Aerobic exercise improves cognitive and motor function by inducing neural changes detected using molecular, cellular, and systems level neuroscience techniques. This review unifies the knowledge gained across various neuroscience techniques to provide a comprehensive profile of the neural mechanisms that mediate exercise-induced neuroplasticity. Using a model of exercise-induced neuroplasticity, this review emphasizes the sequence of neural events that accompany exercise, and ultimately promote changes in human performance. This is achieved by differentiating between neuroplasticity induced by acute versus chronic aerobic exercise. Furthermore, this review emphasizes experimental considerations that influence the opportunity to observe exercise-induced neuroplasticity in humans. These include modifiable factors associated with the exercise intervention and nonmodifiable factors such as biological sex, ovarian hormones, genetic variations, and fitness level. To maximize the beneficial effects of exercise in health, disease, and following injury, future research should continue to explore the mechanisms that mediate exercise-induced neuroplasticity. This review identifies some fundamental gaps in knowledge that may serve to guide future research in this area.

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A single bout of aerobic exercise modulates corticospinal excitability, intracortical circuits, and serum biochemical markers such as brain‐derived neurotrophic factor ( BDNF ) and insulin‐like growth factor 1 ( IGF ‐1). These effects have important implications for the use of exercise in neurorehabilitation. Here, we aimed to determine whether increases in cardiorespiratory fitness ( CRF ) induced by 18 sessions of high‐intensity interval training ( HIIT ) over 6 weeks were accompanied by changes in corticospinal excitability, intracortical excitatory and inhibitory circuits, serum biochemical markers and working memory ( WM ) capacity in sedentary, healthy, young males. We assessed motor evoked potential ( MEP ) recruitment curves for the first dorsal interosseous ( FDI ) both at rest and during tonic contraction, intracortical facilitation ( ICF ), and short‐interval intracortical inhibition ( SICI ) using transcranial magnetic stimulation ( TMS ). We also examined serum levels of BDNF , IGF ‐1, total and precursor (pro) cathepsin B ( CTSB ), as well as WM capacity. Compared to pretraining, CRF was increased and ICF reduced after the HIIT intervention, but there were no changes in corticospinal excitability, SICI , BDNF , IGF ‐1, total and pro‐ CTSB , and WM capacity. Further, greater CRF gains were associated with larger decreases in total and pro‐ CTSB and, only in Val/Val carriers, with larger increases in SICI . Our findings confirm that HIIT is efficacious in promoting CRF and show that corticospinal excitability, biochemical markers, and WM are unchanged after 18 HIIT bouts in sedentary males. Understanding how aerobic exercise modulates M1 excitability is important in order to be able to use exercise protocols as an intervention, especially in rehabilitation following brain injuries.

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