Abstract
1. The recurrent inhibition, brought about by a conditioning H-reflex discharge, was estimated in human subjects by the amplitude of a test H-reflex involving only the soleus motoneurones which fired in response to the conditioning volley. The modifications of the recurrent inhibition during contraction were evaluated by comparing the amplitude of the test H-reflex to a reference H-reflex. Both reflexes experienced the excitation underlying the voluntary contraction, but only the test H-reflex was subjected to the recurrent inhibition evoked by the conditioning H-reflex discharge. 2. Distinct differences were observed between the modifications of the test reflex and those of the reference H-reflex during both tonic and phasic voluntary contractions. Evidence is presented that these differences were due to changes in the amount of recurrent inhibition elicited by the conditioning discharge. 3. The changes in recurrent inhibition were studied while the subjects performed voluntary tonic contractions of various forces. The weakest contractions were accompanied by a decrease in the size of the test reflex. With greater contraction forces, there was no longer an inhibition of the test reflex, but instead a facilitation which grew continuously with increased contraction forces. The test reflex could eventually exceed the reference H-reflex amplitude at the strongest contractions. This is taken to indicate that the recurrent inhibition following the conditioning discharge was progressively decreasing, as the contraction force increased. 4. During ramp contractions, whatever the contraction velocity, the time courses of the variations of the test and reference H reflexes were almost inverse. Evidence is presented that these differential time courses were due to changes in the amount of recurrent inhibition elicited by the conditioning discharge. 5. The possibility of occlusion in the recurrent pathway ;as considered and it was concluded that the decrease in the recurrent inhibition elicited by the conditioning discharge was essentially due to an inhibitory control (spinal and/or suprasegmental) acting on Renshaw cells. This inhibition of Renshaw cells eventually counteracts the increasing excitatory inputs (resulting from the voluntary motor discharge) which they receive via motor axon collaterals during increasing tonic contractions and throughout ramp contractions. 6. The functional significance of the Renshaw cell inhibition during voluntary contraction is discussed in relation to the inhibition exerted through the recurrent pathway on both motoneurones and Ia inhibitory interneurones. It is suggested that the depression of Renshaw cell activity could play an important role during voluntary movements by favouring reciprocal Ia inhibition.