Reciprocal inhibition between the muscles of the human forearm.

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Abstract
Peripheral and central mechanisms of reciprocal inhibition between antagonist muscles in the forearm were studied in 10 human subjects. H reflexes were evoked in flexor muscles by stimulating the median nerve with angle shocks at around motor threshold intensity. Peripheral inhibition of the flexor H reflex was produced by motor threshold stimulation with a single shock of the radial nerve supplying the extensor muscles. The conditioning radial nerve stimulus produced inhibition of the flexor H reflex consisting of 3 phases. In some individuals, an H reflex could be evoked in extensor muscles of the forearm. Stimulation of the median nerve produced inhibition of the extensor H reflex with a similar time course to that from extensors to flexors. The 1st phase of inhibition was apparent when the test median nerve shock was given from 1 ms before to 3 ms after the conditioning radial nerve shock. It was abrupt in onset and short in duration and could be evoked with a conditioning stimulus intensity as low as 0.75 .times. motor threshold. The 2nd and 3rd phases of inhibition were evident when the conditioning radial nerve stimulus preceded the median nerve test shock by 5 to 50 and 50 to 500 ms, respectively. The characteristics of these later phases of inhibition are to be the subject of a separate report. The difference in timing of the peak initial short-latency inhibition from extensor to flexor and from flexor to extensor muscles enabled an estimate to be made of the central synaptic delay of the inhibitory process. This method yielded a central delay of 0.95 ms in excess of that of the H reflex. The 1st phase of inhibition is evidently mediated via large group I afferents acting through a single inhibitory interneuron. Central inhibition of the flexor H reflex was demonstrated with the radial nerve anesthetized by injection of local anesthetic at the elbow. Subjects were asked to try to contract the paralysed extensor muscles. Under this condition, attempted voluntary wrist extension inhibited the flexor H reflex even though no movement occurred. A shock was delivered to the radial nerve at a site proximal to the anesthetic block. When the shock was applied in conjunction with an attempted voluntary contraction of the paralyzed extensor muscles, the depth of inhibition was greater than that predicted from the effect of either a shock or a willed contraction acting independently. The result was consistent with spatial facilitation from descending and peripheral sources acting at the level of a spinal interneuron. The depth of flexor H-reflex inhibition from a radial nerve shock was studied as a function of flexor torque in the intact subject. Over the range of torques used (0-1.5 N m) the depth of inhibition diminished as an approixmate linear function of flexor torque.