The amplitude of the H-reflex during the development and progression of fatigue reflects a complex interplay between central and peripheral factors. The purpose of this study is to characterize H-reflex homosynaptic post-activation depression (PAD) in an online fashion during a sustained submaximal fatigue task. The task required a high motor output in order to increase the likelihood of creating partial muscle ischemia with accumulation of fatigue metabolites, an important potential inhibitory influence upon the H-reflex during the progression of fatigue. Eleven subjects without neurologic impairment maintained volitional, isometric plantar flexion at 60% of maximal voluntary contraction until exhaustion. A paired-pulse stimulus (2 Hz) was delivered to the tibial nerve to elicit paired H-reflexes before, during, and after the fatigue protocol. The normalized amplitude of the second H-reflex (depression ratio) served as an estimate of PAD. Depression ratio increased during the first half of the fatigue protocol (P < 0.001), indicating a diminution of PAD, and then returned as exhaustion approached. The biphasic behavior of homosynaptic H-reflex depression during fatigue to exhaustion suggests a role for metabolic mediators of post-activation depression during fatigue.
Keywords: H-reflex; fatigue; homosynaptic depression; ischemia.
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