptors reduced the VO, during post-exercise recovery. However, after an exhaustive one-leg exercise, muscle temperature and blood catecholamine concentration returned to the control level within 20 min of recovery, but the VO, remained elevated.88 Adaptation in Sports Training SUPRAMAXIMAL, ‘SUBMAXIMAL EXERCISE. EXERCISE GLYCOGEN GLYCOGEN ! GLUCOSE. GLUCOSE: ae at wf! 4 ! ! | PYRUVATE NH PYRUVATE, 1H Veet Scam er a ee LACTATE. | ALANINE LACTATE ALANINE: OXIDATION OXIDATION FIGURE 4-4. Dynamics of post-cxercise oxygen uptake. The dotted area comesponds to alsctatic debt and striated area to lactatic debt. 3. Intensive function of the myocardium and respiratory muscles continuing after exercise need additional energy. It was calculated that the O, cost of moving an additional blood volume through the circulation for the first hour is about 1.3 after submaximal and 0.7 1 after supramaximal exercises.**? The ventilatory cost constitutes 0.1 1 O..** 4, Altered muscle tone may cause changes in VO, There are reports pointing to a long period of persisting elevated oxygen consumption lasting for up to 12 h or even more after vigorous exercises.°**! The prolonged component of post-exercise excess oxygen consumption was found both after exhaustive prolonged submaximal and short-term supramaximal exercises. This component is a function of exercise intensity and duration.***! Special experiments showed that the thermic effect of the con- sumed food was not decisive in the prolonged component of post-exercise excess oxygen consumption. It has been suggested that an increase in the rate of substrate cycling, particu- larly the triglyceride-fatty acid cyele may account fora significant part of the increased energy expenditure after exercise." Additionally, energy expenditure for the reconstructive func tion of the recovery period has to he taken into aecount to explain the prolonged component of excess post-exereise oxygen consumption. - LACTATE DYNAMICS AND PH VALUES IN POST-EXERCISE RECOVERY Post-exercise lactate values are widely used for evaluation of the participation of anacrobic glycolysis in the attaining of energy during strenuous exercises. However, during exercise lactate accumulates because the inerease in the lactate disappearance rate lags behind the increase in the lactate appearance rate.*’ Therefore, the amount of resynthesis of ATTP at the expense of anaerobic glycolysis will be underestimated if the ealeulations are based on the Jactate accumulation in the blood or on the post-exercise oxidation of lactate (lactate debt), ‘One must also take into consideration the various pathways of the fate of pyruvate formed during exercise: besides the oxidation of pyruvate and the transformation to lactate, one part is used for alanine synthesis (Figure 4-5). Pyruvate determination does not help because the measured pyruvate gives only its residual amount in a moment of time. ‘After exercise a part of both the formed pyruvate and lactate is used for glycogen resyn- thesis in exercised muscles. After supramaximal exercises causing blood lactate levels ofPost-Exercise Recovery Period 80 CC Recovery period FIGURE 45. Fate of pyruvate during supramaximal or submaximal exercises. 10 to 16 mmol"! and muscle lactate content of 25 mmol-kg” the proportion of lactate used for the resynthesis of glycogen has been estimated at 75,** $0,.7 and 13 to 27%. Nevertheless, these sources of errors will not make the use of lactate levels and lactate debt meaningless in evaluating the anacrobic energy production, because in supramaximal exercise the largest part of pyruvate is transferred to lactate and lactate production greatly exceeds its elimination, Only the quantitative estimation of the energy released in anaerobic glycoly: may not be exact. “The rate of lactate removal during recovery is directly related to the lactate concentration at the end of exercise. The three main routes for muscle lactate clearance are (a) release ‘into the capillary bed, (b) conversion to pyruvate, and then (c) either oxidation or further conver sion into other compounds.” Using a knee-extensor exercise model inducing exhaustion within 2 to 4 min, it was found that at the end of exercise, the femoral vein plasma concentration of lactate is only a half of that accumulated in the muscle (the muscle-blood ‘gradient was 18 mmol-Y, but 3 min into recovery, the difference was reduced to 5 mmol, ‘and was zero after 10 min of recovery. During 1 h of recovery as much as 82% of the lactate left the muscle as lactate via the blood stream.*? These results are in accordance with the other data. After a 4-min exhaustive exercise the lactate release from working muscle gradually decreased. This process continued for at least 8 to 15 min. After a 3-min exhaustive cycling the blood lactate increased during the first 10 min, while a pronounced drop occurred in the muscle lactate concentration. Thereafter, lactate decreased also in the blood. Approximately 0.5 h post-exercise the lactate ‘concentrations in muscles and blood equalized.“ In the blood the post-exercise lactate curves could be fitted to a bi-exponential t function, consisting of a rapidly increasing and slowly decreasing component A compa son of lactate pattern after 3- and 60-min exercises showed that with exereise duration the values of velocity constants of lactate increase and decrease were reduced. In exercise intensities over the anaerobic threshold, the blood lactate concentration increased with the prolongation of exercise duration from 3 to.6 min, but the constants of kinetics for both post- exercise increase and decrease of lactate concentration decreased. During the first 5 min of recovery after cycling with increasing intensity the pyruvate concentration progressively increased in the blood. ‘The lactate/pyravate ratio decreased.” It is yet to be established whether the decreased lactate/pyruvate ratio is a general phenomenon90 Adaptatian in Sporis Training appearing immediately after cessation of muscle contraction, and if it indicates a relative decrease in the pyruvate conversion by corresponding metabolic pathways. ‘As a result of intensive anaerobic glycogenolysis an accumulation of hydrogen ions appears in the muscles!*7! and in the blood.” The changes in pH values after exercise are parallel to the changes in lactate concentrations.“ An intensive 4-min anaerobic exc resulted in a decrease of the thigh muscle: pH from 7.15 +0.01 to 6.57 + 0.04 and that of the blood from 7.39 £ 0.04 to 7.04 + 0.03. During the first 5 min of recovery the decrease continued and then the pH values began to increase.”» After another 4-min exhaustive exercise low pH persisted for 4 min in the atrial blood and then began to increase. In the venous blood aa gradual inerease began from the first post-exercise minute. Both values returned to a level close to the initial within 20 min. Cycling. at high intensity (mean heart rate 192) until ‘exhaustion resulted in a pronounced drop of pH values in the m. quadriceps femoris (total muscle pH from 7.08 +0.03 to 6,64 0.12), intracellular pH (from 7.004 0.06 to 6.45+ 0.09), femoral venous blood pH (from 7.08 + 0.06 to 6.93 + 0.06), and arterial blood pH (from 7.27 to 7.14), Muscle lactate increased up to 22.0 2.6 mmol/kg (intracellular lactate to-29.1+3.4) «i femoral venous blood lactate up to 15 + 5 mmol/l. At 20 min post-exercise the muscle Jactate remained elevated but both (otal and intracellular pH were normal. The pH values of femoral venous blood normalized within 20 min. At 30 min post-exercise, significantly elevated pH values were found in comparison with the pre-exercise values. At the same the blood lactate was insignificantly lower than the In most cases lactate concentrations normalize within 30 to 60 min after intensive exer cise °7.72 There is old evidence that activity increases lactate removal from the blood.” Moderate exercise performed during recovery also causes a faster elimination of lactate: from the muscle.”"* At first it was supposed to be related to enhanced perfusion.” However, stimulation of the oxidation rate against the decline in oxidation intensity may have its significance as well. Mild exercise following a strenuous one enhanced lactate oxidation” Lactate disappearance after exercise at VO,max level was intensified by exercise at 40% VOsmax, but not by exercise at 65% VO,max." However, other studies indicated that the recovery exercise at 65% VO,max™ or at 60% VO.max™ is optimal for speeding up lactate removal. After a 10-min exercise at 90% VO,max active rest slightly below the anacrobic threshold improves the lactate removal rate compared to complete rest or active rest above the anaerobic threshold ENDOCRINE SYSTEM ‘A number of studies on blood levels of hormones during the first 10 to 20 min of post ‘exercise recovery have revealed the continuation of exercise-induced change before the opposite change occurs. Thus, the endocrine response to exercise may be more prolonged than the exercise itself. In other cases opposite changes were found to begin just after the end of exercise. These opposite changes do not mean a fast normalization of hormone Jevels in the blood. Quite often they reach concentrations significantly differing from the initial valuc. ‘Thus, the exercise-induced rise or drop may be changed by a decrease or an increase, respectively. The new hormone level may now persist for a long time, There are cases of a secondary rise in the hormone level after a certain time of rest. Of course, there are also cases of gradual normalization of the hormone level to the normal concentration. The hormone changes in the recovery period express, abviously, not only the inertia of regulation in regard to exercise-induced changes, but also the following normalization of the endocrine function The regulation of metabolic processes during the recovery period may require specific changes in hormone leve Catecholamines During the first mi tration rose a little. During the follow!Post-Exercise Recovery Period 1 ‘Two months of training accelerated, but the following two months of detraining deceler: the restitution rate of the noradrenaline level. Increase in the power output during exercise from 1480 kpm-min to 1920 kpm-min- slowed down the disappearance of noradrenaline from the circulation." In a recumbent position the noradrenaline concentration decreased jore rapidly than in a sitting position after exercise." A rapid decline in the adrenaline concentration following the highest level has been found after short-term exercise.” After prolonged exercise, high levels of catecholamines may persist for many hours oreven. for days. Both adrenaline and noradrenaline concentrations remained increased for 2 h after 80-min exercises at 75% VO,max. After a marathon race adrenaline concentrations above the initial level persisted for at least 24h! At 24/h after a 24h endurance run or triathlon ‘competition the blood levels of free and sulfated catecholamines were elevated." During a 6 day cross-country ski hike (daily distance 35 to 50 km) immediately after skiing as well as in the evening, the blood levels of catecholamines were clevated, but catecholamine response to the ergometer test, performed immediately after skiing, was normal. Eleven days after the hike the noradrenaline concentration was above the initial level by 25%. In rats the noradrenaline levels exceeded the initial one by 229% immediately after 3-h of swimming and by 144 and 238% 1 h and 4 h tater, respectively.?! According to the results of animal experiments a long time period is necessary for restitution of the catecholamine content in the adrenals. In rats after an 8-hswim the adrenaline content remained low during 7 days due to the disturbed catecholamine synthesis. During the first 5 days of the recovery period the adrenals synthesized mainly noradrenaline. After only a week the adrenaline formation was augmented, but the prevailing adrenaline synthesis, common for the resting state, was not yet observed. The catecholamine content in the heart and the noradrenaline content in the hypothalamus returned to normal levels after 2 days? In the mouse, after a prolonged run (running for 16 and 10 h, interrupted by a 12-h rest period) 6 days was required for the adrenal catecholamine content to return to normal levels.” Glucocorticoids After short-term exercises the increase in the blood cortisol concentration continues within the first 5 to 30 min.” This may be due to the inertia of the activation mechanism or of the secondary response of the adrenal cortex. The highest corticotropin level was found immedi- ately after, but the highest cortisol level 15 min after 1 min of cycling at 120% VO,max.* The elevated blood cortisol after exercise has been shown to be related to the decreased rate of hormone elimination from the blood plasma."™" A fier a 30-min exhaustive exercise the blood cortisol level rose during the first 30 to 60 min, and then declined. The resting level was obtained within 90 to 120 min! After an 80-min cxercise at 70% VO,max a transient increase in the plasma cortisol concentration lasted for Ih after the exercise. A heavy anaerobic exercise (running 3 x 300 m) was followed by a high level of cortisol in the blood that persisted for 3 h. Then a drop in the cortisol concentration followed. At 6 h after the end of the exercise it was substantially below the initial level.” At3toGhafiera 13-to 14-kmruna low cortisol level was observed. After 2h of exercise at 60% VO,max adecreased activity of the pituitary-adrenocortical system was established by evels of both corticotropin and cortisol below the initial ones within 6 to 24 h post-exercise. There were no systematical differences. between data obtained from untrained persons and from well-trained sporismen in endurance events. Low levels of cortisol were found also 24 hafter 60-min cycling at 70% VO,max,! marathon race," and 100-km running. At1.2,and 4 days after running for 34 km, the blood cortisol was insignificantly. and 8 days later significantly, below the initial values. In rats the corticosterone content in the blood plasma?” and in the adrenals" remained augmented for at least 4 h or even 5 days following swimming exercises. The peak values were ‘observed afier 2-days in the adrenals and after 5 days in the plasma. One day later, repetition ‘of the same exercise did not elicit any response. After 2 days the response was inverted92 Adaptation in Sports Training Following 3 t0 5 days after the first exercise the response to the new exercise was cxagger- ated! Js the latter a reflection of supercompensation for biosynthetic activity in the cells of the fascicular zone of the adrenal cortex Anyway, an elevated content of ascorbic acid in the adrenal tissue was found several days after exercise! Pancreatic Hormones Exercise is followed by a rapid increase in the blood level of insulin." This change is so rapid that any measurement of insulin concentration, not carried out while the subject is still exercising, may be misleading in regard to the detection of an insulin drop during: exercise.!!® The concomitant increase in the C-peptide level in the blood indicates that insulin secretion increases just after the end of exercise.!"* ‘After a 100-km tun the insulin level in the blood was still increased 24 h later.!° Running, of 34 km was followed by a decreased insulin level 1 day later." ‘Apart from other results, no significant change in the blood insulin level was observed after ‘an 80-min exercise at 70% VO,max during the period of post-exercise excess oxygen con- sumption. In rats, 3h of swimming was followed by a-4-h period of decreased insulin level.” Using the blockade of the opioid receptor with the aid of naloxone administration, it was shown that in the post-exercise period the glucose-stimulated insulin secretion was enhanced by endogenous opioids. In resting conditions naloxone did not have such effect."* ‘The glucagon level decreases gradually from the highest concentration just after the end of ‘exercise in humans," rats?" and dogs.!!® In men the glucagon blood levels remained elevated for 90 to 120 min after 30 min of cycling until exhaustion." At 1, 2, 4, and $ days after running of 34 km the glucagon concentration was close to the initial level.!® Somatotropin In most cases the recovery period is characterized by a rather rapid decrease in the somatotropin concentration in the blood to normal values if the hormone level was augmented during the exercise.!°!°5116117 The rebinding time is dependent on the fitness level. After the cessation of a 30-min exhaustive exercise the somatotropin concentration returned to the resting level within 30 min in fit persons, but continued to increase for 60 min before declining in unfit ones.%°" A post-cxercise increase in the blood somatotropin level was observed mostly after comparatively short-term exercises: after 20-min aerobic exercises or afier seven repeti- tions of a I-min anaerobic exercise,!""" or after intermittent weight-lifting exercises." An anaerobic running exercise (3 x 300 m) induced even in trained persons a persistently high somatotropin level during the first hour of restitution. Subnormal values were found 6, 24, and ‘72h later.” In athletes the blood level of somatotropin was higher on the night after daytime training exercises than during the control night." Sex Hormones Usually, the pituitary-testicular system does not respond until the recovery period. Within the first 6 hh of restitution after various endurance exercises, a gradual drop in the blood testosterone! and androstencdione"? occurs. Low levels of both components may persist for at least 3 to 4 days.!##05% Prolonged running (15 to 42 km) caused a decrease in the plasma testosterone concentration. The longer the run, the more time it took before the testosterone concentration returned to pre-contest levels. In rats, short-term swimming with a high additonal load (13% body weight) caused a slight increase in the blood testosterone level but was followed during the first 2h of restitution by a decrease in the hormone level. At 4h after the exercise a rise in the hormone concentration was detected, exceeding the resting level by 1.5 to 2.5 times." This exercise bout increased the testosterone, androstenedione, and estradiol contents in the blood, skeletal muscles, and the myocardiuni. In skeletal muscles the hormone content was close to normal after 2, but increasedPost-Exercise Recovery Period 93 after 48 h (Figure 4-6). AU72 h after the exercise a decrease was observed in the androstenedione and estradiol content and a further increase in the testosterone content. The number of androgen- binding sites was increased by 20% 2 h and by 80% 72 h after the exercise. ‘The plasma lutropin level usually returns to the initial values within I h.and does not change further." However, after a 13- to 14-km run the plasma lutropin level decreased within the first 30 min and increased during the next half-hour." After incremental exercise until exhaustion the serum lutropin concentration declined below the basal level reaching nadir values between 60 and 180 min post-exercise. This fall in the serum lutropin concentration appeared to follow a slight but significant elevation of the plasma level of corticoliberin which reached peak values immediately after exercise, The plasma corticotropin paralleled the rise but fell to undetectable levels 60 min post-exercise, The plasma cortisol concentration peaked approximately 30 min after the rise in corticotropin, after which they gradually declined to baseline levels. Plasma testosterone concentrations paralleled to concen- trations of lutropin. It has been suggested that corticoliberin might suppress the secretion of lutropin after exercise.!* Thyroid Hormones Immediately after a marathon run, increased thyroid activity was evidenced by elevated blood levels of free thyroxine, free triiodothyronine, and thyrotropin. Free thyroxine remained elevated 1 hh later as well. At 22 lh after the race the thyrotropin concentration was decreased, and thyroxine and triiodothyronine levels were close to pre-race values. Comparison of the changes of free thyroxine or free triiodothyronine to free reverse triiodothyronine indicated that 22 h after the race a favored conversion of active hormones to inactive reverse triiodo- thyronine stil exists." After an 80-min exercise at 75% VO,max no changes in the free thyroxine levels were found. in rats, 30 m of running (35 m-min‘) induced increased levels of thyroxine and wiiodo- thyronine in the blood for 48 h, with peak values of thyrotropin 1.5 hafter the end of exercise (Figure 4-7). This response was observed even in rats made hypothyroid by repeated injections of mercasolil after 10 of swimming with additional load of 10% b.w.!?" Responses to Test Exercises in Men Substantial changes in the endocrine system during the past-exercise recavery period are evidenced by altered responses to repetition of the same exercise or to test exercise. In swimmers the noradrenaline, adrenaline, corticotropin, cortisol, and somatotropin responses to a 100-m swim, repeated | h after the first swim, were suppressed in comparison response to the first exercise bout. When swimming for 1500-m was repeated, noradrenaline and adrenaline responses were exaggerated, and cortisol and somatowopin responses de- creased. In both exercises the insulin response did not change, Increases in lactate, glycercl, and FFA levels were more pronounced after the second repetition of these exercises.'™ One hour after a 2-h exercise at $3% VO,max the heart rate response to Stroop conflicting color word test or to a 3-min exercise at 42% VQ.max were elevated, but the blood adrenaline responses to handgrip or the Stroop test were lowered. A reducti the adrenaline response might reflect either the altered adrenaline removal or changes in the activation of the adrenal medulla. The plasma noradrenaline and blood pressure responses were similar in the control situation and in post-exercise recovery.!”” ‘When highly qualified weight lifters performed two strength training sessions in 1 day, an increase in serum cortisol as well as in the total and free testosterone concent IS Was. observed only after the second training sessions, One hour after the termination of the afternoon session a decrease in the levels of three. hormones followed. The studied hormones decreased in response to the morning session. It was suggested that the diurnal variation might mask the exercise-induced changes during the moming session.'* However, summation of the94 Adaptation in Sports Training Seranaulzieeraty araapern tet ota K FIGURE 46 Testosterone (0-0), androstenedione (#-#) and estradiol (x-x) levels in blood serum (A), cytoplasin oof myocardium (B) and ckeletal muscle (C) in rats after swimming sox to seven times for 1 min with additional load ‘of 12% body weight (rest intervals 90 s). In the lower part of the figure the specific binding of nortestosterone to cytosol proteins (O-0) and number of binding sites (x-x) are indicated. (From Tchaikovsky, V. S., Fevtinova, LV. and Basharina, ©, B., Acta Comment. Univ. Tartuencis, 702, 105, 1985. With permission ) effect of the training session might also have an essential role. This possibility is indicated by a less pronounced increase in the lactate concentration and also by a more pronounced impairment of the maximal isometric force, the maximal rate of force development, and relaxation time after the second rather than after the first training session. WATER-ELECTROLYTE HOMEOSTASIS inges in the water and electrolyte content in the blood plasn the muscle and other tissues indicate the rate of restoration of the water-electrolyte balance after exercise. At the same time, changes in the levels of hormones controlling the water-clectrolyte balance express the activity of related homeostatic mechani ndPost-Exercise Recovery Period 95 * wee THYROTROPIN 08} oa —- fees THYROXINE . Fe aa ee, nmol" % * . TRIIODO-THYRONINE 144 a C5 eee, 24 aah FIGURE 4-7. Dynamics of thyrotropin, thyroxine, and tniodothyronine in the blood after 30 sin of cunning. (35 ‘emin~!) in rats, Asterisks denote statistically significant difference from the coatrol level Rapid re-uptake of K* by muscles and decrease of plasma K* are secn after exercises." The recovery kinetics of K* re-uptake by muscles were described by a very fast (<1 min) anda slow component (>1 min), The magnitude of the former was equivalent to what had accumulated in the plasma du . The time of restoration of the normal potassium level in the blood plasma varies from some minutes to20to 30 min after various exercises.!'*""" During recovery from anaerobic (exhaustion appeared after 4,6 + 1.3 min of exercise), but not from aerobic exercise (1 h at 65% VOnmax), there was a rapid decrease in the plasma potassium levels while the phosphate values were gradually normalized together with pH.™* While concentrations of scrum potassium and adrenaline returned to their basal levels immediately after incremental exercise until exhaustion, those of plasma noradrenaline and serum aldosterone remained elevated 30 min later." It was suggested that besides other hormones the increased level of plasma noradrenaline, maintained during the first 30 min post- exercise, might have a function in avoiding excessive hypokalaemia through the stimulation of c-receptors.""? a-Adrenergic stimulus produces an inerease in kalacmia through elevating the hepatic release of potassium. The later is obviously related to hepatic glycogenolysis. The function of noradrenaline may also be to compensate for the decreased volume of circulating blood by its vasoconstrictor action,aan aaah a 96 Adaptation in Sports Training Short-term exercises of high intensity performed until exhaustion caused a decrease in the volume: of the circulating blood by 20% in connection with water accumulation in the extra- and intracellular compartments of muscles, and in connection with increased concentrations of sodium and potassium in the blood plasma. At 10 min post exercise the concentrations of electrolytes decreased despite the fact that the volume of intravascular fluid was still dimin- ished. At | h after the end of exercise an increase of 5 to 6% was found in the volume of the circulating blood." In well-trained swimmers the blood volume that decreased during exercise was restored after a 100- or 800-m swim within 30 min, but plasma sodium within 2.5 min After an intensive all-out exercise (duration 10 to 11 min) the increased total persisted for 20 min. Water accumulation in muscles was associated with an increase intracellular water, At20 min post-exercise the intracellular water was normal, but the amount of extracellular water increased. In muscles both the total and intracellular Na* increased, but only the total volume remained beyond the initial level 20 min post-exercise. Total as well as intracellular potassium decreased and did nat normalize within 20 min of recovery. ‘The hormones of renin-angiotensin H-aldosterone, regulating the electrolyte balance, de~ clined slowly after various exercises.%!i08 After short-term exercise the aldosterone and renin normalization rates depend on the body posture. At 15 min aftera 20-min exercise bout both the aldosterone and renin levels remained at higher values in a sitting position than in a recumbent position.!"* Shifts in the water-electrolyte balance, caused by marathon competition, may persist for a prolonged period. Bload volume was increased by 16% on the second post-marathon day. On the third day a tendency to normalization was noticed but the volume remained beyond the initial values. During the first 2 days the sodium concentration was decreased in the plasma, but changes were found neither in the potassium and aldosterone concentration nor in the osmolality of the plasma." At 12 h after a marathon race the increased blood level of atrial natriuretic peptide had changed to a decreased one. At 36h after the race a secondary rise was observed. The elevated level of the peptide persisted for 7 days.!"” During the first I to 2 h after a 24-h endurance run the plasma volume had decreased by 2%, aldosterone, cortisol, and vasopressin concentrations were increased, and atrial natriuretic peptide was decreased. During 3 days of recovery, plasma volume rose, with a peak on the second day (by 24% over the initial level) and remained elevated on the third day. Cortisol, vasopressin, and atrial natriuretic peptide returned to baseline 24h later, and aldosterone 72 ‘h later." At 24 h after termination of the 24-h run the plasma Na* and K* were normal, but ‘the Nat level in the urine was very low and the K* urinary level was elevated in connection with the increased aldosterone concentration in the blood plasma. Differently, after a 10-h triathlon competition, the high aldosterone level was associated with normal urinary sodium and potassium. High blood cortisol was found 2 days after the triathlon but not after the 24- h run, Increased activities of creatine kinase, lactate dehydrogenase, aspartate aminotrans- ferase, and alanine aminotransferase persisted at least 24 h after the 24-h run. Erythropoietin conccatration in the blood was increased at 3 h and, more impressively, 31 h after a marathon run but not immediately after the race. At 31 h after the race a pronounced increase in the plasma volume was established, which led to a hemodilution together with decreased concentrations of both erythrocytes and hemoglobin," After very prolonged exer- cise hypocalcemia persisted for 48 h both in rats!*! and in humans." This was associated witl a high level of calcitonin in the blood plasma."*'!"? Highly intensive anacrobic exercise caused an increase in the magnesium concentration in both the blood and urine. These changes correlated with an increase of lactate in the blood. ‘The blood magnesium level normalized within 2 bh." During a marathon race serum magne= sium increased from 1.44 to 1.68 meq: within the first 2 h. Thereafter the magnesium, Gnicentration dropped to 1.07 meq:I" by the end of the race and returned to its pre-race value ‘water thePost-Exercise Recovery Period 7 by 1 b of recovery. During the first 20 min of recovery a further decrease in the blood magnesium concentration was found.' A further decrease in magnesium concentration was also found in cases of its reduction during exercise.'** Exercise-induced changes in total zine and zinc derived from carbonic anhydrase type I in erythrocytes as well as in total zinc in the plasma disappeared within 30 min. ‘CENTRAL NERVOUS SYSTEM ‘The main features of immediate changes in the status of the central nervous system are a certain inertia of exercise-induced changes in excitability and lability of nervous centers, followed later by undulated changes. The corresponding changes in optical and tactile rheobases'*? and latency of muscle contraction and relaxation! are presented in Figure 4-8. Undulated changes were found also in motor chronaxic. For skeletal muscle a relative hypoexcitability for rectangular electrical stimuli has been found in association with low serum Mg level. The polyphasic nature of changes in the central nervous system after exercise was con- firmed by studies of conditioned reflex responses (CRR} on stimuli not related to muscular activity, Immediately after exercise the CRR were more rapid and stronger than before exercise, It was suggested that the first phase of the recovery period expresses the remaining excitation of the central nervous system. This phase was followed by an inhibition phase: the CRR appeared slowly and were less pronounced. When a certain time period elapsed, the phase appeared, suggesting a normalization of the state of central nervous structures, In a number of cases a further exaltation of reflex responses was later observed. Afier a hard, fatiguing exercise the first phase was not found and the inhibition phase appeared just after H-response of various muscles after all-out exercise (duration less than 10 min) indicated aa decreased excitability of spinal motoneurons during the first 3 to 6 min, Then an increased excitability was found. A complete recovery of motoneuron excitability was detected within 8 to 12 min after exercise.'*! ‘The polyphasic changes appear also in the working capacity during the first minutes or hours after exercise, The recovery of strength is initially rapid with a subsequent two- ‘component pattern,'*? Following rhythmic exercises, the recovery of strength was faster than after a static one.!* Likewise, the recovery of local muscular endurance is initially fast and then a slow period of normalization follows." After a subject squeezed a hand-grip device for as long as possible at a tension of $0% of his maximum voluntary contraction, the percentage of recovery at various time periods revealed a three-component exponential curve. ‘The percentage of recovery, calculated by dividing the holding time of the first bout by the time of the second, ranged from 20% after 5 s of rest (0 87% after 42 min 40 s of rest.!"* The short-term phases of working capacity and strength are probably associated with changes in the nervous centers, acting through alterations in the recruitment of motor unit The alterations may be related to the various levels of excitability ‘of motoneurons or other nervous cells, participating in the organization of movements. However, besides chan, the central nervous system, one must take into consideration the fact that in the first minutes after exercise there may exist an intracellular electrolytic unbalance due to the lagging behind of the Na,K-pump functions, and the interference of depletion/repletion of intramuscular energy stores and metabolite accumulation of working capacity of muscles, The recovery of force is closely correlated to the decrease in intracellular Na’, Inhibition of the Na,K-pump favors the net loss of K*, gain of Na‘, and development of fatigue in the isolated working muscle." In the frog muscle, 15 min after stimulation 30 times per minute (contractile foree decreased 36%, lactate content increased from 3.3 to 18.7 umole! of muscle) recovery ‘occurred in two phases. A rapid increase in contractile force (20% of total recovery) took place during the first 1$ s concomitantly with an increase in ATP from 3.9 to 4.6 wmol-g. LactateSe Ep SneTaeerecreeneeeee co 98 Adaptation in Sports Training ‘Optical Rheocbase (mV) oan 10.0" s| |o 75: [| « 5.0: wsasag 25 Latency of Muscle Contraction (LC) and Fielaxation (LA) N in msec 1235 70 15 20 25 30min IRE 48, Post-exercise changes of the optical sheobase (upper part) and latency period of contraction or relaxation (lower par). Upper part: black colurun — initial level, vertical inferrupied lines — I-min exercise striated columns — levels determine 20 s, 40 s, 80 5, 100 s, 2 min, 3 min, and 4 min after exercise, respectively. (F Krestovnikov, A. N., Survey on Piysiology of Physical Exercise, FAS, Moscow, 1951, With permission } did not change during this period. The second phase of contractile force recovery was completed in 30 min. The recovery of contractile force lagged behind the decrease in the lactate level. A significant correlation (r = 0.91) was established between the two indices. 57 A direct pH-dependence of force recavery was not observed during the initial phase of recovery but if present, such a relationship might have been masked by other factors like P, or H;PO",, During the latter phase of recovery a pH-dependent mechanism could come into- action directly.!** REPLETION OF ENERGY STORES: TIME SEQUENCE OF THE REPLETION OF VARIOUS SUBSTRATES By a general consensus, more rapid repletion of energy-rich phosphates than that of glycogen is accepted. Within the first 60's of recovery approximately 70% of the ATP and phosphocreatine were replenished (Figure 4-9). For complete recovery of the ATP store 2. ofrrecovery was necessary, but for recovery of the phosphocreatine store, more than 3 min sary. During highly intensive intermittent exercise 3-min intervals between exer bouts were not sufficient to avoid a gradual decrease of muscle phosphocreatine content.'@ee Past-Exercise Recovery Period 99 apeeoay o 1 2 a FIGURE 4-9. Restitution of ATP and phosphocreatine contents in skeletal muscles after all-out anacrobie exercise in ma, Results of various persons are indicated, (From Multman, E., Bergstrom, J, and McLennan-Anderson, N.. Scand. J. Clin. Lab. Invest, 19, 56, 1967. With permission) After all-out exercise at 100% VOmax less than 10 min was necessary for the complete recovery of ATP, ADP, and phosphocreatine levels in the quadriceps muscle." However, there are also results indicating that ATP repletion does not always precede phosphocreatine recovery" or even glycogen recovery. After a 3-min one-leg exercise a rapid repletion of ATP and phosphocreatine stores was found in the vastus lateralis muscle ‘during the first 10 min. Later the recovery process slowed down and | h after the exercise the levels of energy-rich phosphates as well as glycogen constituted only 90% of the initial. At 9 days after a marathon race decreased levels of ATP, ADP, AMP, and IMP were found in the vastus lateralis muscle, implying that in alate phase of recovery the adenosine deamination was intensified. At the same time, the muscle glycogen level was slightly increased." At least in rats during the initial 30 min after a short-term running, glycogen synthesis was much slower than during the second 30 min. Between 30 and 60 min after exercising the glycogen synthesis rate was hiighest in various types of skeletal muscle fibers, heart, and liver. Comparison of glycogen synthesis rates showed that this process is fastest in the fast-twitch oxidative-glycolytic (FOG) fibers and in the myocardium. The rate of slow-twitch oxidative (SO) fibers was 2 times slower. The slowest rate was observed in the fast-twitch glycolytic (FG) fibers (Figure 4-10). The resting level was first reached in the myocardium and FOG fibers, then in SO fibers, and lastly in FG fibers and liver." The same schedule in glycogen repletion was found in rats after other strenuous exercises.” In most cases, the resulis obtained both in humans*'©'6 and in rats! indicate that the phase of rapid glycogen synthesis occurs within 4 to 6 h after the end of exercise. In this phase the rate of glycogen synthesis is primarily dependent on the amount of glycogen depletion while the subsequent less rapid phase has been reported to be related to the insulin-induced activation of glycogen synthesis."100 Adaptation in Sports Training SUPERCOMPENSATION “The post-exercise supercompensation for muscle glycogen stores was first reported in the Iate 1940s.!." This phenomenon is dependent on the rate of glycogen depletion during ‘exercise. A little later, supercompensation for the phosphocreatine store was reported (Figure 4-11). When glycogen supercompensation in the rat muscles was found within I to 24h post- exercise, supercompensation for phosphocreatine appeared in the muscle following a shorter me interval, which elapsed after the cessation of exercise.!”" After short-term intensive swimming a rapid resynthesis of phosphocreatine occurred, with a pronounced supercompensation, while after long-term swimming the phosphocreatine synthesis was re- tarded and supercompensation less pronounced. Patterns of glycogen resynthesis were similar in both cases." Phosphocreatine and glycogen supercompensation appeared in the muscles of slow-twitch fibers earlier than in the muscles of fast-twitch fibers.!”* According to these results, it was later shown that in humans the restitution rate of ATP, ATP/ADP, phosphocreatine, and lactate is in correlation with the oxidative potential of the skeletal muscle, estimated by the activity of citrate synthase.'"* While immediately after exercise the concentrations of mitochondrial proteins and mite- chondrial P/O were decreased, 1h later both values were significantly higher than in the sedentary control rats. The increase in mitochondrial proteins was associated with an i 4 concentration of phosphatile inozitol and polyglyceride phosphatide but not of other phospholipids in the mitochondrial fraction of skeletal muscles.."" The post-exercise increases in the succinate dehydrogenase activity, mitochondrial proteins, and P/O were higher after swimming in water of 22 than af 32°C." ‘The involvement of mi substrate supercompensation has been confirmed in several studies. In rats uncoupling of oxidative phosphorylation by administration of 2.4-dinitrophenole decelerated the recovery process, no supercompens for glycogen and phosphocreatine was observed, and elimination of lactate was retarded. ‘The exercise-induced reduction of mitochondrial P/O and respiratory control was followed by an increase in both indices after exercise. Experiments on rats indicated that these changes ‘were accompanied by an elevated ratio of B-hydroxybutyrate/acetoacctatc. At that time, increased reductive properties of the mitochondrial pyridine nucleotides and preferably active ‘oxidation of succinate, accumulated in muscles during exercise, were common.'”* At I h after 15 min of swimming the ATP content and the ratios of ATP/ADP and ATP/(ADP-Pig,) Weke elevated.’ It was concluded that a peculiar ‘synthesizing state’ of the skeletal muscle mitochondria appeared related to the overproduction of ATP and supercompensation for energy stores. The increased ratios of ATP/ADP and NADH/NAD suppress the catabolic e of energy metabolism, favoring the substrate supercompensation. However, suppres- sion of the catabolic phase of energy metabolism creates conditions for a decrease in the ATP resynthesis rate, resulting in a reduced ratio of ATP/ADP. Throughout a new intensification of the catabolic phase of energy processes a return to the basal level will be ensured." ‘The phenomenon of substrate supercompensation has repeatedly been confirmed. In- creased levels of glycogen'®#-!#"5 and phosphocreatine'“*'* were found in skeletal muscles after exercises in certain time periods both in humans™!61814 and rats.!**'* In the rat soleus muscle glycogen supercompensation appeared to be followed by a secondary decrease." Muscle glycogen supercompensation can be. stimulated by carbohydrate feeding."*""” Since there is a positive correlation between the pre-exercise muscle glycogen concentration and the ability to perform prolonged severe exercises," the glycogen supercompensation en hanced by carbohydrate feeding is correlated to the time of competition in endurance events. FIGURE 4-10, Pos-exercise dynamics of glycopen in the myocandium, FG, FOG, and SO fibers in rats. Arrows Indicate the tire of ctu iil eve andthe tie of ease of supercornpemsatoa, Comstructed from results of FLL. “Terjung et al! LLPost-Exercise Recovery Period 101 -1 50 mg-g wet weight 40 20 10 of hot cw ae eee aa eae Control 123 4 Ey 48h mg-g wet weight 1234 24 48h102 ‘Adaptation in Sports Training _ _ Glycogen Nonprotein N 05 Ih 6 2 aah FIGURE 4-11. Substrate superoompensation im rats after exercise. (From Yakovlev, N. N.. Sportbiochemie, Barta, Leipzig, 1977. With permission ) In rats supercompensation was demonstrated also in regard to the liver!“"724% and myo- cardial glycogen content.!7=#*+!% Glycogen supercompensation was found in a period of 1 to 4hafter exercise in FOG fibers. and myocardium, 4h post-exercise in SO fibers, and 24 hpost- exercise in FG fibers and liver.' CONTROL OF GLYCOGEN RESYNTHESIS Rat experiments demonstrated that after exercise the rate of glycogen synthesis was in good accordance with the activities of glycogen synthase, mainly glycogen synthase I”* and hexokinase." The activation of glycogen synthase occurs rapidly in a high correlation with an increase in cAMP-phosphodiesterase activity." In humans a significant increase in glycogen synthase fractional activity was found as early as 5 min after cycling at 75% VO;max. At this time the cAMP-dependent protein kinase activity had reverted to the pre-exercise values.” Glycogen depletion per se induces an increase in the active form of glycogen synthase'*™ and stimulates glycogen synthesis.2% Nevertheless, glycogen synthase fractional activity ine creased markedly during the first 5 min both in conditions of low muscle glycogen (due to previous diet and exercise) and in conditions of high glycogen.'”” In man the rate of glycogen synthesis was still elevated when the increase in the form I of glycogen synthase had disappeared, indicating that other factors must also contribute to the high rate of glycogen synthesis in the post-exercise period. In rats during an initial phase of post-exercise recovery glucose uptake in skeletal muscles took place despite the lack of endogenous insulin.” In this phase a rapid glycogen synthesis occurred despite low insulin and elevated noradrenaline and glycogen levels in the blood plasma." During the second phase, when the glycogen content in the muscles reached the basal level or exceeded it, glucose uptake** and glycogen synthesis were insulin-dependent.!14 Insulin has an essential function also in myocardial glycogen resynthesis and supercompensation. Vigorous running for 45 to 75 min caused a decrease in cardiac glycogen in association with increases in glycogen synthase activity and glucose-6-phosphate content. Within 2 to 8 h of recovery the glycogen store was supercompensated, glycogen synthase I activity decreased, and the glucose-6-phosphate content normalized. All these changes were modest in diabetic rats but they became close to normal after treating diabetic rats with insulin.** Post-exercise supercompensation for cardiac glycogen was enhanced with dexamethasone treatment, eliminated by adrenalectomy and restored in adrenalectomized rats that had beenPost-Exercise Recovery Period 103 given daily doses of dexamethasone.™ In adrenalectomized rats a slow rate of glycogen post- exercise repletion was found not only in the myocardium, but also in skeletal muscles and liver. Dexamethasone treatment restored the glycogen repletion rate in adrenalectomized rats. The blockade of protein synthesis excluded the dexamethasone effect, suggesting that the glucocor ticoid effect was mediated by synthesis of regulatory protein, most likely of glycogen synthase." SUBSTRATES FOR MUSCLE GLYCOGEN REPLETION When subjects fasted during the post-cxercise recovery, they exhibited a small but signifi- cant inerease in the muscle glycogen concentration ** In fasting rats a preferential resynthesis of muscle glycogen was found. Obviously, the resynthesis of muscle glycogen can proceed by utilizing endogenous substrates. Those substrates may be lactate produced during muscular activity and glucose released from the liver. Lactate Lactate has been assumed to serve as a substrate for muscle glycogenesis since the elaboration of the Meyerhof-Hill theory" A number of more recent results.confirm this old postulation.*7="2! However, only muscles composed predominantly of FOG or EG fibers have been demonstraicd to synthesize glycogen from lactate." In the removal of blood lactate, the main role belongs to SO fibers.!* The primary fate of absorbed blood lactate is oxidation." For glycogen synthesis in muscles blood glucose is preferred.2)22» 1g of muscle glycogen stores may be associated with a further decrease in liver glycogen during the first post-exercise hours. Obviously, the fast repletion of muscle stores is actualized at the expense of liver glycogen. ‘The rate of muscle glycogen repletion depends on the blood glucose level,” maintained at the expense of liver glucose output of of ingested carbohydrates,!%! Fructose ingestion produces a slower rate of glycogen resynthesis than glucose or sucrose ingestion." After prolonged exhaustive exercise ora GLUCONEOGENESIS AND LIPID METABOLISM Hepatic Gluconeogenesis ‘The rate of liver glycogen restitution is slow until the person or test animal is refed.2'!2'%25 In subjects recovering from exercise, glucose infusion raised the blood level of glucose up to 12 mmol-T", but the arterio-venous glucose difference across the liver was negligible“ The results confirm that the liver defers its glycogen to supply other tissues, such as cardiac and skeletal muscle, by glucose output. After exercise, there is an intensive gluconeogenesis in the liver. During postexercise recovery the splanchnic uptake of gluconeogenic sub- strates is augmented.2"*221235 Convincing evidence is provided for intensive use of blood lactate, alanine," and glyceral™ in hepatic gluconeogenesis after exercise. In the post-exercise period the main role in gluconeogenesis belongs to alanine” While a considerably higher glycogen synthesis has been detected in exercised muscles after glucose than after fructose infusion,” fructose infusion gives rise to a four-times-larger increase in liver glycogen synthesis than does glucose infusion in man 2 dn exercising rats it was found that the increased gluconeogenic flux was the result of the increased activities of gluconeogenic enzymes, pyruvate carboxylase, and fractose-| biphosphatase, with the concomitant inhibition of glycolytic enzymes, 6-phosphofructoki- nase, and pyruvate Kinase. The increased maximal activities of gluconeogenic enzymes were related to changes in the concentrations of several allosteric modulators: increased acetyl- Coa, decreased fructose-2.6-biphosphate, and decreased fructose-1.6-biphosphate 2104 Adaptation in Sports Training Lipid Metabolism Elevated blood levels of glycerol and FFA were found during 24 h after prolonged exercises" By other results, blood glycerol and FFA concentrations returned to the pre- exercise levels within 20 to 60 min, but despite that, a low respiratory exchange ratio. persisted.5=="2"? This was explained by the utilization of intramuscular triglycerides." Tt Wwas mentioned earlier that the triglyceride-free fatty acid eycle may proceed intensively during the recovery period. During 2 h of recovery after moderate cycting for 100 min the insulin effects on carboby- drates and lipid metabolism proved to be altered. While during exercise insulin infusion enhanced carbohydrate oxidation, in the recovery period the insulin effect was negligible. Nonoxidative carbohydrate metabolism increased during the recovery period and became more sensitive to insulin than in resting conditions. However, an exercise-induced increase in fat oxidation did not appear in the first 100 min of the recovery period despite the persisting elevated levels of both glycerol and FFA. Suppression of the FFA level but not of fat oxidation by insulin infusion was enhanced after the exercise.7” These results suggest that the post- exercise increase in insulin secretion together with the increased sensitivity of lipid metabo- lism to insulin will limit the amount of fat oxidation, stimulated by the increased level of EFA. For interpretation of the changes in lipid oxidation one must take into consideration the possible alteration in carnitine metabolism, Exercise-induced increase of esterified camitine in the muscles persisted for 90 min and was associated with a decrease in free camitine Lipid peroxidation during the post-exercise recovery period has not yet been sufficiently studied, The significance of this problem is indicated by the fact that muscle pain that appeared. 24 hafter the exercise was preceded by an inerease in the serum lipid peroxide concentration. RECONSTRUCTIVE FUNCTION OF THE RECOVERY PROCESS PROTEIN SYNTHESIS IN SKELETAL MUSCLES “The renewal of structural and enzymatic proteins in the muscular tissue can be completed only after the end of muscle activity. Accordingly, elevated intensity of protein synthesis is considered to be common for the recovery period after exercise. The exercise-induced de- crease of protein nitrogen was found to be reversed after the cessation of contractile activity. ‘Approximately 6 h after swimming it was on a higher level in comparison with the level in sedentary rats,!7!2828 ‘The studies of whole body metabolism in men point to nitrogen retention in the recovery period.***® The post-exercise intensification of protein synthesis was proved by the elevated ratc of amino acid incorporation into various fractions of skeletal ‘muscle proteins”? as well as by enhanced incorporation of labeled precursors into RNA.** ‘Accordingly, increases in the ribosomal translational activity” and nuclear RNA polymerase activity®s”2 were detected in the recovery period. However, it would be an oversimplification to regard the post-exercise recovery as @ transition from exercise-induced overall catabolism to anabolism. The picture is more: com- plicated. During the first hours of post-exercise recovery the rate of protein synthesis remains low in the skeletal muscle of man™# and rat.2#2S2%2" In rats the duration of this period varied from 6 to 24 h. It is only after this initial period that the rate of protein synthesis increases. ‘There are significant differences in the intensity of protein synthesis between various protein fractions as well as between muscle fibers of various types depending on the character of the performed cxercise. The immediate effect of 6 h of swimming was a remarkable decrease in the incorporation of 'C leucine into actin and the myosin heavy chains in the gastrocnemius muscle, but it caused an increase in the incorporation into myosin light chains. An elevation of amino acid incorporation into actin and myosin heavy chain was observed 48 h post- exercise A post-exercise increase in protein synthesis was also detected in isolated mito- chondria."Post-Exercise Recovery Period 105 After endurance exercises the main locus of the increased rate of protein synthesis is the mitochondria of FOG and SO fibers (Figure 4-12). The highest rate was found 24 h post- exercise. Instead of increased synthesis of various proteins, in PG fibers the incorporation of labeled tyrosin into myofibrillar, sarcoplasmic, and mitochondrial proteins was decreased within 24 to 48 h post-exercise.*® This fact allows us to suggest that during the recovery period the inhibition of protein synthesis in previously less active muscles and fibers makes it possible to concentrate the adaptive protein synthesis for structures that performed the highest load, ‘The main results of this study were confirmed with the aid of an ultra-autoradiographic study. In this study the comparison of dynamics in label incorporation showed that thyroid hormones may promote post-exercise synthesis of proteins in skeletal muscles. In hypothyroid rats no increase was found in label incorporation during a 48-h recovery period after 30 min \g- In these rats a low level of label was found in the mitochondria as well as in all regions of sarcoplasmit and myofibrils during the recovery period. However, after a short- term highly intensive exercise (10 min of swimming with an additional load of 10% b.w.) a post-exercise increase was observed even in rats made hypothyroid by repeated injections of methimazole. The rise in the blood level of triiodothyronine and thyroxine coincided with the increased incorporation of *H-tyrosine in all types of muscle fibers. The most pronounced increase in label incorporation was found 24 h post-exercise in SO fibers.” These results may be considered to be a justification of the hypothesis about hormonal amplification of adaptive protein synthesis induced by metabolic inductors. Probably, after endurance exercise thyroid hormones ensure hormonal amplifications of this kind. Their function in stimulating the genesis of the mitochondria in skeletal muscles is evidenced by the results of various studies.“ In accordance with the above, mentioned results is also the fact that the thyroxine effect on mitochondrial enzymes is more pronounced in the red muscles than in the white ones.** Thyroid hormones may also contribute to the induction of skeletal muscle myosin. ‘A different situation exists after exercises for improved strength. In these cases the main Jocus of adaptive protein synthesis is the myofibrillar proteins of fast-twitch glycolytic fibers, In men the action of a resistance training session (4 sets of 6 to 12 repetitions of the biceps curl, preacher curl, and concentration curl with a resistance equal (0 80% IRM) on protein synthesis in the biceps muscle was studied, using the opposite arm asa control. Muscle protein synthesis was significantly elevated 4h post-exercise, The increased protein synthesis rate persisted for at least 24 h, The increase appeared to be due to changes in post-transcriptional events, The latter conclusion was founded on the unchanged RNA capacity (expressed as total RNA content relative to noncollagenous protein content) and elevated RNA activity (ex- pressed as the amount of protein synthesized per unit time per unit RNA). In rats a model was employed to imitate the human resistance training: skeletal muscles of anesthesized rats were electrically stimulated to contract againstresistance, Aftera single bout of ‘exercise’ myofibrillar protein synthesis rate increased 50 to 60% 12 to 17 and 36 to 41 h after the exercise. However, skeletal G-actin mRNA and cytochrome ¢ mRNA were not altered at these times.*?2"" AAn increase in translation of protein can be inferred from such data.2! Stimulation of the synthesis of myofibrillar proteins and RNA polymerase activity”? in skeletal muscles by anabolic steroids makes it possible to assume that in normal conditions the synthesis of myofibrillar proteins is amplified by endogenous androgens. To support this suggestion some evidence is necessary to prove that strength exercises, which cause myo- fibrillar hypertrophy, specifically stimulate the production of endogenous androgens. There exist variable changes in the blood level of testosterone during and after exercises for iproved strength. However, the most essential factor is the dynamics of androgens during the recovery period. It has been indicated (see p. 91) that a general characteristic of testosterone dynamics is its low level during the first hours of the first day after exercises. However, apart of runnii106 Adaptation in Sports Training CHANGES IN PROTEIN SYW’ MYOPIBRILLAR SARCOPLASMATIC 5 50 25 25 50 MITOCHONDRIAL 25 50 FIGURE 4-12, Synthesis of myofibrillar, sarcoplasmic and mitochondrial protcins in red (R.Q) and white (W.Q) portioas of the quadriceps muscle and the gastrocnemius muscle (G) after 30-min running (35-m-min in rats. From Vira, A. and Ovplk, V., in Paaver Nurmi Congress Book, Kvist, M., B&., The Finnish Society of Sports Medicine, ‘Turku, 1989, 55. With perranission ) from endurance exercises, in case of strength exercises, there follows a tendency to an increased production of testosterone. It is worth repeating that this change is associated with the augmentation of the testosterone and androstenedione content and also with an increase in the number of androgen-binding sites in skeletal muscles.” Similarly to the exercise effect, single injection of testosterone of 10-nortestosterone caused arapid decrease in the eytoplas- mic androgen receptors in skeletal muscles 1 b afier treatment, which was followed by its twofold increase 5 to 6 h later, Inhibition of protein synthesis by cyclohexamide 1 h after testosterone treatment led to a less pronounced augmentation of androgen receptors over the control values 5 hh later.2"* Results have been obtained to confirm the role of testosterone and related androgens in the postexercise synthesis of proteins in skeletal muscles. Repeated L-min swims with an addi- tional load of 12% b.w. (6 to 7 repetitions over rest intervals of 1.5 min) caused a decreasePast-Exercise Recovery Period 107 in the contents of aspartate aminotransferase and myoglobin in the quadriceps muscle during the first 24 h of recovery. At 48 to 56h postexercise the content of these proteins was increased by 30%. At the same time testosterone concentrations in the blood and muscle as well as the number of androgens binding sites in the cytoplasm of the muscle were substan- tially over the control level?" ‘The specific nature of the amplification of protein synthesis in skeletal muscles by teste csterone has been confirmed by results obtained by A. Saborido et al? Treatment with anabolic androgens increased succinate dehydrogenase activity in the fast-twitch muscle jochondria. This effect was not enhanced when anabolic steroids were administered during training. Moreover, the effect of anabolic steroids on the mitochondrial enzyme was not observed in the soleus muscle. Thus, the typical effect of endurance exercises on the mito- chondria of oxidative muscles was neither reproduced nor amplified by the administration of steroids. » A stimulatory effect on the protein synthesis (probably on the translational level) is produced by insulin and somatotropin.2"* In adults with a somatotropin deficiency, the human growth hormone treatment increased the lean tissue, the total cross-sectional area of the thigh muscle, the strength of the hip flexors, and the limb girdle musele, but not that of number of other muscles.2” Increases were found also in VO.max, anaerobic ventilatory threshold, and maximal power output." However, one must take into consideration the long period of treatment (6 months) necessary for obtaining the above-mentioned effects as well aas the initial hormonal disbalance in the studied patients. In rats, daily injections of somatotro- pin over 36 days resulted in a significant increase in the diameter of both types of fibers (I and I) in the extensor digitorum longus and soleus muscles, The DNA/protein ratio and the number of satellite cells per muscle fiber cross-sectional area increased as wel Hind leg perfusion with insulin at 200 WU-ml- but not at 75 wU-ml stimulated protein synthesis in the white gastrocnemius. After running exercises the insulin effect was not enhanced.” m DEGRADATION AND TURNOVER OF PROTEINS A characteristic feature of postexercise protein metabolism is the coincidence of an increased rate of protein synthesis with an elevated rate of protein breakdown. While protein synthesis is suppressed immediately after exercise and thereafter enhanced, protein degrada- tion remains elevated for a long period. A high level of urea in the blood and urine persists for many hours after strenuous exercises ®*" ‘After exercises the increased urea level is not necessarily caused by retention of the urea on the level of renal excretion. Contrarily, the post-exercise period was characterized by an increased renal clearance of urea in rats after swims of various duration (Figure 4-13). After only 10 h of swimming a lag period of up to 12 h preceded the increased urea excretion and elevated the renal clearance rate. The post-exercise increase in urea renal elimination is glucocorticoid dependent; it is absent in adrenalectomized rats.”5* In rats the increased urinary excretion and renal urea clearance persisted for a longer time than was necessary for the normalization of the blood level after swims of various duration.“ If endogenous production and climination rates are equal, increased production may lead to an elevated urinary excretion without any increase in the blood level, Therefore, the results obtained in rats point to a persisting clevated urea production for a long period after exercise. Accordingly, the activity of hepatic arginase, an important enzyme in urea biosynthesis, remains elevated for many hours after exercise." Exercise-induced increase in tyrosine release from muscles may also persist for hours.°"2"" However, alanine output from muscles decreases rapidly after exercise? Since the elevated net uptake of alanine by the splanchnic bed persists,” the blood level of alanine decreases. 3-Methy histidine is released from muscles as a result of myosin and actin degradation, It will be excreted without any conversion or reutilization. Despite the great variability in the108 Adaptation in Sports Training - ie ; . i é & : B) ee ee ato Fk Usinary Uroa Exeration Rate bdo! Prana 1paeaigue entra aegis 4 Contr Period —-_-Posiercise Period FIGURE 4-13. Urea level of blood plasma (solid line), urinary urea excretion rate (white colurans), urine flow rates (Gtriated columns) and renal urea clearance (interrupted line) in rats after swimming for 3 h (upper part}or 10h (lower part), (From Litvinova, L., Viru, A., and Smimava, T.. Jpn. J. Physiol. 39,713, 1989. With permission.) changes that occur in 3-methylhistidine excretion during exercise, the increased excretion is a post-exercise phenomenon (Figure 4-14). The excretion dynamics were identical when the persons were on a meat-free ration 3 days prior to the exercise or when from the total 3- methylhistidine excretion the amount of 3-methylhistidine containing the consumed food was substracted.2” The post-exercise increase in 3-methylhistidine liberation was also revealed in the blood 3-methylhistidine response*2* and in the accumulation of the metabolite in muscles.2 Increased protein degradation in the recovery period has been confirmed by isotopic methods “2% In humans, 5 h after prolonged exercise, the rate of protein synthesis was elevated together with an increased rate of protein degradation. In rats after 10 h ofPost-Exercise Recovery Period 109 Aa 3-METHYLATSTIDINE i, pllol+ 1g. protein’ PREE TYROSINE peste wot ttooue™! GLYCOGEN — 2 i £19 a7 ¢ 8 21 O26 2 768 FIGURE 4-14. 3-Methyhistsie, fee tyosia, and glycogen level in sed (R.Q) and white (W.Q) portions ofthe quadsiceps muscle in rats after swimming for 10 h, swimming a high intensity of protein breakdown persisted for at least 24h in the soleus muscle. The increased protein degradation was associated with a decrease in the protein content in the muscle during exercise. The increase in the protein synthesis rate followed the period of its suppression and was accompanied by a normalization of the protein content for 24h after the termination of cxercisc. A furthcr intensive protcin synthesis rate did not lead {© an increased protein content due to the persistence of an intensive protein breakdown *! ‘The listed results of various studies justify the conclusion that the increased 3-methylhistidine: liberation and excretion afier exercise must not be regarded as an index of the prevalent breakdown of contractile proteins, but as a sign of their increased turnover. GJ. Kasperek and B.D. Snider found a 3-day period of increased 3-methylhistidine excretion after eccentric exercise. They both believe that this reflects protein degradation due10 Adaptation in Sports Training to the breakdown of muscle tissue that was damaged during the exercise bout. On the other hand, this process can also be considered part of the general renewal of cellular structures in the muscle after exercise. ‘The increased protein turnover contributes to the renewal of the molecular content in the actomyosin complex and other musele proteins in order to eliminate the physiologically exhausted structure elements and to ensure an improvement of the contractile function. However, a question remains of how to interpret the catabolic and antianabolic changes in muscles during and shortly after strenuous exercise. Naturally, itis difficult to assume that the activity causes changes destroying the active organ. Therefore le to suggest that the catabolic and antianabolic changes take place mainly 1g oF less active muscles, As has been repeatedly demonstrated above, the character, intensity, and duration of the exercise determine the degree of recruitment of muscle fibers of various types. This gives ‘us an opportunity 10 compare the catabolic changes in muscles containing various types of fibers for evaluating the significance of the degree of muscle activity. ‘The release of 3- methylhistidine and accumulation of free tyrosine occurred in rats during 10 h of swimming mainly in the white portion of the quadriceps muscle. The red portion of the quadriceps muscle, revealing a more pronounced glycogen drop, produced 3-methylhistidine to a little ‘extent during exercises (Figure 4-14)2' Thus the mobilization of structural proteins is not ‘extended to the contractile apparatus of working muscles. The less active muscles, including their contractile proteins, are: used as a reservoir for mobilizing protein resources. Obviously, activity makes musele tissue less sensitive to catabolic influence. An analogous situation is revealed in the catabolic action of glucocorticoids on muscle tissues: muscle activity decreases their catabolic influence. ‘Compared with the catabolic response during and immediately after exercise, another picture was revealed in protein breakdown in various types of muscle fibers some hours after exercise. In the less active white portion of the quadriceps the 3-methylhistidine content normalized and the increased level of free tyrosine declined after 6 h of post-exercise recovery (Figure 4-14). In the more active red portions of the quadriceps, elevated levels of 3- methyl and free tyrosine were observed after 6 h of recovery. Increased levels were observed 24 and 48 h post-exercise (swimming for 10h) as well.! Thereafter, while during ‘exercise the most active muscle fibers do not contribute to the mobilization of protein resources, in a later stage of post-exercise recovery, catabolic changes take place in most active fibers. These catabolic changes, reasonably, constitute a part of the enhanced protein turnover. ILis tempting to suggest that changes in the testosterone/cortisol ratio are important in the regulation of protein metabolism in skeletal muscles and in the regulation of the protein turnover rate. After endurance exercises the ratio remains low for many hours. Am increase in both cortisol and testosterone concentrations was observed during 30 min of strength ‘exercise without change in the testosterone/cortisol ratio. At 1 h post-exercise, cortisol remained on a high level, but the amount of testosterone decreased. At 6 h post-exereise the levels of both hormones were below the initial values. At 24 h post-exercise cortisol remained ‘on a low Ievel; testosterone concentrations returned to the initial levels, causing a significant increase in the testosterone/cortisol ratio.™ Testosterone has been shown ta antagonize the proteolytic effect of exercise through its action on alkaline proteolytic enzymes." Increased uurea excretion coincided with a decrease in the blood levels of testosterone and androstenedione in rats after muscular activity.°° After an intensive anaerobic interval training session the blood urea level was increased from the second to twenty fourth past-exercise hours concomi- tantly with low levels of testosterone and cortisol.~” The increased post-exercise tumover of myofibrillar proteins seems to be ensured by myofibrillar proteinases. Myofibrillar proteinase activity at alkaline pH had already reachedPost-Exercise Recovery Period i its maximum level during the exercise. Moreover, the maximal proteolytic activity at acidie pH was found 6 h, and at neutral pH 24 h post-exercise.™* After very hard exercises an increased activity of lysosomal enzymes may persist for many days. However, results were reported indicating the postexercise release of free tyrosine after a blockade of lysosomes. ‘This indicates that the: exercise-induced increase in the rate of protein degradation oceurs by increasing the flux of proteins through the nonlysosome degradation pathway.2? Ca-activated proteinases — calpains — may have contributed to a post-exercise increase in protein tumover. After eight swims of 1 min with an additional load of 12% b.w. (rest tervals between repetitions 90 s) the activity of calpains remained at the control level during the first hours. The following increase in the calpains activity led to the highest level 24 h after the exercise. The high level was maintained for 60 h. A return to the control level was found only 96 h after the exercise." Glutamine is known to be a direct regulator of muscle protein synthesis”? and degrada- tion" While alanine and glutamine are synthesized from the same precursor, the relations between alanine and glutamine in muscles may have significance in regulation of protein metabolism. During exercises, the more pronounced production of alanine and, thereby, decreased production of glutamine, promote protein degradation. In the recovery period the increased glutamine production supports the increase in the protein synthesis rate and inhibits protein degradation. CONCLUSIONS ‘The recovery period is not only the time for normalizing functional activities and homeo- static equilibriums, but also the time for repletion of energy stores and for constructive alterations. The repletion of energy stores is actualized in a certain sequence and is followed by a transitory phase of supercompensation for energy substrates. ‘The constructive alterations are founded on increased protein turnover. It is necessary in order to actualize two tasks. First, it spceds up the replacing of physiologically exhausted cellular structure elements with new ones. In this way the enhanced protein turnover warrants the restoration of the functional capacity of cellular structures. The second task is connected with the induction of the adaptive protein synthesis. In order to build something new, one must destroy the old. ‘The rates of protein synthesis and breakdown may exist in various interrelations during post-exercise recovery. ‘The prevalence of protein synthesis leads to an increase either in the corresponding cellular structures or in the number of enzyme molecules. However, an effec- tive renewal of structural elements may also take place without any changes in the content of the related proteins. After endurance exercises there is a good accordance between the synthesis and degradation of myofibrillar proteins. ‘This might be the reason why endurance exercises do not result in an increase in the size of myofibrils and in muscle hypertrophy. After exercise for improved strength there is another interrelation between the synthesis and degradation of myofibrillar proteins. A more intensive synthesis of these proteins, in compasrison with the degradation rate, warrants an increase in the size of myofibrils and thus also in muscle hypertrophy. ‘The results presented above demonstrate that the adaptive protein synthesis is specifically related to the previous functional activity. It is natural that after endurance exercises the main locus of adaptive protein synthesis is in the mitochondrial proteins of oxidative or oxi glycolytic muscles. After exercises for improved strength, adaptive protein synthesis will take place to the fullest extent in regard to the myofibrillar proteins of glycolytic fibers. Naturally, exercise-induced adaptive protein synthesis is not limited to skeletal muscle tissue. One of the locuses of the postexercise adaptive protein synthesis has to be the12 Adaptation in Sports Training FIGURE-4-15, Restitution of performance capacities in swimenérs after training session for improved speed (S), anacrobic endurince (AN) or aerobic endurance (A): | — maximal swimming spood, 2 — anacrobic performance aerobic performance capacity. Both anaerobic and aerobic capacities were evaluated with special myocardium. An increased protein synthesis has been found also in the brain tissue during post-exercise recovery! ‘The reconstructive function is accomplished when the working capacity is completely restored, The restoration of the working capacity is an integral of several processes proceeding in the organism during the postexercise recovery period. On the one hand, this means the elimination of all fatigue manifestations, On the other hand, it means the refilling of energy stores, the effective renewal of the most exhausted cellular structures, the restoration of the functional capacity of various functional systems and of the central nervous system, and the re-establishment of normal homeostatic balances. ‘After short-term nonexhausting exercise the restoration of working capacity appears after a couple of minutes or some hours and depends mainly on alterations in the central nervous system. 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Kikim., 17, 280, 1972:Cn Russian). 257, Silber, Mul-y and Rogozkin, V.A., Action of physical exercise on the activity of nuclear RNA. polymerase ‘of skeletal muscles and liver, Ukr. Biokhim. Zh, 431, $88, 1971 ‘258. Bates, F.C, DeCaster, T., Grimble, G.K., Holley, JO. Millward, D.J., and Rennis, M., Exercise and muscle protein turnover in the rat, J. Physiol, 303, 41P. 1980 259. ‘Virwy A; and Otpliy V., Anabolic aed catabolicecspoascsto training, in Paeo Marml Congress Bork. Kvlst. M., Ed., The Finaish Society of Sports Medicine, Turku, 1989, 55. Effect of glycerol 247,12 Adaptation in Sports Training 260. Rogorkin, V., and Feldkoren, RL, The effect of retabolil and training on activity of RNA polymerase in skeletal muscle, Med. Sci. Sports, 11, 345, 1979. 261. Hamberger, A..Gregson, N, and Lebninger, A... The effect of acute exercise om amino acid incoxporation imo mitochoodtia of rabbit tissue. Biochim Biophys. Acta, 186, 373, 1969. 262. Vitus dn Konovalovs, G OBpik, V., and Masso, K., Thyroid hormones in protein symtbesis during posicsercise recovery, in 60 lit Blockers. Exerc. Conf. Progr. Abstr, Nagoya, 1991, 107. 263. Viru, A., The mechanism of training effects: a hypothesis, fat. J. Sparte Med., 5, 264. Gustafson, R, Tata, JR Lindberg, O., und Exnester,1., The celatioaship berwcen the structure and sctvity offal skeletal muscle mitochondria fer thyroidectomy and thyroid hormone treatment, J. Cet. Biol, 26, 555, 1965. 265, Winder, W.W., Baldwin, K.M, Terjung, RL, and Halos, tration on skeletal masciemitechodrs, Am. J. Phytol, 228, 14 266, Winder, W.W., and Hellacry, J.0., Response of mitochondsia of different types of sketctal muscle to thyrotoxicosis, Am. J. Physiol, 232, C180, 1977. 267. Ianuzzo, C.D., Petel, G., Chen, V...O’Brien, P., and Williams, C., Thyroid trophic influence on skeletal muscle myosin, Nanire, 370, 74, 1979. 268, Chesley, Ax MacDougall, J... Tarnopotsky, M.A. Atkinson, S.A., and Smith, K., Changes in barman muscle peotcin syntbesis afer resistance exercise, J. Appl. Physio, 73, 1383, 1992. 260, Wong, TS, and Booth, EW. Protein metabolism in rat gatroceensus muscle afte stimulated chronic concerti exertise, J. APPL Physiob, 69, 1718, 1990. 270. Wong, TS. and Booth, F-W., Protein metabolism in rot tibialis amerior muscle after stimulated chronic eccente exercise J Appt Physiol. 69, 1708, 1990. 271, Booth, FW and Thomason, D-B., Molecular and cellular aapation of sousce in respomse to exercise: perspectives of various models, Physiol. Rev., 71, $41, 1991 272. Rogozkin, V., Metabolic effects. of anabolic steroids on skeletal muscke, Med. Sei. Sports, 11, 160, 1979. 274. Tehaikovsky, V.Sq Astratenkeva, LViy and Kasharina, O.B., The effect of exercise on the content and receptor of the strcoid hormones in rt skeletal scl, J. Steroid Biochem. 24, 231, 1986. 274, Feldkoren,B.,and Osipova, I Exercise, estosteroac blood levelsand andea ge receptor in skeletal muscle, in Hormona! Regulation of Adaptation te Muvcular Activity, Tarw University, Tart, 1991, 25, 275. Suborida, A., Vila, J, Motano, F., and Megas, A. Effect of anabolic steroids on mitochondria and Sarcotebalar system of skeletal mace, J. Appl PAysiol.70. 1088, 1991 276 Wool, LG.. and Caviceh, Insulin repultion of pretein symthesis by muscle ribosomes, Pro. Natl Acad. Sei, USA, 56, 991, 1966, 27, Cheek, D.B. and Hill, DAE, Effect of growth hormone of cell and somatic growth, in Handbook of Physiotogy, Knobil, E. aod Sawyer, W.H., Eas, American Physiological Society, Washington, D.C, 1974, 139 278, Fryburg, DLA. Gelfand, R.A. and Barret, F., Growth hormone acutely stimulates forearm muscle protein synthesis in normal buntias, Amt. J. Physiol, 260, EAY9, 1991. 279, Cameo, R-C., Salomon, F, Wills, CML, and Sénksen, PIL. Growth hormone treatment in growth hormone deficient adulis, L Effects on mscle mass and strength, J. Appl. Physiol, 70, 688, 1991 280. Cuneo, RS., Salomon, P., Wills, C.M., Hesp, R.,. and Sénksen, PHL. Growth hormone treatment in growth hormone deficieat adults. 1. Fifects om exercise performance, J. Appl Physia.. 70,695, 1991 281. Ullman, Ma and Oldfors, A. Effects of gmth hocroneon skeletal muscle. 1. Seuies oa normal adult ras ‘Acta Physiol Scand. 13S, S31, 1986. Balon, TAW., Zorzano, A. Treadway, J.L~. Goodman, MN. and Ruderman, NB. Elfect of insulin on protein syothesis and degradation in skeletal muscle after exercise, Am. J. Physiol, 258, B92, 1990 283. Refsurn, LE, and Striimme, S.E.. Urea and creatine production and excretion in urine during and after prolonged heavy exercise, Scand. J. Cli. Lab. Invest. 33,287. 1978 284, Gecokboy, AL. A stidy of id-base balance and urea in blood of sportsmen, Teor. Poakt. Fiz: Kal. 1,22, 1976 (ia Ressian). 285, Buhl, H., Newmann, G., Gerber, G. and Gottschalk, K., Der extreme Davereistang. Fall stu6e ctnes 24+ ‘Stenden bzw 100-km Lautes, Med. Sport, 18, 334, 1978 286, Fancoen, G MLE. Degenau, C.P., Mensbeere, P-P.C.Ax Habets, ML, and Gervesten,P.,Plasmatca {reatinine ric and lbomin ad ttl protcin concentrations before and afer 1S, 25-and 42-km contests, Int. J. Sports Med., 10 (Suppl, 3), $132, 1989. 287, Lenkova, RL, Usik,S.K., and Yakovlev, N.N;-Changes in urea contentin blood and tisucs dering scalar activity in dependence on the adaptation of onanism, Sechenow Physiol. J, USSR, 39, 1097, 1973 (in Russian) 288, Litvinova, L’ Viru, A.,and Smirnova, T, Renal wa clearance in normal and adrenalectomized rats after exercise, Spa J. Physiol, 39, 713, 1989. Yakeviev, N.N., Omithine metabotism and adsptation to augmented muscular activity, Sechenov Physiof USSR, 6S, 979, 1979 {in Russian)oT ee aS | | . : je | = A | 296, 291. 301 302, 303, 308. 310. 3h 312. 313, 314, . Nazarov, LB., Baboshina, O.V., Rogozkin, V. | Post-Exercise Recovery Period 13 Kasperek, GJ., and Snider, R.D., The effect of exercise on peotein turnover in isolated soleus and extensor digitorum longus muscle, Experimenria, 41, 1399, 1985. Varrik, E., Viru, Ax Qopiky V. and Virw, M., Exercise indced catabolic responses in vatous muscle fibers, Can J. Sports Sci. 17, 125, 1992. ‘Wahren, J., Felig, P, Hendler, R., and Ahlberg, G. Glucose and amino acid metabolism during recovery aftr exercise, J. Appl. Phyl, 34, 88, 1973. Brosks, GA. Amino acid and protin metabolism during exercise and recovery, Med. Sei Sports Exerc. 19, S150, 1987. Dohm, G.L., Williams, R.T., Kasperek, G.J., and van Rij, A.M. Increased excretion of urea and N- methylhistidine by rats and humans after a bout of exercise, J. Appl. Physiol, 52, 27, 1982. Dohm, G.Lq Israel, K.G., Breedlove, RL, Williams, B.L., and Askew, E.W., Biphasic changes in 3- rmethylhistidine excretion im head after exercise, Am. J Physiol, 248, 588, 1985 ‘Varrik, Ex, and Vira, A., Excretion of 3-methylhistidine in exercising rats, Biol. Sport, 5, 195, 1988. Dobm, G.L., Tapscott, E.B., and Kasperek, GJ., Protein degradation during. endurance enereise and recovery, Med. Sci. Sports Bxerc.. 19, $466, 1987. ‘Vira, A., Mobilization of structural proteins during exercise, Sports Med., 4, 95, 1987. Sci, and Viru, A.,3-Methylhistidae exrcion i raining for improved power and strength, Sport: Med Training Med. Rehab, 3. 183, 1992. Kaspereh, GJ, and Solder, RID. Incrased prfcin degedation after escentic exercise, Eur J. Appl Physi, $4, 30, 1985. arr E, Odplk, Vand Virw, A. Protein metabolism in muscles afer their activity. Med. Spor. 4,7, ig, ‘Hickson, R.C., and Davis, J.R., Partial prevention of glucocosticoid-induced muscle atrophy by endurance training, Am. J. Physiot. 281, E226, 1981. ‘Seene, T and Viru, A., The catabolic cffect of glucocorticoids on different types of skeletal muscle fibers adits dependence upon muscle activity and interaction with anabolic steroids, J. SterifBiochem., 1, 349, we. ‘Warimie, T., Karen, K., Smirnova, T.,and Viru, A., The cffect of a single-circuit wei ght-trining session. ‘on the blood biochemistry of untrained university students, Eur. J. Appl Physiol., 61, 344, 1990. ‘Dahlman, B., Widjaja, A., and Reinauer, H., Antogonistic effects of endurance training and testosterone on alkaline proteolytic activity im rat skeletal muscles, Eur, J. Physiol, 46, 229, L981. Doin GL, and Lous, TM, Changes in androstenedione, etocroe and protein metabolism asa result of exerise, Prog. Sec. Exp, Bol Med. 158,622, 1978 . Fry, R.W., Morton, A-P., Garcia-Webb, P., and Keasl, D., Monitoring exercise stress by changes in ‘metabolic and hormonal responses over a 24 h period, Eur, J. Appl. Physiol, 63, 228, 1991 Vika, V., Salminen, A., and Rantamiki, J.. Acid hydrolase activity in red and white skelctal muscle of fice ducing a two-week period following exhausting exercise, Pfligers Arch ges. Physiol, 378, 99, 1978. . Salminen, A., and Vihko, V., Acid hydrolase activities in mouse cardiac and skeletal muscle follawing exhaustive exercise, Eur, J. Appl. Physiol. 47, $7, 1981 Kaspereh Gan and Salder, D -Eflectof execs on fetal and myotsil pon degrsdaion a soleus muscle, Can J. Sposts Sci, 13, 20F, 1988, ta = a ees bs VA Tk, NV Ite of pil execs eae of myeloperoxidase in skeletal muscles of rats, Ltr. Biokhim. Zi, MacLennan, FLA. Brown, Rut. and Rennie, MJ. A positive relationship between protein synthetic rate and iniracellular glutamine concentration in perfused rat skeletal muscle, FEBS Lew, 215, 187, 1987. MacLennan, P.A., Smith, K., Weryk, B., and Rennie, M.J., Inhibition of protein breakdown by glutamine in perfused rat skelctal muscle, FEBS Left, 237, 133, 1988. Platonor, V.N., Adaptation in Sports, Zdarowya, Kiev, 1988.Chapter 5 SPECIFIC NATURE OF TRAINING ON SKELETAL MUSCLES ‘The principle of specific adaptation to various kinds of muscular activity was first formu- lated and argued by N.N. Yakovlev.'5 Later, striking evidence of the specific nature of training effects was obtained from a great number of studies carried outin several laboratories. Each exercise determines the degree of activity of various organs, different type of muscles, and motor units. Within each active cell the main metabolic pathways that permit the accomplishment of necessary functional tasks also depend on the nature of training exercises. The activity of the metabolic control system at various levels as well as the activity of the system directly regulating bodily functions is also dependent on the nature of training exercise. Correspondingly, the organism's adaptation bears the imprint of the type of exercise system- atically used in training (Figure 5-1). HYPERTROPHY OF MYOFIBRILS ‘The most prominent result of training for improved strength is hypertrophy of skeletal muscles.” A very pronounced muscle hypertrophy is displayed by athletes exposed to long- term vigorous strength training.'*" Muscular hypertrophy is primarily the result of an in- creased size of the individual fibers.!*2" In its turn, the latter is based on the enlargement of myofibrils," obviously due to the augmentation of myofibrillar proteins.“32"" Also, an increased number of myofibrils has been found, indicating some: hyperplasia?" It is assumed that the myogenic response to strength training involves mainly the synthesis of new contractile proteins. In rats a model of strength training, consisting of a repeated serics of fast climbing up a slope with an attached load (100 to 400 g), induced an increased rate of synthesis of actinomyosin proteins in fast-twitch glycolytic (FG) and fast-twitch oxidative-glycolyt (FOG) fibers. Accordingly, a period of strength training resulted in an increase in the cross- sectional area mainly in the fast-twitch fibers of the rat.'**2" Olympic weight-lifters may possess fast-twitch fibers that are two times larger in diameter than slow-twitch fibers of the same muscle." The great growth potential of fast-twitch fibers allows the area of muscle occupied by fast-twitch fibers to increase by 90% with strength training, despite retaining a fiber-type composition within the normal range.” However, a moderate enlargement of slow-twitch fibers cannot be excluded from having contributed to this hypertrophy.!®* ‘The effect of training for improved strength differs from that of aerobic endurance training, ‘which does not cause a substantial increase in the cross-sectional area of muscle fibers. The cross-sectional area of thigh muscles remained essentially unchanged during about 6 months of strenuous bicycling. In one study even a decrease in the volume fraction of myofibrils occurred after endurance training of 2 months duration.‘ However, a selective and moderate enlargement of slow-twitch oxidative (SO) fibers and in some cases also FOG fibers is possible in endurance training." In endurance training no enlargement of myofibrils was found, The increase in the fiber diameter is mainly due to the elevated volume of sarcoplasma.79" “The increase in the sarcoplasmic space is thought to be due to the glycogen content increase." ‘The elevated glycogen content also explains the increase in the volume density of cytoplasm as a result of strength training.* 3s126 Adaptation in Sports Training eg Most active Most active visceral Change in activity muscle ‘organs, notvous of endactne structures, connective ‘systems. | tissue elements | Most active ‘Change of hormonal type of fibers Tavels in body fuids x Nest colulay slructures Main metabolic ea metabolites “quiver ‘Synthoss Functional Improvement of most active structures, FIGURE: S-1. Factors determining the specificity of the influence of training exercises. Endurance training induces an elevated rate of myosin heavy chain and actin turnover in all fiber types. In sprint-trained rats a more rapid turnover of the myosin heavy chain was found only in FG and FOG fibers in comparison with sedentary rats. No increase in the content of myosin or actin has been found after endurance training." Sprint training increases the cross-sectional area of both slow- and fast-twitch fibers.*? This effect is greatest for the fast-twitch fibers. The end result is that they occupy a slightly greater area in the sprint trained athletes.“* The effect of sprint training on fiber size is less pronounced than that of strength training. ‘: “The area of slow-twitch fibers constituted 51 10 76% of muscle in distance runners, the percentage of slow-twitch fibers was 63 to 74%, and in sprinters the respective values were: 15 to 32 and 21 to 27%, with no significant difference in individual fiber area between the two groups of athletes, In middle- _ mainiyin oxidative slyeohyte and acolyte ibors ineeased senctaty of enzymes: |" olyeatysis to activating actions ‘Synthesis of isozymes ~ Lo») “tesistve fo reduced pH Increased butter > capacity Ty Increased Anaerobic Working Power and Capacity FIGURE $10, Adaptation to anacrobic exercise ‘of up to 25 mmol-1+ in the blood and 30 to 35 mmol-kg~ in the musele tissue were recorded at the finish of 400- and 800-m races. At the same time, pH was 6.9 (in some cases 6.8) in the blood and 6.4 in the muscle tissue." ‘Training experiments on rats have shown that a 4-min intensive run (60 m-min') caused in interval trained rats a less pronounced lactate acccumulation in FG fibers, and in rats trained with short-term dashes or continuous running, a more pronounced one than in control rats. In $0 fibers an elevated lactate accumulation was revealed only in sprint-trained rats.** These results obviously emphasize the significance of improved lactate elimination in lactate re~ sponse to exercise. ‘The increase in anaerobic working capacity as a result of using concerned exercises is summarized in Figure 5-10. INTRAMUSCULAR ENERGY STORES AND MYOGLOBIN ATP ‘There is no convineing evidence that training increases the ATP store in muscles. No changes were detected in rat muscles with either endurance or strengih training.** A mild increase in ATP concentration has been reported in the limb muscles of adolescent!” and adult!"495 males after a program of endurance training. However, these reports seem 10 describe the initial effect of waining. PHOSPHOCREATINE There are old evidences that training elevates the phosphocreatine content in skeletal muscles.'*“!5 Rats trained by repeated short-term intensive exercise increased the phospho- creatine content in skeletal muscles, but the effect of continuous exercise was only modest. ‘Some of the human biopsy studies confirm the increase in muscle phosphocreatine!" However, an increased phosphocreatine store is not considered a common result of training144 Adaptation in Sports Training It was suggested that in humans an increased amount of phosphocreatine will be achieved by a moderate hypertrophy without any change in the substrate concentrations. It was considered a seeontl way for the increased total amount of energy for fast contractile activity." GLYCOGEN ‘The taining effect on muscle glycogen store has been known since 1927." In rats no difference was found between training with continuous exercises and interval training, but the effect of high-power exercises was less pronounced.™* In one study no effect of sprint training on the glycogen content of any of the fiber types was found." A comparison of various kinds of training effects confirmed that sprint training does notalter the glycogen store of either SO or FG fibers. Aerobic training with continuous running or swimming was highly effective. In SO fibers these effects were more pronounced than the response to interval or strength training. In FG fibers all he training variants produced approximately the same changes. Also, in this study glycogen compartmentalized to the SR was detected. It increased as a result of all the training variants used, including sprint training, which was otherwise ineffective in regard to inducing a total glycogen increase, The largest increase in glycogen compartmen- talized to the SR resulted from interval training in both SO abd FG fibers. In humans a higher value of muscle glycogen stores in trained than in sedentary individuals. hhas been demonstrated repeatedly since the first biopsy studies."””%* Both longitudinal and cross-sectional studies indicate that subjects undergoing strength-, sprint-, or endurance- training: programs possess a larger store of muscle glycogen than untrained persons or the: same person before training.*?-"-" The augmentation of glycogen stores may be related to the increase in glycogen synthase activity in trained muscles.!-2% TRIGLYCERIDES In humans an inerease in the triglyceride content of the quadriceps muscle was detected after endurance training 2° This change was not confirmed in a one-leg training experiment." In rats a reduced triglyceride content was observed in both the white and red parts of the gastrocnemius muscle after training.” MYOGLOBIN “This protein increases the rate of O, diffusion in muscles through the eytoplasma to the mitochondria." Endurance training. increased the concentration of myoglobin in skeletal muscles of rats 462%!" Analogous results were obtained with speed and power training 4 Incontrast, biopsy studies did not demonstrate an increased myoglobin content in endurance trained humans*2" Six weeks of sprint training decreased the intramuscular myoglobin content in human museles.'" MUSCLE CAPILLARIZATION ‘An endurance training-induced increase in capillary densities was detected in animal muscles during 1934 to 1936" Later it was shown that the human skeletal muscle also adapts to increased use by increasing the number of capillaries *'"*"* This effect of endur- ing becomes apparent in regard to increases of capillaries per fiber, capillaries per limeter, or number of capillaries found around a fiber. Soccer players, as com- pared with untrained persons, also possess a significantly greater mean number of capillaries surrounding each fiber.2!? The number of capillaries per fiber in trained muscle is closely inked to the whole body maximal oxygen uptake of a subject 2"* If during exercise all fiber types are involved, both the number of capillaries around the various fiber types and the size of the fibers are increased.2!*?" The increase in capillaries is larger than the increase in the fiber area each capillary has to supply.eS say Fr Lo amma ae ei ae al Ope Specific Nature of Training on Skeletal Muscles 145 Endurance training induces an increased number of capillaries in animal skeletal muscles," mainly around slow, not fast, fibers. In experiments of chronic stimulation of muscles it was found that capillaries begin to proliferate before changes can be noted in the: ‘oxidative enzymes 2 4 close coupling is assumed between the number of capillaries and the capacity for oxidative metabolism of the fibers they supply.*> ‘Heavy resistance training does not change capillarity.° Olympic weightlifters and power- lifters display lower capillary density than untrained subjects, whereas the number of capil- laries per fiber of m. vastus lateralis was cqual in these athletes and nonathletes. The increased muscle capillarity seems to be a specific phenomenon characteristic of endurance training. “There is undoubtedly a true proliferation of capillaries associated with prolonged muscular | activity. The adaptation occurs in the exercised muscle and only around fibers that are recruited in the training schedule? Hypoxia is known to increase the growth rate of cultured vascular cells. Therefore it was suggested that hypoxia may play a role in blood vessel growth in vivo” However, in motorically highly active Japanese waltzing mice, a 2-week period in lowered atmospheric pressure (approximately 3000 m altitude) gave no evidence of the development of new capillaries. The capillaries became tortuous and many capillary cross-bridges were developed, hence: enlarging the endothelial surface. On the basis of these results it was suggested that | higher capillary counts on cross sections are mostly derived from the altered capillary pattern but not actually from new capillaries. This situation will not occur in endurance training, | at least in rats. After 4 weeks of endurance training the number of capillaries per muscle fiber increased by 30% in association with an increased citrate synthase activity in the soleus muscle. Capillary tortuosity was not affected by endurance waining*” ‘Against the significance of hypoxia in increased capillarization of active muscles speak the results of an investigation of permanent high-altitute residents (3700 m). When the high- altitude residents were divided into physically active and inactive groups, the first group had } a higher number of capillaries per fiber, similar to the results found in sea-level residents” Im rats.a 13- to 17-weck period of endurance training increased the total blood flow in hind limb vessels by 50%. The highest was the increase in the blood flow of the red part of the gastrocnemius muscle (up to 200%). Maximal capillary infusion was in trained rats 70% higher than in untrained ones. Thus, endurance training warrants a total increase in vascular transport capacity and mainly in muscles of high oxidative potential! FIBER TYPE TRANSFORMATION PROBLEM Fast- and slow-twitch fibers can be distinguished by their specific myosin light chain patterns.2 Both “fast” and ‘slow’ myosin were found in fast- as well as in slow-twitch fibers, but in different ratios" Changes of these ratios are not excluded in training. However, there are limited possibilities for tl Tn guinea pigs 30 days of treadmill running influenced the specific myosin light chain pattern and probably also the myosin isoenzymes content. While running at 0.7 m:s' on a 5° slope decreased the DINB light chains and increased the A2 light chains both in m. pstias ; major and m. vastus lateralis, running at 0.4 m-s*! on a 45° slope caused an increase im the DTNB light chains and a decrease in the A2 light chains. ‘Under appropriate conditions muscle fibers are mutable indeed. Perhaps the first of these situations occurs during maturation after birth. Data obtained indicate the change of slow- to fast-twitch fibers during the early postnatal period. Fiber type transformation is possible with cross-innervation™ and specific electrical stimulation.75* \ Chronically increased contractile activity by low-frequency stimulation induces a transfor- mation of fast- into slow-twitch muscle fibers in the rabbit, Early changes in enzyme act146 Adaptation in Sports Training and isozymes of energy metabolism result in a ‘white-to-red’ metabolic transformation. Simultaneously, cytosolic Ca’* binding and Ca® sequestering are reduced by a decrease in paralbumin and a transformation of the sarcoplasmic reticulum membranes, The fast-to-slow transformation is completed by an exchange of fast- with slow-type myosin isoforms. Changes in total RNA and qualitative and quantitative alterations in translatable mRNA indicate that the various transitions result from altered translational and wanscriptional activities.* The phenotype of'a muscle fiber thus appears to be dynamic and is modified according to the actual functional demands." More recent studies have confirmed that endurance training can ange the isomyesin pattern in fast- and slow-twitch muscles" and in the diaphragm? and thereby alter the myosin phenotype of muscle fiber. Results were obtained indicating that training may also produce changes similar to fiber type transformation, In prolonged endurance training a transformation of type Ile fibers into type I fibers*? and type IIb fibers into type Ila fibers * was suggested. A 50-day program of skiing induced a reduction of the total population of Ha and IIb fibers that was partly compensated for by an increase in the Ic fiber population.'** When the intensity of endurance exercises was over the anaerobic threshold, the training result was a decrease in type I fibers accommodated by an increase in type Ic fibers? A study of skiers demonstrated the coexistence of slow and fast isoforms of myosin and troposin in various types of muscle fibers.“ According to the obtained results, it was suggested that in endurance training the following fiber type transformations may exist; Ha — To— I. Anaerobic interval training during a 13-week period also increased the percent of type I fibers (from 41 to 47%). The percent of type IIb decreased from 17 to 12%, and the percent of type Ha did not change in the vastus lateralis muscle.*“ The endurance training-induced increase in myofibrillar ATPase intermediate fibers was confirmed in another paper.*” With sprint or strength training, changes in different fiber types are mainly restricted to alterations in the myofibrillar to mitochondrial volume ratio."* Nevertheless, data were obtained about an increase in fast-twitch fibers,” mainly type Ila fibers,"%.as a result of sprint training. After 16 weeks of isokinetic training the percent of fast-twitch fibers decreased when ‘one training session consisted in 5 sets of 5 repetitions, while in the case of 15 sets of 10 repetitions no changes were revealed? In contrast, 6 months of bicycle exercises did not alter the percent of fast- fiber despite the doubling of the oxidative potential of the studied vastus lateralis muscle." Differences in the percent of fast- or slow-twitch fibers were not found after endurance or sprint training practice with one. leg either.* In the distribution of type I, Ha, and IIb fibers, no change was found in the same muscle after endurance training of 6 months. In rats no changes were detected in a population of various types of fibers in the gastroc- nemius muscle after either an endurance or sprint training program. This result was not confirmed in another study. After 18 weeks of endurance training the percent of type Land type Ila fibers increased and the percent of type IIb fibers decreased in the plantaris and extensor jigitorum longus muscle. In the deep portion of the vastus lateralis a pronounced increase from 10 to 27% in type | fibers occurred. A rise in slow type myosin light chains accompanied the histochemically observed fiber type transition in the deep vastus lateralis muscle, Changes in peptide pattern of the SR occurred both in the deep and superficial portion of the vastus lateralis muscle, suggesting a complete transition from type Ilb to Ia in the superficial portion and from type Ha to I in the deep portion. A complete type Ha transition to type I in the deep ‘vastus lateralis muscle was also suggested by the failure to detect parvalbumin in this muscle after 15 weeks of training. Changes in the parvalbumin contentard! in the SR tended to precede the transition in myosin light chains. It was concluded that high-intensity endurance training is capable of transforming specific. characteristics of muscle fibers beyond the commonly ‘observed changes in the enzyme activity pattern of energy metabolism.*? The fiber type-specificSpecific Nature of Training on Skeletal Muscles 47 transition in the enz: a study of this group. In 3-weck-old rats during 8 weeks following heavy resistance training, the type I fiber population decreased significantly and fiber Ib population insignificantly in the deep vastu lateralis muscle. In the superficial portion of the muscle the ratio between type Tia and IIb fibers did not change,** Presently, it seems correct to assume that under certain appropriate conditions, an influence on the muscle cell genetic apparatus might be born by training, resulting in switching of muscle fibers from one subgroup to another. activity pattern by this kind of training was previously established in CONCLUSION In skeletal muscles, the main manifestations of various forms and regimens of training are + Myofibrillar hypertrophy + Adaptation of myofibrillar ATPase * Increased possibilities of the SR + Improved function of Na. K-pumps + Increased activity of glycolytic enzymes of alterations of their susceptibility to activa- tors and inhibitors + Increased. volume density of mitochondria and activity of oxidative enzymes + Augmented capillarization + Increased energy stores Resistance to muscle conraction is the main fact Repeated strong contractions (heavy resistance exercis this change. Continuous exercises of moderate intensity stimulate increases in the volume density of mitochondria, activity of oxidative enzymes, and capillarization. However, these also appear in interrupted exercises of rather high intensity. Therefore, the most essential ‘condition is a prolonged period of a high rate of oxidation, It may be warranted by a prolonged continuous cxercise, but alsa by interrupted exercises if a high rate of oxidation persists during rest periods between exercise bouts. However, a question remains whether there exists. limit for exercise intensity, bearing in mind the possibility that exaggerated accumulation of lactate and proteins may suppress 0 ‘Adaptation of myofibrillar ATPase means, first of all, an increased activity of the eazyme. It isa typical result of strength or speed training. This change is less pronounced in endurance training, In this case a possibility for decreased enzyme activity arises. While the increased myofibrillar ATPase activity is necessary for rapid and augmented transfer of chemical energy to mechanical energy, the decreased activity of myofibrillar ATPase enables economizing the utilization of the produced energy. Further studies are necessary in regard to this aspect. Possibilities for both rapid sequestering and rapid reaccumulation of calcium ions are essential conditions in performance of sprint or power exercises. The velocity of muscle contraction as well as the necessity to form a high number of cross-bridges in ashort time have to be the factors stimulating the improvement of the function of the SR. Less effective are heavy resistance exercises. Endurance exercises may even exhibit an opposite effect. Again ‘a question arises whether the latter is related to the sparing effect of endurance training. “Evidence has been obtained on the improved functions of Na,K:pumps in trained muscles. However, further detailed studies are necessary to specify the dependence of the improved Na,K-pump functions on the exercises used. imulating myofibrillar hypertrophy. -s) are necessary for actualization of148 Adaptation in Sports Training ‘The stimulus for adaptation at the level of glycolytic enzymes is provided by exercises founded on a high rate of anaerobic glycogenolysis. However, the life span of glycolytic enzymes is rather short. Therefore, the increased activity of these enzymes, resulting from corresponding exercise, may persist only for some days. Recently, a possibility was indicated that anaerobic exercises may elevate the susceptibility of glycolytic enzymes to their activa- tors and inhibitors, or induce a synthesis of isozymes resistive to low pH. This possibility needs further confirmation and specification. “The training effect on intramuscular energy stores is the most pronounced in regard to glycogen content. Endurance exercises seem to be more effective than sprint or strength exercises. However, the differences are not always convincing. Results are not unanimous in regard to increased phosphocreatine content. One may suggest that sprint exercises have to be the most effective in regard to augmentation of the phosphocreatine store. Up to now, this has not been convincingly evidenced, The increase of the ATP store is doubtful. Besides the function of energy donor, ATP possesses an essential role in control of intracellular metabo- lism. The increased ATP content would mean decreased possibilities for mobilization of cellular resources during exercise performance, {All these training manifestations are dependent on the type of muscle fibers. Some of them are favorable in FG and others in SO fibers. This dependence is founded on the: differences in recruiting various motor units and, thereby, fibers of various types. The increase in force application or intensity of performance makes it necessary to recruit more motor units, In heavy resistance as well as highly intensive exercises, the recruiting of motor units is close to maximal. Thereby, the training effects of these exercises are less specific in regard to the influence on muscle fibers of various types. REFERENCES 1. Vakowley, 8.N., Biochemical foundations of muscle training, Usp. Sevrem. Biol (Moscow, 27, 257. 1949 (in Russian), 2 Yakewley, N.N., Problem of biochemical adaplation of muscles in dependence on the character of their activity, Zk. Obshck. Biot, 19, 417, 1958 (in Russian). 3. Yakovlev, NIN., Biochemical mechanisms of adaptation of skeletal Biokhim. Zh. 48, 388, 1976 (in Russian). 4, Yakovley, NIN. Sporthiochemie, Bath, Leipzig 1977, 5. Yakavlew, NN, Biochemische and Morphologishe Verinderungea der Maskelfasem in Abhingigheit von der Act des Training, Med. Spart, 18, 161, 1978. : 6 Marpurge, B. Ucber Activitatis Hypertophie der wilkurlichen Muskeln, Virchows Arck Pathol. Ana. 150, $22, 1897. 47. Hettinger, E.. Physiology of Strength, Chacles C, Thomas, Springfield, 1961. 8 Hollmann, W., and Hettinger, T., Sportmedizin — Arbeite and Trainingsgrundlagea, FX. Schattaver, Stungant, 1976. 9, Booth, F-W. Perspectives on malecular and cellular exercise physiology, J. Appl Pays. 65, 1461, 1988. ipes, TV, Physiologic charactensi of elite bodybuilders, Physician Sporamed., 7, 116, 1979. 11, Katch, VL Kate, FAL, Moffatt, R. and Gittleyen, M., Muscular development and lean body weight in body builders and weight lifters, Med: Set. Sports Exerc, 12, 240, 1980. 12, Hiikkinen, K, Aléa M.,and Komi, P-V..Newommscula, anaerobic, and aerobic performance characteristics ‘of elite power athletes, Eur. J. Appl Physiol. 53, 97. 1984 13, Tesch, P-A., and Larsson, Le, Muscle hypertrophy im bodybuilders, Eur. J Appl. Physiol, 49, 301, 1982. 14, Prince, EP, Hikida, RS. and Hagerman, F.C., Human muscle fiber types in power lifters, distance tuntery and untrained subjects, Fylagers Arch. ges. Physiol, 963. 19, 1976. 15, Thorstensson, A. Hulrén, B., von Déblen W., and Karisson, J., Effect of strength training on enzyme sctivities and fibee characteristics in human skeletal musete, Acta Payaiol, Scand , 56, 392, 1976. 16, Dons, B., Bollerup. K.,onde-Peterson, F, and Hancke, S., The effect of weight-lifting exercises related to-muscle fiber composition and muscle crass sectional area in humans, Eur. J. Appl. Physiol, 40,95, 1978 wseles to muscular sctivity, Uk: a i eeSpecific Nature of Training on Skeletal Museles 149 17. Wiggmark, 7, Jansson, B., and Svane, B.,.Cross-cectioeal area of the thigh muscle in man macasured by ‘computed tomography, Scand, J. Clin. Lab Invest, 38, 355, 1978. 18. Hiikkinen, K., Kemi, P-Y., and Tesch, P.A.. Effect of combined concesiric and eccentric strength training and detraining on force-time, muscle fiber and metabolic characteristics of leg extensoe ruscles, Scand. J Sports Sci, 3, 0, 1981 19. Young, A., Stakes, M., Round, J.M., and Edwards LT. The effect of high-resictance training on the strength and cross-sectional area of the human quadiceps, Eur J. Clin. favest, 13, 411, 1983, 20, MacDoughall, LD, Elder, G.C.E, Sale, D.G., Moror, J.R. and Sutton, JR., Effects of sircagth training ‘and immobilizalion on homan muscle fibers, Eur. J. Appl. Physiol 43, 25, 1980. 21. Yakovleva, E-S., Micromorphological changes in skeletal muscle fibers of white rats in working strain, Arch. ‘Anat. Khistol. Embriet, 17, 519, 1968 (in Russian). 22. Lilthi, ML, Howald, H..Claasen, H., Riser, K. Vock, P:, and Hoppler, H., Structural changesin skeletal ruscle tissue with heavy-resistance exercise, Int. J. Sports Med., 7, 123, 1986. 23, Helander, E.A.S., Influence of exercise and restricted activity on the protein composition of skeletal muscle, Biochem. J, 78, 478, 1961 24, McDonagh, MJM., and Davies, C:TM,, Adaptive response of mammalian muscle to exereise with high loads, Ear. J Appl. Physiol, 52, 139, 1984 25. Goldspink, G., The combined effects of exercise and reduced food intake on skeletal muscle fibers, . Ce. Comp, Physiol, 63, 30, 1964, ‘Gudz, P., Reforming of muscular structre, their innervation and blood supply under the influcnce of iensive physical loads, in Abstr. Pup: Presented In. Congr. Sports Sct, Tokyo, 1964, 142, 27. Gude, P,, Adaptive transformations of stractures of the organism as material foundation for endurance in ‘conditions of enhanced muscular activity, in Physiological Characteristics af Endurance and Methods af tts Estimation in Sports, Zimkin, NV, Ed, iS, Moscow, 1972, 41 (in Russian) 28. Mamosh, M., Lesch, M., Baron, J, and Kaufman, S., Enhanced protein synthesis i a cell-free system from hypectrophicd skeletal muscle, Science. 157, 935, 1967. 29. Goldberg, A.L., Protein synthesis during work-induced growth of skeletal muscle, J. Cell Biol, 36, 653, 1968, 30. Gollnick, P.D., Cellular adaptation to exercise, in Frontiers of Fitness, Shephard, R.J.. Ed., Charles C. Thomas, Springfield, 1971, 112 31. Hoppeter, H., Exercise induced changes in skeletal muscle, fat. J Sports Med. 7, 187, 1986. 32. Pehme, A., and Seene, T.. Importance of the relation of power to total volame of work on the procein symtbesis in different types of skeletal muscles during suength training of rats, Acta Comment. Univ Tarwensis, 814, 15, 1988, 33, Yakovlev, NIN, and Vakovleva, ES. Influence of various kinds of training on ‘white’ and ‘red’ muscles ‘of animals, Sechenow Physiol. 4. USSR, $7, 1287, 1971 Gn Russian). 34. Edstrim, L., and Ekblom, B., Differences in sizes of red and white muscle fibers ia vastus Intralis of ‘musculus quadriceps femoris of normal individuals and athletes. Relation to physical performance, Scand. J Glin Lab Invert, 30, 178, 1972 35, Cestill, Dil Cayley EAF., Fink, WF» Lesmes, G:Ry and Witzman, FA., Adaptations in skeletal mescle following strength training. J App! Physiol, 46, 96, 1978, 36, Kemi, PV, Training of musele strength and power: interaction of ncuromotoci, hypertrophic, and mccban sal factors, fat J. Sports Med. 7 (Suppl. 1} 10, 1986, 37, Tesch, P.A., and Karkson, J., Muscle fiber types and size in tained and untrained muscles of elite athletes, J. Apph Physiol, $9, 1716, 1985. 238, Tesch, P.An. Skeletal muscle adaptations consequent to Iong-termbcany resistance exercise, Med. Sci. Spert Evere., 20, $132, 1988 39, Salmons, S:, and Henriksson, J., The adaptive response of skeletal muscle to increased use, Muscle Nerve, 4,94, 1981 40, Hoppeler, I, Howald, H., Conley, KE, Lindstedt, S.L., Clazsen, HL, Vock, P., and Weibel, ER, Endurance training in humans: aerobic capacity ad structure of skeletal muscle, J. Arpt. Physiol, $9, 320, 1985, 41, Risler, Ke Conley, EK Classen, Hy Hewald, HL, and Hoppeler; HL, Transfer cffocts in cadurance ‘exercise: Adaptations in trained and untrained muscles, Fur. J Appl. Piysiol, 54, 355, 1985, 42. Gollnick, F-D., Armstrong, KLE, Saltin, B., Sauber, CW. Sembrovtict, W.L. and Shephard, E.R, Effect of training on enzyme activity and fiber composition of human skeletal muscle, J. App. Physiol, 34, 107, 1973. 43. Bylund, A-C., Bjari, T-, Cederblad, G., Haim, J, Lundholm, K., Sjistedm, M., Angguist, K.A., and ‘Scherstén, T., Physical training in man, Skeletal muscle metabolism in relation to muscle morphology and running ability. Eur. J. Appl. Physiol. 36. 151, 197 44, Howald, HL, Hoppeler, HL, Claasen, HL, Mathieu, ©., and Straub, R, Influences of endurance taining on ‘the ultrastructural cornposition of the different muscle fiber types inihumans, Aligers Arch. ges. Physiol, 403, 369, 1985,150 Adaptation in Sports Training 45, James, DE, and Kracgen, EW, The effect of exercise taining on glycogen, glycogen synthase, and Phosphorylase in muscle and liver, Eur J Appl. Physi, $2, 276, 1984 46, Seene, T,and Aley, K., Effect of muscular activity the turnover rae of actin and myosin heavy abd light chains in different types of skeletal muscle, int J. Sports Med. 12, 208, 1991 4]. Mackavi, E., Melichna, J, Havlickova, Ly Placheta, Za» Blahové, D., and Semiginavsky, B., Skeletal rusele characteristics of sprint According to differences in anaerobic and aerobic training effects, the anaerobic threshold constituted 65.9 + 0.3% of VO,max in swimmers-sprinters, compared to 90.4 £ 0.1% in swimmers-skiers.” The specificity of the training effect on the anaerobic threshold was confirmed in various studies.°!#* In case of a similar training protocol, running resulted in Jarge improvements in the anaerobic threshold for both cycling and running, with a larger improvement in the running anaerobic threshold. Cyclic training resulted in an improvement in the cycling anaerobic threshold with no change in the running anaerobic threshold"* (Figure 6-3). EXERCISE ECONOMY ‘The increased oxidative capacity of working muscles warrants a possil of utilizing a smaller fraction of it for performance of exercises of moderate intensity. Accordingly, it is affirmed that successful distance running is dependent on the economical utilization of a highly developed aerobic capacity and the ability to employ a large fraction of that capacity with minimal accumulation of lactic acid.° This specific effect of waining has been considered ina number of papers, and its significance for endurance performance has been confirmed.*!- * Among Sweden's best runners the lowest VO, during running at 15 m-t! was found in those who were specialized for 10,000 m or marathon (Figure 6-2). However, in a number of studies no good accordance was found between running economy and endurance perfor- mance.'®! In female athletes correlation coefficients between the running pace for 5 km, 10 kin, and 10 mile distances on the one hand, and maximal oxygen uptake, speed at 2.0,.as well as at 4.0 mmol of Plasma lactate, on the other hand, ranged between 0.84 and 0.94. The ‘oxygen casts of running at cach of the three distances moderately correlated with the pace of each race (r = -0.40 to 0.63). xercise economy and correspondingly the employed fractions of aerobic capacity are specifically related to training exereises in two ways: (1) the specific effect of exercises on the oxidative enzymes of related muscles, and (2) the spec improvement of muscle coordina- tion that warrants the more accomplished biomechanical utilization of muscle forces and thereby, an increased mechanical efficiency. MAXIMAL OXYGEN UPTAKE An integral index of the aerobic capacity of the organism is maximal oxygen uptake. ‘This index only partly depends on the oxidative capacity of muscles. VO,max depends also onSpecificity of Training Effects on Aerobic Working Capacity and the Cardiovascular System 161 oxygen binding in erythrocytes. Moreover, fundamental studies have established that VO,max is mainly sot by cardiovascular determinants.*5* Ttis possible to find a great number of studies indicating the relation of individual VO,max values to endurance performance (for instance, Reference 59-68). The high performance capacity in sprint, power, strength, and skill events is not related to VO,max. The usual finding in endurance athletes is that the longer the main distance, the higher is the maximal oxygen uptake (Figure 6-2). In this regard an exception is revealed when marathon runners are compared with runners of 5000 to 10,000 m.‘" However, changes in running performance with training may occur without equivalent changes in VO,max. ‘VO,max was found to be a good interpreter of endurance performance when a heterog- enous group of persons with quite different athletic abilities were studied.26*14.7 How- ever, it is a relatively poor predictor when athletes of similar ability are evaluated !*«##1«676 ‘When two athletes with the same VO,max were compared, the runner with a higher running. economy was faster.7? Cases are possible where runners with quite different ¥O,max values have the same running ability.” It was also found that in runners with the best marathon result, within 2 h 30 min to 2h 35 min, running economy was quite different, and in runners with similar VO,max values of 65 to 71 ml-min-kg", the best marathon result ranged from 3 bh 12 min to 2h 8 min.” Furthermore, the factor predicting endurance performance may be related to ‘muscle power’, measured as the peak workload reached during maximum treadmill running” or isokinetic muscle power measured in swimmers.® A relationship was found between VO.anax and total work output during maximal isokinetic exercise of 30s duration." However, a question remains whether the increased “muscle power’ is a result of specific acrobic exer- cises, or whether special exercises are necessary for developing ‘muscle power’, Strength training in prepubertal boys" as well as sprint training in rats* increased VO,max without increasing muscle oxidative capacity. These findings were explained on the basis of training- induced increases in muscle power, enabling exercise at higher work loads. This explanation disagrees with the main role of the heart and the circulating function limiting VO,max. Both strength and sprint training are also ineffective in increasing the functional capacity of the cardiovascular system (sce below). However, these results agree with the suggestion that the possibilities for oxygen transport system can be measured only in sufficiently intense exercises. ‘The highest peak VO; for each aihlete was measured in performing the exercise for which he was specifically trained. “The ‘specificity of training’ concept has been supported by researchers on training-induced changes in VO.max measured in various exercises. Significant differences were found when VO,max was compared in running vs. swimming,“*** running vs. cycling"? running vs. rowing and kayaking vs, cycling” The specificity of training response appears also to be present in regard to muscle groups utilized in training vs. test exercises.” The comparison of training on a standard swim-bench pulley system and swim training supports the specificity of aerobic improvement with training and suggests that local adaptations significantly contrib- tute to improvement in peak VO,”" ‘A specific effect of aerobic endurance training may be not only the improvement of maximal aerobic power, measured as VO,max, but also- increased capacity to perform pro- longed aerobic exercise (maximal aerobic capacity). Acrobic training during a 20-week period enhanced the mean maximal acrobic power by 33% and maximal aerobic capacity by 51%. “The latter was computed as the total work output accomplished during a 90-min maximal ergocycle test,” ‘Cycling exercises lasting 18 weeks and performed 3 times weekly increased maximal ‘oxygen uptake both in case of 25-min exercise at 80 to 85% VO,max and in case of $0-min exercise at 45% VOsmax. Thus, VO.max increases as a result of exercise performed at levels oth above and below the anaerobic threshold. When 8-week training was performed with continuous running? or aerobic gymnastics at intensities causing increases in heart rate up162arg aan ud ore anol sree ou) ze (HNL) A eS 25 0S ar gy rr ar oF Specificity of Training Effects on Aerobic Working Capacity and the Cardiovascular System 163Adaptation in Sports Sweden's best runners Vv. max a 80 75 70 6 400 The personal best a 400m 2 $5.6348.33 800 m 6 14764-15042 500-1500 m 5 149.071.5066 438.51 1500-000 m 6 3419-3. 1357.1—14004 s000—10000 5 14 713.59.1 29.210 1000. marathon 5 29.48.8 My, during running at 15 ian a 80 ce] 70 66 “LLL FIGURE 6-2 (left) gSpecificity of Training Effects on Aerobic Working Capacity and the Cardiovascular System 165 Running velocity causing blood lactate 4mmoti* 55 5.0 45 Blood lactate 3 min after mM-1 competition 19 FIGURE 6-2. VO,max, % VO.max during 7 sswiraming at 15 kine, running velosity causing blood lacie level of 4 mmol! and blood 4g lactate levels after incremental test exercise foe ‘VO.max determination, blood lactate levels atthe finish of competition in best Swedish runners. Constructed by results of J. Svedenhag and B. Shou 15— 166 Adaptation in Sports Training TREADMILL PROTOCOL (run group, n=5) 1997 Velocity m-min — 199 AN — 140 \\\ ANI \ \ # a NY AN \\\ A i A iM A Pre Post BICYCLE PROTOCOL (run group, n= uo, Power output Ww ANI A Ni Pre Post FIGURE 6:3. Effect of 10 weeks (four training sessions per week) of serobic training in running or in cycling on. the lactate threshold determined by incremental cxercises on treadmill or on bicycle ergometer. Mean + SEM are indicated. Asterisk denotes statistically significant difference between pre- and post-training values, Constructed by results of EF. Pierce etal” to 140 to 150 or 165 to 175 beats/min, intensitics of aerobic gymnastics and at Ul lower intensity as well as anaerobic exercise regimes (interval run with periodic use of exercises of anaerobic intensities) were ineff training program consisted of low- intensity continuous running d continuous running at a higher intensity (during 2 weeks) and finally 2 weeks of inte female” university students nificant increases in VO,max were found at both raining at the ing or aerobic gymnastics However, when the ing the first 3 weeks, then 1 her running intensity. Running aerobic regimes of exercises are effective only after prior erobic exercises. Further, it was found that female students with x (25 + 3.5 ml-min-Lkg~!) exhibited a greater increase in aerobic ‘preparation’ Jow initial values of VO,Specificity of Training Effects on Aerobic Working Capacity and the Cardiovascular System 167 TREADMILL PROTOCOL (cycle group, n=6) aay Velocity _ memin BICYCLE PROTOCOL (cycle group, n=6) ta, Power: output W FIGURE 63 (continued. 32 + 1.6 ml-min“'-kg-!) In a group with the initial level of VO.max of 38 + 2.5 ml-mi the training regime used was ineffective. ‘A number of studies indicate the effectiveness of interval training for improvement of VO,max. Obviously, the exercise intensities used and the previous fitness level of the persons necessary accordance, It was established that in anaérobic interval training the intensity, rather than the distance, is the most important factor in improving VO,max.*” ‘The gains in VO.max were independent of training frequency both in men! and women." During a 2-month interval waining period (three times per week) VO,max increased. The waining regimes based on 3-min periods were more effective than 15-s periods.! Interval taining programs lasting § weeks (3 days/week) induced equal increases in VO,max for 30- stuns with 19 repet readmill speed of 15 to 17 kmh or 120-sruns with 7 repetitions at 10 t0 12 kmh to 12° in both cases, rest intervals until heart rate decreased to 120to 140 beats/min). In neither case were there changes in the amount of lactate accumulated jin the blood during 4- to 8-min runs to exhaustion.»-“ However, taking into consideration the experience of sports practice, there can be no doubt about the effect of interval training on power than those with higher initial valu exer168 Adaptation in Sports Training TREADMILI PROTOCOL (control group, n=5) 10, Velocity _; 100 40 * cee BICYCLE PROTOCOL (control group, ta, Power output W 120 100 40% 0 * Pre Post F capacity for anaerobic performance, In runners, an imerval period results in middle-distance more than other tools improved endurance." Increases in blood lactate levels up to 20 mmol or more and drops in pH to 7.0 during an interval taining session evidence a great strain on anaerobic metabolism. !%™” In turn, the lactate accumulation depends on the duration of both the exercise bout and the rest intervals between repetitions.'™* Repeated uphill running gives a combined improvement of VO,max, leg muscle power, and indices of anaerobic performance capacity." Endurance training effect on the maximal oxygen uptake was also confirmed in an experi ment with rats.!!° In contrast tc nce training, high-resistance strength training induces no increases in maxi gen uptake." Olympic weight-lifters and body-builders show VO,max values similar or slightly above those of untrained individuals." Concurrent performance of endurance and resistive training does not affect the magnitude of increase in acrobic power induced by endurance training only.!"""5!¥ ‘The situation may change in two ases: (1) when moderate resistance exercises are repeated over a prolonged period with short are used.Specificity of Training Effects on Aerobic Working Capacity and the Cardiovascular Systems 169 5 5. 4 ‘ 3 3 - 2 = a * 1 1 0. © ° 71000 2000 3000 0 7000 2000 "3000 to wo 5 5 4 ‘ at 3 4 2 2 1 1 ish) 0 © o 7000 2000 ‘300 O 100) 200 oto @ @ FIGURE 6-4. Dependence of VO,snax ianprovement (ml-min-kg-t) on volume of various training exercises per ‘year in km, A — total volume of running exercises, B — volume of serobic exercises, C — voluine of aerobic- anaerobic exercises, D — volume of anaerobic exercises. Constructed by N. Volkov. (Human Bioenergetics in ‘Surenaows Muscular Activity and Pathways of Improved Performance in Sportsmen, Anckin Res. Inst. Normal Physiol, Moscaw, 1990) In the latter case an increase in the blood lactate concentration up to 13 or 16to 17 mmol: was observed. However, 16 weeks of high-intensity, variable-resistance strength training did not change either VOmax or hemodynamic responses to submaximal exercise. Muscle strength increased by 44% in one study.""* Probably, to improve VO.max, a considerable exercise duration and a sufficient intensity is necessary. Accordingly, the lack of effect of strength as well as sprint training can be explained by insufficient duration of exercise influence (exercise time plus recovery time at high oxygen uptake level). In runners the VO.max improvement correlated with the total volume of running exercises, the volume of aerobic exercises, as well as with the volume of anaerobic exercises during a training year. ‘The relationship between VO;max improvement and the volume of anaerobic exercises was inverted (Figure 6-4). In any case, ly qualified decathlonists exhibited a VO,max level of 55 t 1.3 mb-min-!-kg#,1 which is higher than usually found in power athletes, Only minimal increases in aerobic power''* and in the oxidative potential of the muscle cell!!? were found as a result of ice hockey training. When maximal or submaximal cycling was employed in hockey players, no training-induced alterations were found except for a reduced heart rate during submaximal cycling.!'* Thus, the adaptation process possesses specific peculiarities also in the case of ice hockey training. _ SPECIFICITY OF TRAINING EFFECTS ON THE CARDIOVASCULAR SYSTEM: HEART HYPERTROPHY ‘The effect of endurance training is pronounced in regard to adaptive change in the structure and function of organs of the functional system responsible for oxygen intake and transport, ‘As was affirmed by E.A. Newsholme,!*! except only for the 100-m sprint, it is enormously advantageous from a metabolic point of view to increase the blood flow to the working muscles.170 Adaptation in Sports Training Since the accurate chest percussion studies from the end of last century," enlargement of the heart is known as a typical result of endurance training. Subsequent X-ray studies confirmed this fact." The background for heart enlargement in endurance sportsmen is both myocardial hypertrophy as well as increase in heart cavities. Three variants of heart dilation were discriminated: (1) myogenic dilation due to damages in the myocardium, (2) tonogenic dilation caused by loss in myocardial tone, and (3) regulative dilation, expressed by low myocardial tone in the resting state and by high contractility and tone of myocardium in a strain simation caused by exercise or other factors.! fer Variant is the usual result of endurance training."*' An expression of regulative dilation is the augmented residual blood volume in the heart during resting conditions and its almost maximal utilization for the increased strake volume during exercise.'"%"! In the resting state, endurance athletes revealed 3:1 ratio between residual and stroke volumes.!”” In sprinters, field athletes, gymnasts, and fencers the heart volume, estimated from X-ray Pictures, is clase to values in untrained persons."™.!2\" Heart enlargement was found in weight-lifters, However, differently from endurance athletes the enlargement was mainly on account of the right ventricle in these cases. More than half a century ago it was assumed that the increase in the right heart ventricle is caused by exercises connected with short-term but intensive muscular effort and with respiration stop in the inspiration phase. ‘An enlarged heart in endurance athletes was confirmed by autopsy material of sportsmen who had perished in accidents. Boih increased volume of heart cavities and heart weight were detected. However, only in a single case did the weight of an athlete's heart exceed 500 g,"* This heart mass was considered to be critical; larger human hearts were associated with cardiovascular efficiency." Accordingly, myocardial fibers thickness of over 20 stm was considered to be critical. After 16 weeks of swim training the maximal duration of swimming was shorter in rats with aan increase in heart mass by 18% or more, in comparison with rats who exhibited a less Pronounced cardiac hypertrophy.!™ A comprehensive study of (raining-induced cardiac hypertrophy showed that endurance exercises induced an increase in the diameter as well as cross-sectional area of myocardial fibers from both the left and right ventricles of the dog heart. This change was associated with an augmentation of the number of capillaries per myocardial fiber." Instead of the increase in the number of myocardial fibers found in rats," in dogs a slight decrease was observed.!38 In rats heart hypertrophy was also associated with an increased amount of sarcoplasmna in individual myocardial fibers." A 7% increase in heart weight with endurance training in rats Was accompanied by a slight increase in sarcomere length and compositional changes in the sarcolemma."? ~ ‘The increased capillarity and capillary-to-fiber ratio in the myocardium of endurance. ied animals has been evidenced by results of various studies." Increased capillary diffusion capacity,‘ precapillary vascularity and total size of the coronary tree,'‘6!” ‘development of extra coronary colletrals,"*"? and increased coronary artery lumina! have also been found. ‘When heart rate, afterloads, and perfusion pressure were all kept constant in isolated hearts, the coronary blood flow was much greater in the hearts from trained animals. The coronary blood flow increased with a rise in heart rate in hearts, but not in hearts from untrained rats.!"° A further specification of training effects on the human heart became possible with the use of the echocandiographic method, Cross-sectional echocardiographic studies demonstrated larger right!s""® and left ventricular diameters!™“"% and calculated left ventricular masses!*#15* in endurance athletes ax compared to sedentary persons. Different palterns of left ventricular hypertrophy exist among different types of athletes, with mainly increased wall thickness in athletes trained primarily with static exercises (wres- ters) and increased volume in dynamically trained athletes (runners)!Specificity of Training Effects on Acrobic Working Capacity and the Cardiovascular System 171 In contrast, in regard to an old opinion, the echocardiographic studies show that resistance training increases absolute left ventricular wall thickness and left ventricular mass.!95!2161 These increases are not as evident when expressed relative to body surface or lean body mass."'S There is little or no change in the left ventricular internal dimensions in absolute terms or relative to body surface area," resting heart rate and blood pressure, 410.1641 and diastolic dimensions of the left ventricle'**4 due to resistance training. No changes or slight positive effects are noted in systolic function of the left ventricle with strength train- ing.!@1216. & group of nationally ranked U.S. weight-lifters had normal left ventricular mass/volume ratios in spite of an increased septal/free wall ratio," In long-distance runners and cycle racers the left ventricular mass ficantly increased as compared to sedentary subjects.' This resulted from thickening of the intraventricular Septum and the left ventricular posterior wall as well as from enlargement of the left ventricu- lar internal diameter.!' Although the left ventricular wall was enlarged in weight-lifters, their left ventricular mass was not significantly increased as compared to sedentary persons! A study of 7- to 16-year-old boys showed that endurance training resulted in an increased volume of the left ventricle and stroke volume in association with a slight increase in the thickness of veniricular walls, Training in power events induced a pronounced myocardial hypertrophy, but changes in the left ventricular volume and stroke volume were insignifi- cant™ In adolescent boys VO,max increased significantly together with a slight enlargement of calculated left ventricular mass as a result of endurance training. Ina group that underwent sprint training these changes were insignificant, In a strength-trained group a less pronounced increase was found in the left ventricular mass in combination with a pronounced rise in muscular strength." In endurance-trained female athletes the aerobic capacities were 30 to 40% greater than in sedentary subjects. The athletes also exhibited wends toward higher left ventricular end- diastolic dimensions and volumnes, stroke volume, left ventricular mass, and left atrial dimen- sions when data were standardized for body surface area.!7? J. Morganroth et al.!* considered the training effect on the heart in power athletes a concentric hypertrophy, as opposed to ‘pure dilation” in endurance athletes, in regard to the inéreased pressure work during static or power exercises and to the predominant volume work during dynamic exercises, respectively. However, R. Rost!” did not confirm concentric hypertrophy in power athletes. He found only some examples of such hypertrophy in power athletes, but for an unknown reason this could also be found in endurance athletes. He assumed that cardiac hypertrophy takes place in a uniform way as eccentric hypertrophy. The differ- fences between the hearts of sportsmen of various events are only quantitative, according to his data. A common result of many years of training is the increased volume of the left ventricle at the end of diastole during exercise.!™ According to the generalization by J, Keul and collaborators," as a result of dynamic endurance training the reduction in the sympathoadrenal drive causes a decrease in heart rate, blood pressure, contractility, and oxygen and substrate consumption. The diastolic filling velocity accelerates and stroke volume increases. As a result of growth processes, the heart enlarges. These changes are the prerequisites for a high increase in cardiac output, and a higher efficiency of heart work can be achieved (Figure 6-5). As a result of strength training the muscle mass of the heart increases at the expense of the heart cavities. Cardiac output docs not increase, and neither does the sympatho-adrenergic drive, A study of arm vs, leg training indicated that in cardiovascular adaptation, specific and general training effects can be discriminated. The central circulatory function (stroke volume) plays a more dominant role in arm exercise after training, suggesting that the metabolic and circulatory responses during arm work become more like the responses observed during leg work.!"6im Adaptation in Sports Training Endurance Trained Trained {Dynamic Training) (Static Training) sialele|alele 15/14/31 ele fg | FIGURE 65. A schemafired summary of the development of the athlete's heart. The modification ta exercise is at first a functional one, followed by growth. As. aresult of the reduced sympathetic drive in endurance trained athletes: ‘the beart rate, the contractility, and the myocardial oxygen consumption all decrease; the diastolic filling velocity lsccelerates, and the siroke volume ix moderately increased. These valocs remain unchanged as a result of sta training, or even develop in the opposite direction. Growib, as a result of dynamic training, leads to an increase io the heart velume, the end diastolic volume and the muscle mass, at the expense of the end diastolic volume. In this way there isa favorable influence on the relationship of the muscle mass tthe end diastolic volume, and the stroke ‘volume to the heart volume in endurance trained athletes. ‘Static training, on the other hand, has a negative effect on these relationships. (From Keul, J, Dickhuth, H-H. Lehmann, M., and Staiger, J ni. J. Sports Med. 3 (Supp. 1) 33, 1982. With permission) “Against the background of the results of echocardiographic studies, it was necessary to re- evaluate the standpoint on the critical size of the athlete"s heart. Corresponding analysis led to the conclusion that the physiological heart hypertrophy as a healthy process always remains within restricted borderlines. Even in a very early onset of top training in childhood, the limits of physiological hypertrophy are maintained. However, in contrast to the old hypothesis of “critical heart size’, the maximum of physiological hypertrophy cannot be considered a really critical limit: it seems to be an individual rather than absolute parameter, depending on the athlete's body size and heredity." In regard to the body size, arelative maximum critical heart weight of 7.5 g-kg b.w. was suggested.'” “Myocardial hypertrophy is not an unavoidable result of endurance or other kinds of exercise training. For example, in a study of 271 members of the Italian Olympic Team, pronounced heart hypertrophy was detected only in 23 sportsmen (9 cyclists, 9 rowers, 2 ‘basketball players, 1 volleyball player, and 2 weight-lifters).' More than 10 years ago it was ‘concluded that the large heart of athletes is mainly caused genetically or by intensive training from an early age.” CARDIAC PERFORMANCE Endurance training increases the cardiac performance in both humans!" and test ani- mals.!+! The major adaptation to endurance training is the generation of a greater stroke ‘volume at any given level of exercise as well as a greater maximal stroke volume (Figure 6-6).Specificity of Training Effects on Aerobic Working Capacity and the Cardiovascular System 173 stroke volume increase during exercise 1%) a 10 8 SJ BSSS Lonll 120! dal mi 1071 mi heart volume stroke volume Increase |%] A 50 100. 150 WATT Duntiained 2 trained FIGURE 6-6. Stroke volume increase during exercise in untrained persons and in athletes. On the upper panel the stroke volume increase im sportsmen pocsessing enlarged athlete's heart f= compared to the volume in untrained ‘persons. On the lower panel the stroke volume increase during an incremental exercise is shown in untrained persons ‘and trained subjects who have not increased the size of the heart. Constructed by J. Keul et al! This adaptation has been attributed to the Frank-Starling mechanism resulting from an increased end-diastolic volume, as well as from cardiac hypertrophy. In regard to the first mechanism, it was indicated that the larger stroke volume of the trained heart is related to the increase in blood volume," actually caused by endurance training."*' An experimental expansion of plasma volume by infusion of dextran solution increased the stroke: volume by174 Adaptation in Sports Training 11%. Any further increase in the volume of the circulating blood did not cause additional Increase in stroke volume. However, the stroke volume can increase with training without any increase in the heart or central blood volume." This is accomplished by increasing the ‘contractility of the myocardium to decrease the end-systolic volume. ‘The endurance-training effect on the myocardium contractility is proved in various kinds of experiments. The active tension is much greater in the strips of columna camae taken from trained hearts.!"°" Experiments on isolated papillary muscle preparation confirmed the training-induced improvement of the myocardial function." Several studies have demon strated an increase in the intrinsic contractile performance of isolated perfused hearts taken from exercise-trained rats as compared to untrained animals," If the rat heart isolated after training with daily running, the increase in heart mass by 14% was accompanied by increases in maximal stroke volume (+67%), maximal stroke work (+1119), and in maximal Power output by the left ventricle (+112%). However, in hearts exceeding the heart mass of sedentary animals by 30%, the maximal stroke volume was increased by only 45%, and maximal power output by the left ventricle by 36%. Further experiménts on isolated working heart preparations indicated increase with training in percent changes of systolic Pressure, stroke work, ejection fraction, circumferential shortening velocity, and relaxation rate working at 20 em H,0 of the atrial pressure,” The contractile performance appeared to be in relation with the magnitude of coronary blood flow generated by the preparation *° In a study, no enhanced performance was found in the hearts of female rats conditioned by running." The papillary muscle contractile responses to calcium, noradrenaline, or hypoxia were not altered by training == Relatively small differences were seen in the left ventricular performance in trained and Untrained animals investigated in sineunder a variety of conditions such asincreased aficrload and/or inotropy stimulation. However, the systolic tension at any given diastolic tension Was greater in rats trained by swimming.*” The maximal velocity of shortening is also increased in the trained myocardium. In dogs, endurance training improved the stroke volume potential in association with increased left ventricular relaxation sate." In rats, training enhanced VO,max by 16 10.20% ‘on the background of an increase in stroke volume (11%) and Oy extraction (8%).2!! CONTRACTILE MECHANISM OF THE MYOCARDIUM The ATPase activity of myosin,” actomyosin,”#2"2 and myofibrils?!52!* is increased by 1510 30% in male rats conditioned by swimming for’8 to 18 weeks. In female rats the response is similar, but its magnitude is not so great as compared to the results on male rats.2!3 ‘Significant changes were not found in a study.?” The increase in ATPase activity has been attributed to conformational changes in the heavy meromyosin component of the myosin molecule.24421219 In contrast to swimming training there is a relatively small increase in ATPase activity of the cardiac contractile proteins of rodents in response to endurance treadmill running 2°°22' In some studies no changes in ATPase were detected after running training in rats 27222 dogs. or guinea pigs. In a study, a decrease in myosin ATPase activity was found in female rats after a running training 2* On the other hand, a high-intensity interval running Program resulted in a 15% increase in myofibrillar ATPase activity. ‘The cardiac muscle can express three different isoforms of myosin. The predominance of the ¥ isoform has been associated with greater eross-bridge cycling economy at the expense of contraction intensity, whereas the predominance of the V, isoform has been associated with less economical but intensive contractions.#!* In running training of rats the myosin isozyme Profile indicates.a modest conversion to greater V, predominance." The shift in isozyme forms induced with swimming is mediated through thyroid hormone influence, because the alteration was blocked in swim-trained, thyroid-deficient rats.°"* Controversially, enduranceSpecificity of Training Effects on Aerobic Working Capacity and the Cardiovascular System 175 running waining induced a greater V, expression without a compromise in exercise capac~ ity." It is noteworthy that this adaptation was cnhanced if the involvement of the sympa- thetic nervous system was severely reduced by sympathectomy. At the same time, the maximal exercise capacity of trained sympathectomized rats was increased even though 50% of the cardiac myosin expressed in these animals was V,. These changes were associated with reduction in the specific activity of myofibrillar Ca-ATPase. and myosin Ca-ATPase.?772* Tt was found that myosin light chain phosphorylation decreased the ATPase activity of cardiac myofibrils and inereased the myosin affinity for actin.” These findings suggest possible link between myosin phosphorylation and the level of mechanical activity of the heart.” Further, it was demonstrated that training induced alterations in cardiac sarcolemma composition and functional properties, Asa result, an increased calcium influx appears, which can potentially enhance activation of the contractile machinery? These adaptations can contribute to the higher level of cardiac performance that is achieved with waining, ‘The maximal force of the papillary muscle, studied in vitro as.afum of external calcium concentration, improved in female rats with running training in association with decreased affinity of calcium binding sites on the sarcolemmal membrane.™' The specific content of sarcolemmal phosphatidy! serine (a sarcolemmal phospholipid, critical for sarcolemmal cal- cium binding moiety) increased by approximately 50% in the trained myocardium.?* These data provide a possible mechanism by which more externally bound calcium could be made available to the interior of the cell during the action potential.2!* ‘The cardiac sarcoplasmic reticulum has a grester capacity to sequester and bind calcium in swim-trained vs. control rats.?"”224 However, calcium sequestering and binding capacity of the cardiac sarcoplasmic reticulum did not improve after running training.** Within great limits of heart rate the heart of a trained rat exerts a greater level of left ventricular pressure than that of an untrained rat.’ Consequently, adaptive mechanisms to economize eross-bridge cycling may be necessary to buffer the high degrees of contractile activation that can be achicved at high-intensity levels of exercise in the trained state” In dogs, an improvement of the contractile state of myocardium occurred during. exercise following training in spite of the lack of change in contractile protein ATPase.™*! Eleven weeks of progressive treadmil running for Ih daily did not increase the concentration of myofibrillar protein, nor the myofibrillar ATPase activity. The time course of isometric twitch af the papillary muscle did not change. However, tension output per unit area increased and this appeared to be due toa greater amount of Ca* being made available to the contractile apparatus.*™ In the context of the specificity of training effects, it is important to emphasize that in this experiment as well as in other investigations the use of similar training programs did not produce marked degrees of cardiac hypertrophy. Consequently, there are two versions of heart adaptation to training. One of them is connected with myocardial hypertrophy. In rats this version appears mainly as a result of swimming training. The other version of cardiac adaptation is connected 10 adjustments that do not necessarily include heart muscle hypertrophy, increased amount of contractile protein, and elevated activity of ATPase in myofibrils. The other version of adaptation is revealed mainly as a result of running training and seems to be related to adjustment on the level of intracellular Ca** metabolism. At the same time these training programs induce a pronounced enhancement of oxidation potential in skeletal muscles. * In dogs also, running training increased the maximal rate of the left ventricular pressure devel- ‘opment but not the content of myofibrillar proteins and ATPase activity. ENERGETICS OF THE MYOCARDIUM With the exception of some earlier studies,2°2* a common result is that neither endurance nor other kinds of training increase the amount of cardiac mitochondrial protein per gram wet tissue or the activity of mitochondrial enzymes.*2"" In rats the activity of oxidation enzymes increased neither with swimming nor running training. In the untrained organism the176 ‘Adaptation in Sports Training oxidative capacity of the heart already exceeds that of the oxidative skeletal muscles by approximately three times.” With training, the skeletal muscle can approximately double its oxidative capacity (see above), while that of the heart remains unaffected under intense training regimes,” Jt is suggested that the n mitochondria is chronically main- tained in @ maximal ‘up-regulated’ state. This property permits the heart to maintain a positive ‘energy balance in the face of a constantly changing availability of substrates. Hence, the endurance training effect on skeletal muscle mitochondria implies the reduction of differences between skeletal and heart muscles’ oxidative capacities. In regard to the heart muscle, it was assumed that training induced a proportional increase in myofibrillar and mitochondrial protcin.””2"! Moreaver, endurance training normalizes the decrement in mitochondria-to- myofibril volume ratio, seen with pressure-overload hypertrophy. In mice, endurance training induced a stable cardiac hypertrophy (by 6 to 7%), but not changes in the activities of myocardial actomyosin ATPase, citrate synthase, succinate dehy- drogenase, cytochrome c oxidase, malate dehydrogenase, and adenylate kinase. B- Gluceronidase: activity increased by 20-25%.2° ‘The myocardial lactate dehydrogenase activity may increase with endurance taining. However, it is not a common result. Training does not affect the activities of phosphofruc slyceraldehyde-3-phosphate dehydrogenase, adenylate kinase, or creatine ki- the heart, No significant difference was found in the mechanical efficiency of isolated hearts obtained from trained and untrained rats." Training did not change the ATP/O ratio of mitochondria ‘obtained from the myocardium." Calculations made on the basis of recording the blood Pressure contour in the axillary artery (diastolic pressure time index, tension time index) during a progressive multi-stage treadmill test, led to the conclusion that in humans, jogging aining reduces myocardial O, demands, increases potential O, supply, and improves the supply/demand balance at any submaximal workload together with the increase of the whole body working capacity ** At the same time endurance training suppresses the free radical oxidation of lipids. A prolonged swimming training program that caused a significant increase in cardiac weight, decreased activities of catalase in the right ventricle and in the subendo- and subepimyocardium. ‘The activity of thioredoxin reductase decreased in cach part of the myocardium and that of glutathione reductase in the right ventricle and in the subepimyocardium. The activity of glucose-6-phosphate dehydrogenase increased and the activity of glutathione peroxidase as well as the tissue content of carnosine and anserine and tissue sulphydryl groups remained unchanged, Only minor changes were found in the regional distribution of antioxidants.” Coronary vasodilation during exercise can produce a three- to fivefold increase in coronary flow.35! Even in strenuous exercise the myocardial oxygen delivery appears to be adequate: and the existing flow reserve seems capable of handling the increased oxygen demand. Correspondingly, the coronary flow reserve is not changed by chronic endurance exer- cise. However, experiments on dogs indicated that endurance training significantly inereases the coronary transport capacity, A 26 and 82% increase in maximal blood flow and capillary diffusion capacity, respectively, were detected 2 There is also.a difference hetween the effects of endurance and high-resistance waining. Endurance-trained rats exhibited a higher left and total coronary cast weight when compared to cither control or resistance- trained rats. In resistance-trained rats, a higher right coronary cast weight was observed in comparison with their sedentary counterparts." It seems correct to conclude that exercises that substantially increase the cardiac output and coronary blood flow, stimulate a neovascular response, at least at the capillary level 295297 Endurance training increases the glycogen store in the myocardium,®*2* but no changes ‘were found in the contents of phosphocreatine, ATP, ADP, and AMP." Myocardial triglyc- erides* as well as phospholipids and cholesterol™# did not alter with training.Specificity of Training Effects on Aerobic Working Capacity and the Cardiovascular System 177 ADDITIONAL ADAPTIVE CHANGES IN THE OXYGEN TRANSPORT SYSTEM “The adaptation to endurance exercises is also connected with an increased capil of the lung alveolus,2! as well as changes in the respiratory muscles. In the diaphragm, activities of oxidation enzymes increase.” Increased glycogen content was found in Land type Tib fibers of the diaphragm but not in type Ifa. Increased capillarization per area of musele fiber was found in type IIb fibers of the diaphragm.*® No changes in the oxidation ‘enzymes were found in the intercostal muscles. The activity of glycolytic enzymes remained. without change.” Endurance training stimulates erythropoietic processes in the bone marrow. 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Sci Sporae Ener, 15, 472, 1983. 146. Tepperman, J., and Pearlman, D,, Effects of exercise and anemia on coronary tries of small animals as revealed by the corrasion-cast technique, Cire. Res... 56, 1961 147, Stevenson, LA.P, Felehi, V., Rechnitzer,P., and Beaton, JIR, Effect of exercise on coronary ce sire ia the rat, Cire Rex, 15, 265, 1964 148, Bloor, C.M., and Teen, AS. Interaction of age and exercise an the heart and its blood supply, Lab. Jest 22, 160, 1970. 149, Koerner, J.B. and Texjung, R.L., Effect of physical raining on covanary collateral circulation of the rat, J Appl. Physiol, $2, 376, 1982 150, Penpargkul, S, and Scheuer, J., The effect of physical taining upoa the mechanical and metabolic performance ofthe rat ear, J. Clin. Invest, 49, 4859, 1970, d Kirchhoff, HLW.. Kretslawfrepalation, Georg Thieme Verlag.182 Adapiation in Sports Training 151. Roeske, WIR, O'Rourke, R.A. Klin, A, Leopold, G., and Karliner, JS.. Noninvasive evaluation of ventricular hypertrophy in professional athletes, Circulation, $3, 286, 1976. 152, Underwood, R.H. and Schwade, J.D... Noniavasive analysis of candiae function of elite distance ruaness — echocardiography, vectorcardiography, and cardiac intervals, Ann. NY Acad. Sci, 301, 297. 1977. 158, Allen, HD, Goldberg, SJ., Sahn, DJ., Schy, No, and Wojcik, R.,A quantitative echocardiogeaphic study of champion childhood runners, Circulation, $5, 142, 1977. 154. Morganroth, J, Maron, BL, Henry, W-L., and Epstein, S., Comparative left ventricular dimensions in trained athletes, Aim. Patera. Med, 82, 521, 1975 15S, Tkaheima, M.J. Palatsi, LJ., and Takkunen, J.T, Noninvasive evaluation of the athletic heat: sprinters versus endurance manners, Am. J. Cardiol, 44, 24, 1979, 156. Longhurst, J.C., Kelly, A.R., Conyea, W.J., and Mitchell, J.H., Echocardiographic left ventricular masses in distance mianers and weight lifters, J. Appl. Physiol, 48, 154, 1960. 157. Gilbert, C-A., Nutter, D.O., Felner, J.M., Perkins, J.V., Heysficld, S.B., and Schlant, R.C., Echocantiographic stody of cardisc dimensions and function in the endurance-tiined athletes, Am. J. Cardiol, 40, 528, 1977. 158. Paukon, W., Boughner, D.R., Ka, P., Cunsingshan, D.D. and Persaud J.A., Left ventricular function in marathon runners: echocardiographic assessment, J Appl Plysiol, SI, 881, 198], 159. Cohen, J... and Segal, K.R., Left ventricular hypertrophy in ahlctes: an exercise echocantiogsaphic study. Med. Sed Sports Exerc, 12, 695, 1985. 160, Dickhuth, H.H, Simon, G.,.indermana, W., Wiberg, 4., and Keed, J, Fchocardiograpbic sties on athletes of various sporttypes and noe-athletie persons, Z. Kardiol, 48, 449, 1979. 161, Brown,S, Byrd, R, Jayringhe, M.D. and Fones,D., Echocardiographic charactristics of competitive and recreational weight lifters J. Cardiavasc. Ultrason, 2, 163, 1983, 162. Monapace, FJ, Hammer, W.1., Ritzer, T.R., Kessler, K.M., Warner, HLP.Spann, J.F..and Bove, A.A.. Left venicula size in competitive weight lifters: an echocardiographic study, Med. Sci. Sports Exerc, 14, 72, 1982, 163. Fleck, SJ. Candiovascular adaptations to resistance training, Med. Sci. Sports Exerc., 2, $146, 1988. 164, Stone, MAL, Wioson, G.D., Blessing, D. and Rezenck, R.. Cardiovacolae responses to short-term olympic style Weight-traésing in young men, Can. J. Appl. Sport Sc, 8, 134, 1983, 165. Pearson, A.C., Schiff, M., Mrosek, D., Labovitz, Al, aid Williams, G. fonction in weight lifters, Am. J. Cardiol, $8, 1254, 1986. 166. Fleck, SJ, and Dean, LS. Resistance training experience and the pressor response during resistance exercise, J Appl. Physio, 63, 116, 1987 167. Colan, S.D., Sanders, SF, McPherson, D., and Borrow, K.M., Left ventricular diastolic function in elie athletes with physiological candise hypertrophy, J. Am. Coll. Cardiol, 6, $48, 1985, 168. Snoees, LIE, Abeling, HFM. Lambrechts, J.A.C. Schinits, J.P Verstappen, F-TJ4 and Reneman, RS. Echocardiographic dimensions in athletes in relation to thei taining programs, Med. Sci Sports Exerc., 1, 428, 1982. 169. Cox, M.L., Benet, JB, and Dudley, G.A., Exercise taining: indoced alterations of cardiac momphology, J Appl. Physiol 61, 926, 1986, 170, Fomin, N.A., Gorokhov, NIM, Vlassov, A.V., and Beshetoy, A.V., Dircstion of adaptive transformations of hear in young sportsmen, Teor. Pratt. Fiz. Kult. $, 18, 1991 (in Russian). 171. Ricci, G» Lajoie, D, Petielerc, R., Perounet, F, Ferguson, RJ, Fournier, M., and Taylor, A.W, Left ventricular size following endurance, sprint, and strength waining, Med. Sc. Sporis Exere.. L4, 344, 1982. 172. Rubal, B.J., Al-Mubailani, A-R., and Resentswieg, J» Effcels of physical conditioning oa the eart size ‘and wall thickness of college women, Med. Sei. Sports Exerc, 19, 423, 1987. 173. Rost, R, The frontiers between physiology and pathology in the athlete's heart: to what limits can it enlarge and beat slowly, in Sports Candiology,Lubich,T., Vencrando, A..and Zeppill.P, Eds., Aulo Gaggi, Bologna, 1989, 187 174, Past, B., and Peve, J, The influence of endurance training on left ventricular function, J Sports Med. Phys: Fimess, 20, 359, 1990. 17S. Kea, Jo. Dickhiith, Hf Lehmann, M., and Staiger; J, The athlete's heart — hsemedynamics and structure, dnt. J. Sports Med, 3.>189 Specificity of Training Effects on Control Functions and the Connective Tissue (Coops cpp “61 ‘6 “60 Fay Hyg PAN sods fA “SUETATH OH) ay PUT OPAL .Sure, eBuawe ur safwnys aa ueyos ayy uEowaq diysuoNEfaL om pur (y) SuuTEN vans 01 paucsnoce scofgns ogy nt uorsuoine 2 rear cunautos euNe pu HS GOS AAFC Se] SEA JO FOIA PEBEHBAG WOH} POIR|IOED FOLIO OUINFOWWAL OPIN “ToL AMNOLA -ye Butpaodsarses ox} raye (Gq) 22u0) Alea, eFeeane wl soduey> an ‘uans afi (somo) anrsoldxe yoame-pz: pur -Z| aq19Ue pure as0soq Buu ‘ip 2uunp posnpoxd sofoemu (4g) suoUEY smADcE Paw CN,A) STTEPIUH SraseA (Guujen syaew yz CuuNp %v) (ou SOUOs JOVESAY (002—n0r) (oor—oneXoce—002)(002—00 LKo0k—0), epee Rik Hoe aak ay cca Te wit ‘SCOIU3d SIL } ONINIVEL HLONSHLS IAAL ‘BAISOTAXE SHBEM $2 URLIY = = SWgEM 21 UaLdy ++ ONINIVHL S033 — zo (= Au) ‘ONS! JOWUSAY (Guujan, syoom Fz BUUNP %6¥) NaI SOVUaAY190 Adaptation in Sports Training D.G. Sale” considers as possible mechanisms of neural adaptation in training: Increased activation of agonists Selective recruitment of motor units within agonists Selective activation of agonists within a muscle group Co-contraction of antagonists Pepe In addition, the training effects on motoneurons’ excitability and lability have to be taken into consideration. Strength training with weight-lifting or isometric exercises causes an increase in the reflex potentiation of EMG responses. Reflex potentiation is enhanced in weight-lifiers" and elite sprinters."* The potentiation of reflex responses by voluntary effort is probably related to elevated motoneuron excitability." Training increased the time that the highest threshold motor units could be kept active in sustained maximal contractions.” Training allows both low- and high-threshold motor units to maintain regular firing intervals at lower rates than before training.” Naturally, a marked specificity exists in the response to strength training, including its action on motoneuron excitability.‘ Isometric strength training resulted in an elevated ability of subjects to discharge motor units at regular firing intervals, whereas high repetition dynamic taining resulted in a trend towards reduced ability to maintain regular firing intervals.** A comparison of various training methods for improved strength showed that the force improvement was the highest in maximal voluntary isometric contraction as well as in maximal electrically evoked tetanic contraction when isometric training was used. The lowest improvement was found with isokinetic training at the movement velocity of 160°-s7. Isokinetic training with the movement velocity of 40°-s* gave medium effects. The training effect on the torque at various velocities of movement was the highest when the movement velocity corresponded to the movement velocity of training exercises." This result is in accordance with others indicating that at least in isokinetic training the taining velocity contributes in improving peak torque.** It was calculated that in a 60-day training with the aid of maximal isokinetic knee extensions at an angular velocity of 2.09 rads“, hypertrophy accounted for 40% of the increase in force while the remaining 60% was attributable to an increased neural drive and, possibly, to changes in muscle architecture.!® A taining program that included various types of jumping exercises resulted in an earlier preactivation of leg extensor muscles before impact in the performance of test exercises. This was associated with a more powerful eccentric working phase. Higher preactivation of muscle, higher flexion of knee, and increased dorsioflection of ankle joints in the beginning of contact, caused an increased tendomuscular stiffness, possibly through more powerful reflex activation.*? Six weeks of daily clectrostimulation sets augmented the muscle force by changing peripheral processes associated with intracellular events, without modifying the nervous ‘command of the contraction. Comparison of the peripheral changes recorded during submaximal training by electrostimulation and voluntary contractions suggest that clectrostimulation is less efficient, but complementary to voluntary training because the number and the type of trained motor units are different in the two procedures.!* It was noted eatlier that there are certain differences between the effects of training for improved strength and for improved power (Figure 7-2). The main difference between exercises applied in heavy resistance and power training is founded on the time of develop- ment of peak force during movements. In heavy resistance exercises the aim is to apply the highest possible force or one close to it. The time for force development is not the main condition of these exercises. In power exercises the aim is to achieve the highest possible power output by the movement. Therefore, the time of force development becomes a main determinant. Correspondingly, there are substantial differences in the results of systematical use of heavy resistance or power exercises. These differences have to be related to adaptive changes on muscle level (hypertrophy vs. improvement of the excitation-coupling system,Specificity of Training Effects on Control Functions and the Connective Tissue 191 GE MUSCLE FIGRE AREA rary units) 7-35 veavr Resistance STRENGTH TRAINING 200 275 250 EXPLOSE TYPE STRENGTH TRAINING (a 0 @ 20 WEEKS TRAINING PERIOD FIGURE 7-2 Average (arbitary units + SE) total fiber arca of the fast-and slow-twitch fiber types of the vastus. lateralis during the 24-week heavy resistance strength training and during 24-week explosive type strength training, in subjects accustomed to strength training. (From Hikkinen, K., J. Sports Med. Phys. Fitness, 29, 9, 1989. With permission.) sarcoplasmic reticulum function, and cross-bridge formation rate) or on the level of central nervous control. Usually, both groups of adaptive changes are revealed together. Only the ratio between them is different depending on the training exerises. There also seems to be a certain time sequence in development of various adaptive changes in training, for improved strength Early changes in voluntary strength can usually be accounted for largely by neural factors with a gradually increasing contribution of hypertrophy factors as the training proceeds.* During prolonged heavy resistance training the capacity of the neuromuscular system for fast force production may even decrease after the initial slight improvement? CHANGES IN THE CENTRAL NERVOUS SYSTEM In a number of studies, training-induced structural, biochemical, and functional changes were found in the nervous system. Mice subjected to physical activity during late post-natal development show significantly higher brain weight than inactive controls. Histological examination of the cerebellum revealed significantly greater dendritic field, branch length, synaptic density of dendritic spikes, and total number of spikes per unit length per cell.” The training effect on spinal neuron size was recorded in rats. histochemical study indicated increased oxidative potential of motoneurons? A high significance belongs also to the increased activity of cholinesterase in motor end-plate® and changes in axonal conduction velocity. Most of these adaptations appear to be specific to motor unit types and cannot be gencralized beyond motor unit population.** The responsiveness of the monosynaptic compo nent of the spinal stretch reflex to training has been demonstrated in limb muscles of monkeys. In conclusion, the mechanism of neurall adaptation includes increased activation of prime movers in a specific movement, and appropriate changes in the activation of synergists a antagonists.” AAll these manifestations are essential not only for improved muscular strength ind power, but also for improved speed of movement and endurance. The neural adaptation mechanism is decisive for improved skill and coordination, CROSS-EFFECTS OF TRAINING ON UNTRAINED MUSCLES ‘There are very old evidences that resistive training with muscles of one limb increases the strength of the muscles of the contralateral limb." During the last half-century it has been confirmed by physiological experiments. More recently, it was demonstraicd that the strength increase in the contralateral untrained arm was associated with an increase in intepral192 Adaptation in Sports Training electromyogram® but not in muscle size.“ Consequently, the cross-training effect was considered to be the result of neural adaptation.” In an experiment of one-legged exercise a positive cross-effect on the contralateral leg was confirmed in regard to peak torque of both quadriceps and hamstring muscles. Also, an increased endurance of these muscles of the untrained leg was found after € weeks of training of the contralateral ie ‘The cross-training effect is revealed also in regard to-the velocity of movement. However, the training effect on the muscle strength as well as on the velocity of movement is more pronounced in the trained than in the untrained leg“ ‘The one-leg training experiments are rather conclusive that endurance exercises affect only muscles directly involved in mechanical energy production.“ This is the case in regard to enzyme adaptation as well as energy stores. The glycogen concentration of the trained leg was from 6 to 60 mmol-kg"' wet wt. higher. In bicyclists and swimmers the muscle glycogen content is higher in the trained than in the other muscles with differences varying from 20 to 101 mmol-kg-' wet wt. One-leg training experiments indicated the inerease of glycogenetic ‘enzymes (glycogen synthase and hexokinase) only in trained muscles." In triathlonists the mean percentage of type [fibers was 58, 63, and 60% in the gastrocne- ius, vastus Jateralis, and deltoid muscles, respectively. However, the respiratory capacity as well as the activity of citrate synthase were lower in the deltoid muscle compared with leg muscles.” In another study, 8 weeks of cycling increased the peak VO, by 13%, capillary density by 15%, and volume of mitochondria by 40% in the vastus lateralis muscle. In the unexercised deltoid muscle the peak VO, increased by 9%, but the volume of mitochondria decreased by 17%, Capillary density did not change.” ‘The dependence of adaptive changes within muscular fibers on their actual use indicates that the: inductors of these modifications are local in nature and depend on the internal conditions within the muscle fibers. The cross-cffects of unilateral tr through any possible influence acting gencrally on muscle tissue. TRAINING EFFECTS ON THE CONNECTIVE TISSUE ‘The main types of connective tissue (ligaments, tendons, collagenous structures within muscles, bone, and cartilage) contain collagen, which is extracellularly located and which constitutes 25 to 30% of the total body protcin. To continue discussion on the specific nature of training effects in regard to the connective tissue, the main questions are (1) does training influence the synthesis and turnover of collagen and other proteins of the connective tissue? (2) how are these effects related to the training specificity? and (3) do the training-induced changes in the connective tissue improve the strength of the structures of the tissue? Most of the animal studies indicate that endurance training can increase the maximum strength of tendons? and ligaments." Accordingly, the breaking load of ligaments and tendons increases. These changes were accompanied by an increased mass of studied tendons and ligaments. However, these results were not obtained in all studies. There seems to exist a number of factors determining the action of training on connective structures. Among these the significance of age, sex, and localization of the structure is demonstrated. As a result of endurance training, an increased number of nuclei and an increased tendon mass were found in young mice,” but this was not found in elder animals.” Endurance training programs increased the maximal load that the attachment of the medical collateral ligament to tibia could sustain in growing male rats and male dogs.” ‘This effect was not ‘observed in female rats.” However, in a paper a training-induced increase in the load Recessary to disrupt the medical collateral ligament in female rats was reported" In contrast to the positive training effect on the maximal tensile strength of various tendons,” this effect was not observed using a Calcaneus-Achilles tendon-gastrocnemius-femur preparation.Specificity of Training Effects on Control Functions and the Connective Tissue 193 Hypophysectomy,® adrenalectomy, and diabetes,” but not thyroidectomy" or ovariectomy,® exeluded the training effect on ligamentous strength. Treatment of hypophysectomized rats with thyrotropin restored the training effect." Treatment of hypophysectomized rats with somatotropin”4® or corticotropin'* was ineffective in regard to restoring the training effect. Collagen can be measured determining the hydroxyproline content. As expected, training increased both hydroxyproline concentration and the breaking strengths of tendons” or ligaments.‘ However, a possibility was also indicated that the breaking sirength increases without any change in the hydroxyproline content. It is likely that this discrepancy may be related to the increase in collagen degradation, found in the Achilles tendon of trained animals. ‘The water content of ligaments and tendons does not change with taining."' The acti of acrobic enzymes increases in tendons." Sprint training has been seen to-enhance ligament weight and the weight/length ratio The same is assumed as a result of resistive training.” °5 The maximum voluntary contraction represents approximately 30% of the maximum tensile strength of tendons.” This leaves a great safety mar Exercises for improved flexibility are connected with stretching ligaments and tendons. It ‘was shown that an experimental stretching of a tendon to 108% of its original length altered the tendon’s qualities. The tendon remained at 104% of its original length when unloaded. In the second trial the tendon was stretched more. Nevertheless, there were no changes observed in the maximal load at breaking.” ‘Systematic physical activity also increases bone density and mass.°*!"" First of all, the bone ‘mass of the main active limbs increases." In regard to changes in the bone tissue, the major factors are training intensity and load-bearing.” However, there are differences in stimulation of bone density and of bone length growth. Low-intensity training may stimulate the growth in bone length and in bone girth in growing animals, Relatively high-intensity training inhibits these processes, but results in increased bone density. Lower-intensity train- ing does not change bone density.” Increased bone density with high-intensity training or increased load-bearing is founded on increases in calcium and hydroxyproline concentration” in bones. Bone enlargement together with increased bone density, collagen concentration, and mineral content warrant in breaking strength" The thickness of cartilage in all joints was greater in trained than in nontrained rab) "Training also induces changes in the endomyseal connective tissue, In rats a compensatory hypertrophy of the soleus muscle after severing the attachment of the gastrocnemius and plantaris muscles to the Achilles tendon, doubled the number of fibroplasts in the soleus." ‘After severing the gastrocnemius from the Achilles tendon the collagen content increased in the plantaris muscle.'!? Endurance exercises did not increase the total collagen of the endomyseal connective tissue sheaths." On the other hand, life-long endurance training maintains higher level of biosynthesis''S as well as hydroxyproline concentration in the soleus muscle ‘Swimming training, which lacks weight-bearing and eccentric components, caused an crease in prolyl 4-hydroxylase and galactorylhydroxylysy] glucoryltransferase activities in the soleus, suggesting that muscle contractile activity per se is a positive regulator of collagen biosynthesis. '"7 In the rectus femoris muscle the training effect on hydroxyproline concentra. tion was not observed. In slow muscles the basement membrane is more collagenous than in the fast muscle, Aging and training further distinguish the composition of the basement membrane in slow and fast muscles. Jn young mea, strength training stimulated the endomyseal connective tissue growth. Tn body-builders the collagen amount was increased in the biceps muscle, but the proportion of collagen in the total amount of noncontractile proteins was similar in untrained persons, elite, and novice body-builders.'™ no194 Adaptation in Sports Training In the rat heart, endurance training decreased the hydroxyproline concentration.2! How- ever, this result was not confirmed in the mouse heart. In young mice no changes in myocardial hydroxyproline concentration were found with daily running." Myocardial col- lagen content increased with endurance training (running) in 4-month-old rats but not in $.5- month-old rats." During training the hydroxyproline concentration increased in the skin of mice." Atthe same time, training may improve the skin elasticity in older men and women. = REFERENCES: 1. Vira, A. Hormones ta Muscular Activity. Vol. H, Adaptive Effects of Hormones in Exercise, CRC Press, Boca Raton, FL. 1985. 2. Kjaer, M., Epinephine and some other hormonal responscs to exercise ia man. With special reference to physical wining, nt J. Sports Med. 10, 1, 1989. 3. Vendsalu, A.. Sindies on adcenaline and noradrenaline in human plasma, Acts Physiol. Scand. 49 (Suppl. 173), 1960 4, Hiiggendal, J Hartley, 1-H, and Saltin,B., Artcrial nocalrcaline eneceatation during exercise in relation torthe relative work levels, Scand J. Clin. Lab: Invert, 26, 337, 1970, 5. Brooks, 8, Cheetham, M.E., and Williams, C., Spriat uaining and the catecholamine response to brief ‘maximal exercise in man, J. Physiol, 369, PTL, 1988. 6 Brooks, S., Cheetham, M., and Williams, C., Endurance training and the catecholamine response to bricf ‘maximum exercise in ma, J. Physiol, 361, P81, 1985 7. Mallina, ES and Kass, G.N., Mctabolismof catehcolamines during physical exercise in man and animals, Usp. Fiz. Nauk, 2, 13, 1976 (on Russian) 8. Viru, A. Functions of the Adrenal Coriex in Muscalar Activity, Medizina, Moscow, 1977 (in Russian). 9. Kassil, G.N., Valsfeldt, LL, Matlina, E-S., and Schreiberg, G.L., Humoral-Hormonal Mechanisms of Regulation of Functions in Sports Activities, Nauka, Mescow, 197% (in Russian) 10. Viru, A. and Matsi, Functional stability of adrenocortical activity during bicycle ergometer and running exercise, Biol Sports, 8, 305, 1988 1. Vira, A., and Seene, T, Peculisitics of adjustments inthe adrenal cortex to various training regimes, Bil. Sports, 2,91, 1985, 12, Niveri, H., Kuoppasalmi, K., Karvonen, SL, Hubtanieml, L, and Harkimen, M.. Andropeas and physical exercise in the male rats, at. J. Sports Md, Suppl. (2nd World Congr. Sports Med.) 62, 1982. 13, Makkinen, K., Pakarinea, Ay Alen, M., Kaukanen, HL, and Kami, P.V., Neuromuscular and hormonal ‘daptations in athletes to strength training:in two years, J. Appl. Physia, 6S, 2406, 1988. 14. Sato, J., Osawa, L, Osbida, ¥,, Sato, Y., Kikura, Y., Higuchi, M., and Kobayashi, S., Effects of different ‘ypet of physical training a insulin action in human peripheral tissucs — use of the euglycemic clamp technique, 8th fot. Biochem. Exerc. Conf, Nagoya, 1991, 133. : 15. Ika, M.. and Fukunaga, T., A stody on training effect on strength per unit cross-sctional area of mascle by means of wltrtonic measurement, Eur. J. Appl. Physiol, 28, 173, 1970 16. Thorstensson, A...Obscrvations on strength training and detrsining, Acta Physio Scant, 100, 491, 1977. 17. Komi, PL., Viitasale, J, Rauramas, Rand Vihko, V., Effect of isometric strength training on mechanical ‘lectrical and metabolic aspects of muscle function, Eur. J. Appl. Physiol, 40, 45, 1978, 18, Cosi, DL, Coyle, E-F., Fink, W.F., Lesmes, G.R, and Witzman, F.A., Adaptation in skeletal muscle following strength training, J. Appl Physiol, 46. 96, 1979, 19, MeDonagh, MJ.N, Hayward, CM, and Davies, CT. muscles, J Bone Joint Surg, 65., 355, 1983, 20, Hakkinen, K., nd Koml, P.V., Training induced changes in newronscular performance under voluntary And reflex cinditions, Eur: J. Appl. Physiot. $5, 147, 1986, 21. Rutherford, OM, and Jones, D.A., The role of learning and coordination in sicogth taining. Eur J. Appl Physiol, $8, 100, 1986, 22, Lindh, M, Increase of muscle strength from isometric quadriceps exercive a different Knee angles, Scand. J. Rehab. Med. 11, 38, 1979. 23. Komi, P-V., and Buskirk, LR. Effect of cocentic and concentric muscle conditioning o@ tension and and Sutton, JR., Muscle fiber number ia biceps brachit in bodybuilders and control subjects, J. Appl. Physiol 57, 1399, 1984. 121. Tomanck, R.J., Taunton, C-A.,and Liskop. 1-S., Relationship between age, chronic exercise and collagen tissue ofthe hean, J. Gerontol, 27,33, 1972 122, Kiiskinen, A., and Heikkinen, E, Physical tsining and connective tissues ia young mice-heart, Ber J. Appl. Pirysiol, 35, 167, 1976. 123. Bartosors b., Chvapil, M., Korecky,B., Poupa, 0, Rakusan, K., Turek, Zand Visck, M.,The growth ‘of the muscular and collagenous parts ofthe rat hast in various frm of cardiomegaly, J. Physi, 200, 285, 1969, 124. Kiiskinen, A., and Heikkinen, I, Physical training and cosnective tissue ia young mice, Br. . Dermatot. 93,925, 1976 125, Suominen, H., Heikkinen, E., Moisio,H., and Vijama, K., Physical and cbemical properties of skia ia habitual tained and sedentary 31 1070 yeas old mea, Br. J. Dermatot, 99, 187. 1978.Chapter 8 MOLECULAR MECHANISMS OF TRAINING EFFECTS In the previous chapter it was shown that systematically repeated exercises induce a great ‘variety of changes in the body. These include morphological changes, up to the subcellular structures, metabolic and functional changes, and improved coordination of the body's activi- ties regarding nervous, hormonal, and cellular autonomic regulations. They are specifically related to the training exercises used, Improvements in performance and various body facul- ties are founded on these changes. There was never any doubt that changes induced by training express adaptation to condi- tions of increased muscular activity. Thus, various concepts related to these adaptive processes. swere used fo explain the mechanism of training effects: 1, J.B. Lamarck’s! statement that function creates organ 2. W. Roux’s? postulation that any functional change induces a trophic stimulation and thereby specific action on the organic form 3. W. Weigert’s law! of supercompensation for energy expenditure 4, W.A. Engelhardt's* rule that the degradation process is always a specific stimulus for the synthetic process. 5. LP. Pavlov's* theory of conditioned reflexes These concepts cannot be considered alternatives. Partly, they are additive, contributing mechanisms for different changes (changes in organic form vs. supercompensation for energy stores, improvement of the body's resources and cellular structures vs. coordination of functions). At the same time there exists a possibilty for regarding some of these concepts as ‘expressions of the process of development in understanding the same manifestation. J.B. Lamarck’s idea was based on analysis of the process of evolution. Ik was speculative to use this idea for understanding processes going on within the ontogenesis of an individual ‘organism. Therefore, an additional postulation like that of W. Roux's was necessary, But what does trophic stimulation mean, and what is the mechanism by which it acts? These questions have remained without answers. A number of biochemical results enabled W.A. Engelhardt toestablish a close relationship between synthetic and degradation processes in the organism, Soon evidence was obtained that this relationship is founded on cellular autoregulation of ‘enzyme activities as well as on various mechanisms of neurohormonal regulation. What was important in Engelhardt’s rule was the affirmation that a stimulus for the synthetic process is thorn in the degradation process. Consequently, this rule made it possible to recognize the trophic stimulus as a result of previous degradation. In the same way the stimulus for repletion of energy stores and their supercompensation can be understood. However, the trophic stimulus must not only warrant restoration of the previous steres and abilities, but also induce improvement of the organism's faculties. Therefore, the changes constituting the background for improvement of the organism's faculties have to wansfer various qualities to a new, more cor less stable level. Only if this is the case, can the training effects be understood. Analysis of recovery processes after various exercises (Chapter 4) showed that restitution of the body's abilities is followed by a period of intensive adaptive protein synthesis and supercompensation for energy stores. However, this period is only transitory. Consequently, 199200 Adapuation in Sports Training the effect of a single exercise bout is not enough for achieving any training effects. Accord ingly, the experience of sports practice is very striking: only systematically repeated exercises can lead to training effects. “The concept of symmorphosis postulates that the quantity of structural elements is regu- lated to satisfy but not to exceed the requirements of the functional system.* Chronically maintained high demands are necessary for a stable improvement. Sportsmen's experience also shows that progress in sports results is possible only by using ‘exercises requiring extensive mobilization of the body’s abilities. Animal experiments per- formed in N.N. Yakovlev's laboratory likewise led to the conclusion that. systematically repeated exercises promote the improvement of fitness only if they cause substantial changes in the biochemical content of the internal milieu, ie., alterations in the ‘biochemical homeo- stasis’? “Therefore, training effects can be achieved: (1) if the exercises are repeated, and (2) if they demand an extensive mobilization of the adaptation abilities of the organism. ‘The classical studies by W.B. Cannon* and H. Selye” laid the basis necessary for intimate understanding of adaptation processes. Subsequent progress in the theory of adaptation helped todraw a more complete picture about the training mechanism. In this context, understanding of the connection between a high functional activity and the activation of the cellular genetic apparatus is the most important item, In 1965 it was suggested by F.Z. Meerson!® that an intracellular mechanism exists that interrelates the physiological function and the genetic apparatus of cells. Through this mechanism, the intensity of the functional activity of cellular structures determines the activity of the genetic apparatus. Thereby, a specific stimulation of protein synthesis follows. The significance of adaptive protein synthesis in the development cf fitness has been assumed by various authors.""* It has been hypothesized’* that the: mobilization of bodily resources and their utilization during training exercise causes accumu- lation of metabolites that will specifically induce adaptive synthesis of structure and enzyttie proteins related to the most active cellular structures and biochemical reactions, respectively ‘The accompanying activation of the mechanism of general adaptation warrants hormonal changes necessary for amplification of the inductor effect of metabolites as well as for the supply of protein synthesis by “building materials’, As a result, an effective renewal of protein structures, their enlargement, and increase in the number of molecules of the most responsible enzymes will be created (Figure 8-1). In order to evaluate this hypothesis it is necessary (1) to demonstrate the specific relation between training exercises and induction of adaptive protein synthesis, (2) to establish what the metabolic inductors in various kinds of training exercises are, (3) to obtain evidence for the cssential role of hormones in amplifying the action of metabolic inductors, (4) to confirm the necessity for repeated series of training exercises in order to achieve any training effects, and (5) to clarify interrelations hetween series of repeated exercises. PROTEIN SYNTHESIS IN TRAINING ‘The above-presented data are collectively rather conclusive that (a) training exercises stimulate an enlargement of cellular structures and correspondingly increase the contents of various proteins, and (b) these processes are: specifically related to the training exercises used. Differences in training effects suggest that in the training process the adaptive protein synthesis is utilized in many ways. The main locus of the adaptive protein synthesis varies between tissues and organs. In striated muscle tissue different distribution of the adaptive protein synthesis exists between muscles, and within a musele between motor units (types of muscle fiber). Within a cell, the adaptive protein synthesis is differently distributed between cellular structures and between individual proteins. In all cases there exist two main determi- nants of the distribution of the adaptive protein synthe:Molecular Mechanisms of Training Effects 201 Exorcise | TT enccerne ganas Fupetional activity Scan — Augmentation Increase ot of enzyme the most active Terres oe) jikosbeee Metaboites Hormones te Nasal Adaptive proten tnaxtore Synthesis i ~~ cantor gonetic “=~ pesreal FIGURE 8:1. Indoction ofthe adaptive protein synthesis and its results 1. The rate of functional activities during exercise performance or in the first stage of the recovery period 2. ‘The significance of the organ, musele, motor unit, cellular structure, and metabolic pathway in acute adaptation to the performed exercise and in the realization of the concrete motor task Undoubtedly, the proteins in which synthesis is stimulated, are different in training for improved endurance and in training for improved strength. Strength training mainly increases the content of myofibrillar proteins in the first place in fast-twitch glycolytic fibers, but rather significantly also in fibers of other types. However, these changes arc almost exclusively located in the muscles bearing the most strain during exercise. The increased activity of oxidative enzymes and elevated content of mitochondrial proteins indicate that the effect of endurance training is located in the first place in mitochondria. This effect has been found in various types of muscle fibers. It has been demonstrated that in the recovery period after an endurance exercise the protein synthesis rate increased in fast-twitch oxidative-glycolytic fibers but not in fast-twitch glycolytic fibers (see Chapter 4, Figure 4-12). Within oxidative~ glycolytic fibers the synthesis rate of mitochondrial proteins increased more than that of myofibrillar proteins. EVIDENCES OF AUGMENTED PROTEIN SYNTHESIS IN TRAINING ‘A number of results have confirmed the increased rate of protein synthesis in muscles during their hypertrophy."™!*>" Simultaneously, an increase in the RNA content takes place.”!? The increased activity of genome of the skeletal muscle fibers was indicated by clevated activities of DNA-dependent RNA polymerase®** and amino-acyl-RNA-synthase.?"7” This result was obtained both with endurance and strength training. An increased synthesis of RNA’ in vivo was detected within 24 b after initiating the compensatory hypertrophy of muscles.” ‘The increased physical working capacity resulting from endurance training was found to be influenced by actions on the induction of adaptive protein synthesis. Actinomycin D, a blocker of DNA-dependent synthesis of RNA, decreased the working capacity. At the same time, exercise decreased the resistance of animals to actinomycin. Administration of a com- bination of cofactors and precursors of nucleic acids (folic acid, vitamin B,,, and orotic acid) promoted the increase in working capacity during training. Actinomycin D- administra prevented the compensatory hypertrophy of muscles ‘A program of chronic treadmill running induced an increase in citrate synthase activity of 301041% together with a similarrise (27 to 37%) inmRNA for cytochrome c in the rat soleus, plantaris, red quadriceps, and gastrocnemius muscles. An increase was also found in mRNA. for o-actin but only in fast-twitch fibers.”202 Adaptation in Sports Training ‘The results are in a good accord with data obtained in experiments with chronic indirect electrical stimulation of the extensor digitorum longus or tibialis anterior muscles. In these experiments the muscle contractions were moderate in force output, but the period of daily ulation was up to 24h. A pronounced elevation in the activities of citrate synthase and cytochrome oxidase accompanied with an increase in mRNA for citrate synthase," B-subunit of F,ATPase, VIC subunit of cytochrome oxidase, and cytochrome b= In a study of the muscle-disuse effect, parallel changes of cytochrome ¢ protein synthesis and cytochrome © mRNA were confirmed. It was concluded that in muscular activity similar to endurance type exercises, the chronic adaptation is founded on a pre-translational control mechanism." ‘To imitate human resistance training, 2 model was employed in rats. Calf muscles were electrically stimulated to contract against a heavy resistance, resulting in plantar flexion. Both ankle extensors and flexors in the same limb were induced to contract, the gastrocnemius muscle (ankle extensor) shortened while the antagonist tibialis anterior muscle (ankle flexor) lengthened during active cross-bridge formation. Using a vigerous program of such heavy resistance training, the concentrically trained gastrocnemius muscle did not reveal hypertr phy. A significant hypertrophy was established in eccentrically trained tibialis anterior muscle ‘A milder resistance training program caused similar hypertrophy in the eccentric and concen- ‘rie contracted muscle. After a single bout of either 192 concentric or eccentric contractions, both mixed and myofibrillar protein synthesis rate increased 50 to 60% in the post-exercise recovery period (between 121041 h alter the exercise bout). However, skeletal o-actin mRNA and cytochrome ¢ mRNA did not change.***” While mitochondrial adaptation is not expected in heavy resistance training, the lack of change in c-actin mRNA suggests that the myofibrillar protein synthesis might be stimulated thr protein translation." The i ‘creased protein synthesis after concentric contractions was not associated with muscle hyper- trophy when this kind of activity was used in training."* Obviously, the increased protein synthesis rate, caused by a protein translation control mechanism, was balanced by a compa- rable increase in protein degradation. Against this background, a post-translational control mechanism was suggested in concentric resistance training.!* ‘The eccentrically trained tibialis anterior muscle enlarged, however, in relation with daily contraction. After a 10-week heavy resistance training program, increases of 41% in actin mRNA, of 38% in total RNA, and of 28% in protein were recorded in the tibialis anterior muscle. Consequently, multiple control sites (pre-translational, translational, and post-trans ational) can be elicited by training."* ‘When a weight is chronically attached to the wing of a chicken, a 140% increase in the protein content occurs in the slow-twitch anterior latissimus dorsi muscle." It was calculated that only 20% of the increase in the protein synthesis rate accounts for net muscle growth, while 80% of the increase contributes to an increased tumover of proteins. In fast-twitch muscle hypertrophy, even a larger proportion of increase in protein synthesis contributes to the normal replacement and wastage of protein structures (up to 91%). The actual muscle growth was warranted only by 9% of the increase in protein synthesis.” In regard to the action of increased muscular activity on protein tumover, there is-no full agreement between the results of various authors. First, it was observed that the compensatory hypertrophy is founded on both increased protein synthesis and decreased protein breakdown in muscles bearing the highest load.*™' Later, a 73% increase in the fractional rate of protein degradation was detected in fast-twitch muscle during the third to seventh day of its compen ssatory hypertrophy. Most of the increase in the degradation rate was blocked by administration ‘of a prostaglandin inhibitor. In rats a study of the action of exercises causing muscular hypertrophy indicated the ‘existence of significant differences depending on the fiber type. In brachialis muscle, contain- ing mainly fast-twitch fibers, the protein content increased due to the elevated rate of protein synthesis while the breakdown rate did not change. In slow-twitch soleus muscle the protein synthesis rate remained stable but the degradation rate dit ed.