Changes in corticomotor plasticity induced by cardiovascular exercise and strength training in sedentary young adults
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Recent studies have further elucidated the properties of cardiovascular and strength training-induced changes in motor cortex (M1) plasticity (i.e. the strengthening and reorganization of neural connections). However, the degree of change in M1 plasticity following the completion of an exercise prescription remains unknown. The purpose of this study was to examine global changes in M1 plasticity of a small hand muscle in sedentary young adults following a 10 week exercise program. Electromyographic recordings were taken from the right abductor pollicis brevis (APB) muscle of 12 young subjects (5 women, 7 men; range 19-23 yrs). Subjects completed a 10 week exercise prescription consisting of two weekly resistance training sessions with a shorter aerobic session at the end as well as a third aerobic session. Exercises were changed to avoid adaptation, and aerobic session workloads were determined by heart rate response. Transcranial magnetic stimulation (TMS) of the left hemisphere was used to assess changes in APB motor-evoked potentials (MEPs) and input-output curve (IO curve). Changes in neural plasticity were induced using paired-associative stimulation (PAS), which consisted of 90 paired stimuli (0.05 Hz for 30 min) of median nerve electrical stimulation at the wrist followed 25 ms later by TMS to the hand area of the left M1. VO2 increased by 24.9% (P ≤ 0.05; n = 13) and BDNF levels did not significantly change after 10 weeks of exercise (P = 0.623; n = 12). Resting motor threshold (RMT) taken 5 minutes (RMT5) and 30 minutes (RMT30) after PAS did not increase significantly in exercise participants. Control subjects showed a significant decrease in RMT30 MEP amplitude in response to repeating PAS after 10 weeks (P ≤ 0.05; n = 11) and a significant increase in BDNF levels (P ≤ 0.05; n = 8). Post-PAS IO curves in control subjects revealed a significant decrease in excitability of lower threshold motor neurons after 10 weeks. The longitudinal use of PAS appears to yield varying results and our findings indicate that exercise may induce protective benefits against the perhaps diminishing effect of PAS-induced LTP. Findings yielded different excitability levels in RMT5 and RMT30, suggesting that PAS may be used to measure capacity for early-phase and late-phase LTP distinctively in the M1. Future work examining chronic exercise and BDNF levels should aim to control confounding factors shown to influence BDNF production.