Depression of activity in the corticospinal pathway during human motor behavior after strong voluntary contractions

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Abstract

The corticospinal system plays an important role in control of voluntary movements in primates. Recently, we demonstrated that the effectiveness of this system is depressed after maximal exercise. Because the depression was absent after antidromic activation of the motoneurons, we argued that transmission across corticospinal synapses was involved. Here, we explore the possible functional consequences of such a depression. In humans, direct electrical stimulation of axons of corticospinal neurons at the cervicomedullary level evokes motor potentials in elbow flexor muscles. When tested during relaxation after a maximal voluntary contraction (MVC) of the elbow flexors, potentials in biceps brachii and brachioradialis were depressed for ∼90 sec. The potentials were also depressed, although less markedly, when tested during a weak elbow flexion. Brief intermittent MVCs abolished the depression transiently, but during the intervening periods of relaxation, the depression appeared similar to that during continuous relaxation. The depression was greatest during relaxation after a 10 sec MVC and smaller after submaximal contractions. To look for effects of the depression on voluntary activity, we compared bilateral matching weak elbow flexions. After a conditioning 10 sec maximal elbow flexion of one arm, the electromyographic activity produced on that side was reduced relative to the activity on the contralateral side. Our findings support the view that synapses in the corticospinal system are depressed after strong voluntary contractions during both relaxation and activity. Furthermore, this depression can affect the production of voluntary movement.

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Petersen, N. T., Taylor, J. L., Butler, J. E., & Gandevia, S. C. (2003). Depression of activity in the corticospinal pathway during human motor behavior after strong voluntary contractions. Journal of Neuroscience, 23(22), 7974–7980. https://doi.org/10.1523/jneurosci.23-22-07974.2003

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