Excitability of reciprocal and recurrent inhibitory pathways after voluntary muscle relaxation in man

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Abstract
We studied the potential contribution of postsynaptic mechanisms to the depression of reflex excitability which occurs immediately after a voluntary release from tonic muscle contraction. The excitability of the Soleus (Sol) motor pool was tested at rest and after voluntary muscle relaxation. In both cases the Sol H-reflex was conditioned by 1. a single shock to the peroneal nerve, in order to activate the Ia interneurones (INs) mediating the reciprocal inhibition via a peripheral input, or by 2. a short-lasting voluntary contraction of the Tibialis Anterior (TA) muscle, to activate the Ia INs via a central command. Changes in excitability of Renshaw cells were also tested at rest and after release, to assess the role of recurrent inhibition in the release-induced inhibition of the Sol H-reflex. It was demonstrated that: 1. the excitability of the INs mediating the reciprocal inhibition was only slightly enhanced in comparison with resting conditions; 2. the H-reflex of the antagonist muscle (TA) evoked after Sol release was not consistently facilitated with respect to rest; 3. the command to contract the TA muscle reduced the H-reflex of the Sol muscle during rest but not after Sol release; 4. recurrent inhibition did not increase its effect in the post-release period. Such features suggest that recurrent and reciprocal post-synaptic inhibitions do not play a major role in reducing the reflex excitability of a relaxing muscle; rather, the command to release prevents the reciprocal inhibitory effect which accompanies the contraction of the antagonist muscle. The findings support the concept that release-induced reflex depression is mediated mainly by presynaptic inhibition of autogenetic spindle afferences (Schieppati and Crenna 1984).