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1.
École de kinésiologie et des sciences de l'activité physique (EKSAP), Faculté de médecine, Université́ de Montréal, Montreal, QC, Canada; Centre de recherche de l'Institut universitaire de gériatrie de Montréal (CRIUGM), Montreal, QC, Canada; Centre interdisciplinaire de recherche sur le cerveau et l'apprentissage (CIRCA), Montreal, QC, Canada.
Authors
Youssef L
1
Harroum N
1
Pageaux B
1
Neva JL
1
(4 authors)
2.
Department of Physical Therapy, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada.
Authors
Francisco BA
2
(1 author)
3.
School of Behavioural and Health Sciences, Faculty of Health Sciences, Australian Catholic University, Melbourne, Australia.
Authors
Johnson L
3
(1 author)
4.
Direction des bibliothèques, Bibliothèques des sciences de la santé, Université de Montréal, Montréal, Québec, Canada.
Authors
Arvisais D
4
(1 author)
5.
École de kinésiologie et des sciences de l'activité physique (EKSAP), Faculté de médecine, Université́ de Montréal, Montreal, QC, Canada; Research Center of the University Institute of Mental Health of Montreal, Montreal, QC, Canada.
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Abstract
Evidence continues to accumulate that acute aerobic exercise (AAE) impacts neurophysiological excitability as measured by transcranial magnetic stimulation (TMS). Yet, uncertainty exists about which TMS measures are modulated after AAE in young adults. The influence of AAE intensity and duration of effects are also uncertain. This pre-registered meta-analysis (CRD42017065673) addressed these uncertainties by synthesizing data from 23 studies (including 474 participants) published until February 2024. Meta-analysis was run using a random-effects model and Hedge's g used as effect size. Our results demonstrated a decrease in short-interval intracortical inhibition (SICI) following AAE (g = 0.27; 95 % CI [0.16-0.38]; p <.0001), particularly for moderate (g = 0.18; 95 % CI [0.05-0.31]; p <.01) and high (g = 0.49; 95 % CI [0.27-0.71]; p <.0001) AAE intensities. These effects remained for 30 minutes after AAE. Additionally, increased corticospinal excitability was only observed for high intensity AAE (g = 0.28; 95 % CI, [0.07-0.48]; p <.01). Our results suggest potential mechanisms for inducing a more susceptible neuroplastic environment following AAE.
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