Papers by Richard Casaburi
Journal of applied physiology (Bethesda, Md. : 1985), 1987
To investigate the mechanism by which ventilatory (VE) demand is modulated by endurance training,... more To investigate the mechanism by which ventilatory (VE) demand is modulated by endurance training, 10 normal subjects performed cycle ergometer exercise of 15 min duration at each of four constant work rates. These work rates represented 90% of the anaerobic threshold (AT) work rate and 25, 50, and 75% of the difference between maximum O2 consumption and AT work rates for that subject (as determined from previous incremental exercise tests). Subjects then underwent 8 wk of strenuous cycle ergometer exercise for 45 min/day. They then repeated the four constant work rate tests at work rates identical to those used before training. During tests before and after training, VE and gas exchange were measured breath by breath and rectal temperature (Tre) was measured continuously. A venous blood sample was drawn at the end of each test and assayed for lactate (La), epinephrine (EPI), and norepinephrine (NE). We found that the VE for below AT work was reduced minimally by training (averaging ...
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Respiratory Medicine, 2007
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Medicine & Science in Sports & Exercise, 1997
Patients with severe chronic obstructive pulmonary disease (COPD) are limited in their exercise t... more Patients with severe chronic obstructive pulmonary disease (COPD) are limited in their exercise tolerance by the level of ventilation (VE) they can sustain. We determined whether acutely increasing blood bicarbonate levels decreased acid stimulation to the respiratory chemoreceptors during exercise, thereby improving exercise tolerance. Responses were compared with those obtained during 100% O2 breathing (known to reduce VE in these patients) and to the responses of healthy young subjects. Participants were six patients with severe COPD (forced expired volume in 1 s = 31 +/- 11% predicted) but without chronic CO2 retention and 5 healthy young subjects. Each subject performed three incremental cycle ergometer exercise tests: 1) control, 2) after ingestion of 0.3 g.kg-1 of sodium bicarbonate and 3) while breathing 100% O2. During these tests VE was measured continuously and arterialized venous blood (patients) or arterial blood (healthy subjects) was sampled serially to assess acid base variables. Bicarbonate loading increased standard bicarbonate by 4-6 mmol.L-1 and this elevation persisted during exercise. In both groups, bicarbonate loading resulted in a substantially higher arterial pH; arterial PCO2 was either unchanged (healthy subjects) or mildly (averaging 5 torr) higher (COPD patients). However, in neither group did bicarbonate loading result in an altered VE response to exercise or an increase in exercise tolerance. In contrast, superimposing hyperoxia on bicarbonate ingestion yielded, on average, 24% reduction in VE and 50% increase in peak work rate in the patients (but not in the healthy young subjects). We conclude that acute bicarbonate loading is not an ergogenic aid in patients with severe COPD.
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Journal of Cardiopulmonary Rehabilitation, 1994
During an incremental exercise test, three consequences of the onset of anaerobic metabolism can ... more During an incremental exercise test, three consequences of the onset of anaerobic metabolism can be observed: rise in blood lactate (lactate threshold, LT); fall in standard bicarbonate (lactic acidosis threshold, LAT); nonlinear increase in CO2 output (V-slope gas exchange threshold, GET). We compared these thresholds in 31 patients with COPD. We found that the GET and LAT overestimated the LT. A better relationship was found between LAT and GET, even though GET was significantly higher than LAT (by 124 ml/min; p < 0.0001). However, since the bias is appreciably greater at lower LAT values (likely because VCO2 kinetics are slower than VO2 kinetics), we separated the studies into two groups: (A) tests where LAT occurred within the first 2 min of the increasing work rate period, and (B) tests where LAT occurred after 2 min. For Group A, there was a substantial bias between LAT and GET (323 ml/min, p < 0.0001), whereas the bias was much smaller (only 5.4%, though statistically significant) for Group B (57 ml/min, p < 0.01). We conclude that when lactic acidosis occurs after the first 2 min of incremental exercise, the GET closely approximates the point at which blood bicarbonate begins to fall.
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European Journal of Applied Physiology and Occupational Physiology, 1995
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European Respiratory …, 2009
Incremental cardiopulmonary exercise testing work rate ideally increases linearly to the subject&... more Incremental cardiopulmonary exercise testing work rate ideally increases linearly to the subject's tolerance within approximately 10 min. Widely used treadmill protocols often yield shorter exercise times in debilitated patients. We compared a recently described ...
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Medicine and Science in Sports and Exercise, 1995
We sought to determine whether exercise intensities not elevating blood lactate produce alteratio... more We sought to determine whether exercise intensities not elevating blood lactate produce alterations in physiological responses to exercise associated with training. Twenty-seven sedentary young men performed five cycle ergometer training sessions.wk-1 for 5 wk. Training power outputs were randomized to power outputs corresponding to either 80% of the lactic acidosis threshold (LAT), 25% delta or 50% delta (where delta is the difference between LAT and peak VO2 power outputs estimated from incremental exercise tests). Exercise sessions were 30 min for the 50% delta group and were proportionately longer for other groups, so that total work did not vary among groups. Before and after training, subjects exercised for 15 min (or to tolerance) at pretraining 80% LAT, 25% delta, 50% delta, and 75% delta power outputs. Continuous O2 uptake, CO2 output, ventilation and heart rate, and end-exercise blood lactate, norepinephrine, and epinephrine were measured. For the 80% LAT group, posttraining end-exercise values for the 75% delta test were significantly lower for each of these variables. There were similar reductions in each variable in all three training groups; no significant differences among groups were seen. Thus, in healthy subjects exercise which does not elevate blood lactate alters constant power output responses as effectively as exercise which elevates lactate, provided that total training work is the same.
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CHEST Journal, 1994
To evaluate the accuracy of noninvasive estimates of VD/VT in clinical exercise testing, we compa... more To evaluate the accuracy of noninvasive estimates of VD/VT in clinical exercise testing, we compared measurements of standard VD/VT with estimates based either on end-tidal CO2 (VD/VTET) or a published estimate of arterial PCO2 (VD/VTest) at peak exercise in 68 patients. Using regression analysis, we identified highly significant differences (p < 0.001) between each method and VD/VTstand across a broad range of observed VD/VT. Assuming a normal exercise VD/VT < or = 0.30, estimate methods were specific but were insensitive (50 percent for VD/VTET and 57 percent for VD/VTest) for identifying patients with abnormal gas exchange during exercise. Separate analysis of subgroups based on resting pulmonary function did not identify any group for which either method was acceptable. Our analysis showed that errors in estimating PaCO2, which are amplified by the Bohr equation when calculating VD/VT, are responsible for the inaccuracies of each noninvasive method. We conclude that noninvasive estimates of PaCO2 cannot replace measured arterial PCO2 for calculation of VD/VT during exercise.
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CHEST Journal, 1995
Patients with COPD usually are limited in their exercise tolerance by a limited ventilatory capac... more Patients with COPD usually are limited in their exercise tolerance by a limited ventilatory capacity. Lactic acidosis induced by exercise increases the stress on the ventilatory system due to CO2 generated by bicarbonate buffering and hydrogen ion stimulation. Patients with COPD are often observed to increase blood lactate levels at low levels of exercise. We wished to determine whether patients with COPD who experience lactic acidosis do so because of respiratory muscle production of lactate. Eight patients with moderate to severe COPD (FEV1 = 43.5 +/- 11.6% predicted) and 5 healthy subjects performed 10 min of moderate constant work rate exercise either breathing spontaneously or volitionally increasing their ventilation for 5 min to approximate the peak minute ventilation seen during incremental exercise. During volitional increased ventilation, 3% CO2 was added to the inspirate to prevent alkalosis and hypocapnia. In neither the healthy subjects nor the COPD group was the end-exercise lactate level significantly higher during volitional ventilation increase than during spontaneous ventilation. Further, in the COPD patients, the blood lactate levels during volitional ventilation increase were much lower than during maximal exercise (averaging 2.4 vs 5.3 mmol/L) despite similar ventilation levels (averaging 50 and 53 L/min). We conclude that it is unlikely that the respiratory muscles have an important influence on the blood lactate level elevation seen during maximal exercise in COPD patients.
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CHEST Journal, 2005
We hypothesized that endurance exercise training would reduce the degree of hyperinflation for a ... more We hypothesized that endurance exercise training would reduce the degree of hyperinflation for a given level of exercise and thereby improve submaximal exercise endurance. Twenty-four patients with COPD (mean FEV(1), 36.4 +/- 8.5% of predicted [+/- SD]) undertook a high-intensity cycle ergometer exercise training program for 45 min, three times a week for 7 weeks. Before and after training, the patients performed both an incremental exercise test to maximum and a constant work rate (CWR) test on a cycle ergometer at 75% of the peak work rate obtained in the pretraining incremental test. Ventilatory variables were measured breath-by-breath, and inspiratory capacity (IC) was measured every 2 min to assess changes in end-expiratory lung volume. After training, the increase in peak oxygen uptake was not statistically significant; however, the peak work rate increased by 12.9 +/- 10.3 W (p < 0.01). For the CWR test performed at the same work rate both before and after training, ventilation and breathing frequency (f) were lower after training (average, 1.97 L/min and 3.2 breaths/min, respectively; p < 0.01) and IC was greater (by an average of 133 mL, p < 0.05), signifying decreased hyperinflation. The increase in IC at the point of termination in the shortest CWR test for each individual (defined as isotime) correlated well with both the decreased f (r = 0.63, p = 0.001) and with the increase in CWR exercise endurance (average, 13.1 min, r = 0.46, p = 0.023). Exercise training in patients with severe COPD dramatically improves submaximal exercise endurance. Decreased dynamic hyperinflation may, in part, mediate the improvement in exercise endurance by delaying the attainment of a critically high inspiratory lung volume.
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CHEST Journal, 2000
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Summary Recovery from heavy exercise requires clearance of lactic acid from the blood and body t... more Summary Recovery from heavy exercise requires clearance of lactic acid from the blood and body tissues. Although it has long been felt that the liver plays the major role in lactate removal, it has more recently been asserted that skeletal muscle plays the dominant role. We felt it relevant to this controversy to determine whether patients with liver dysfunction have slowed
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Medicine & Science …, 2000
... Sports & Exercise: August 2000 - Volume 32 - Issue 8 - pp 1365-1368. CLINICAL SCIENCES: C... more ... Sports & Exercise: August 2000 - Volume 32 - Issue 8 - pp 1365-1368. CLINICAL SCIENCES: Clinical Investigations. ... DEBIGARÉ, RICHARD; MALTAIS, FRANÇOIS; MALLET, MARCEL; CASABURI, RICHARD; LeBLANC, PIERRE. Article Outline. Collapse Box Author Information. ...
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Journal of Applied …, 1992
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Journal of Applied …, 1987
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During exercise at critical power (CP) in chronic obstructive pulmonary disease (COPD) patients, ... more During exercise at critical power (CP) in chronic obstructive pulmonary disease (COPD) patients, ventilation approaches its maximum. As a result of the slow ventilatory dynamics in COPD, ventilatory limitation during supramaximal exercise might be escaped using rapid sinusoidal forcing. Nine COPD patients [age, 60.2 ± 6.9 years; forced expiratory volume in the first second (FEV(1)), 42 ± 17% of predicted; and FEV(1)/FVC, 39 ± 12%] underwent an incremental cycle ergometer test and then four constant work rate cycle ergometer tests; tolerable duration (t(lim)) was recorded. Critical power was determined from constant work rate testing by linear regression of work rate versus 1/t(lim). Patients then completed fast (FS; 60 s period) and slow (SS; 360 s period) sinusoidally fluctuating exercise tests with mean work rate at CP and peak at 120% of peak incremental test work rate, and one additional test at CP; each for a 20 min target. The value of t(lim) did not differ between CP (19.8 ± 0.6 min) and FS (19.0 ± 2.5 min), but was shorter in SS (13.2 ± 4.2 min; P < 0.05). The sinusoidal ventilatory amplitude was minimal (37.4 ± 34.9 ml min(-1) W(-1)) during FS but much larger during SS (189.6 ± 120.4 ml min(-1) W(-1)). The total ventilatory response in SS reached 110 ± 8.0% of the incremental test peak, suggesting ventilatory limitation. Slow components in ventilation during constant work rate and FS exercises were detected in most subjects and contributed appreciably to the total response asymptote. The SS exercise was associated with higher mid-exercise lactate concentrations (5.2 ± 1.7, 7.6 ± 1.7 and 4.5 ± 1.3 mmol l(-1) in FS, SS and CP). Large-amplitude, rapid sinusoidal fluctuation in work rate yields little fluctuation in ventilation despite reaching 120% of the incremental test peak work rate. This high-intensity exercise strategy might be suitable for programmes of rehabilitative exercise training in COPD.
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American Journal of Respiratory and Critical Care Medicine, 2011
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Papers by Richard Casaburi