The physiological lengthening of CoSP end latency during fatigue was not observed in the SCI patients.
This reduced intracortical inhibition, probably secondary to decreased activity of the GABAergic inhibitory interneurons that modulate the corticomotoneuronal output, could represent a 鈥榩ositive鈥?neuroplastic response in an attempt to compensate for the loss of corticospinal axons.
The investigation of motor cortex excitability during fatiguing exercise may shed light on the role of exercise therapy in promoting brain reorganization and functional recovery in humans.