Regular physical activity can have positive effects on brain function and plasticity. Indeed, there is some limited evidence that even a single bout of exercise may promote plasticity within the cortex. However, the mechanisms by which exercise acutely promotes plasticity are not clear. To further explore the effects of acute exercise on cortical function, we examined whether a single bout of exercise was associated with changes in cortical excitability and inhibition. Using standard techniques, cortical stimulus-response curves [90% resting motor threshold (RMT)-150% RMT] were investigated in nine subjects (four females, 31.1 ± 11.7 years) and short-interval intracortical inhibition (SICI) [interstimulus interval 2 ms and 3 ms, conditioning intensities of 80% active motor threshold (AMT) and 90% AMT] in 13 subjects (six females, 28.4 ± 5.1 years) before and at 0 and 15 min following 30 min of ergometer cycling at low-moderate or moderate-high intensity. There were no changes in cortical excitability following exercise but less SICI at both 0 and 15 min post-exercise (F [2, 24] = 7.7, P = 0.003). These findings show that a short period of exercise can transiently reduce SICI. Such a change in inhibition after exercise may contribute to the development of a cortical environment that would be more optimal for plasticity and may partially explain previous findings of enhanced neuroplasticity following low-intensity exercise.

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There is some limited evidence suggesting that the spaced application of repetitive transcranial magnetic stimulation (rTMS) protocols may extend the duration of induced neuroplastic changes. However, this has yet to be demonstrated in the human primary motor cortex (M1). We evaluated whether the paired application of an inhibitory rTMS protocol [continuous theta burst stimulation (cTBS)] at 10-min intervals prolonged the duration of induced M1 plasticity. Motor evoked potentials (MEPs) were recorded from the right first dorsal interosseous muscle before and following single and paired cTBS protocols applied with two intensities: 80% of active motor threshold (AMT 80 ) and 70% of resting motor threshold (RMT 70 ). Single cTBS protocols did not significantly influence MEP amplitudes. Whereas paired trains applied at AMT 80 had no effect on MEP amplitudes, paired cTBS trains at RMT 70 significantly reduced them. MEP amplitudes remained suppressed for at least 2 h following the second train. Control experiments suggested that the contraction used to establish active motor threshold prior to cTBS application may be responsible for blocking the effect of paired cTBS trains at AMT 80 . The results suggest that the spaced application of cTBS protocols may be an effective approach for establishing long-lasting M1 neuroplasticity only in the absence of prior voluntary motor activation. These findings may have important implications for the therapeutic application of rTMS.

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Background: The potential of non-invasive brain stimulation (NIBS) for studying, and