Abstract
1. Previous work has shown that the H reflex excitability of the human soleus motoneurones is reduced during fatigue and is accompanied by a corresponding decrease in electromyographic (EMG) activity during maximal voluntary contractions. These findings were consistent with the existence of a reflex whereby alpha-motoneurones are inhibited by sensory input from the fatigued muscle. 2. To elucidate the contribution of different-sized afferents in such reflex inhibition, compression of the sciatic nerve was used in an attempt to block large myelinated afferents prior to fatigue. 3. Fatigue of the soleus muscle was induced under ischaemic conditions by intermittent electrical stimulation at 15 Hz in ten healthy subjects. These subjects also participated in a control test in which the compression block was followed by ischaemia without fatigue. 4. Following nerve compression alone, both the mean maximal plantarflexion torque and the associated EMG for all ten subjects declined by 18.8 +/- 16.2% (S.D.) and 13.4 +/- 17.2%, respectively. 5. Following fatigue, there were five subjects in whom the large afferents remained blocked and the experimental findings were consistent with the existence of reflex inhibition during fatigue. The mean maximal plantarflexion torque decreased further by 36.2 +/- 7.6% from the value following the compression block compared to a decrease of 5.0 +/- 9.9% in the ischaemia control. The mean EMG associated with these contractions also decreased from post-block values by 56.8 +/- 19.6% following fatigue and by only 6.4 +/- 8.0% following ischaemia alone. 6. The peripheral excitability of the neuromuscular junction and muscle fibre membrane was adequate following fatigue as evidenced by only modest changes in the M wave (muscle compound action potential). The descending motor drive was deemed sufficient because of the absence of any large interpolated twitches superimposed upon the maximal voluntary contraction in all but two subjects. 7. The declines in maximal plantarflexion torque and the associated EMG activity were very similar to those found in a previous study in which the sensory input was unaltered. The findings demonstrated that any reflex inhibition of the alpha-motoneurone pool during fatigue was probably not mediated by large diameter afferents. Rather, it is suggested that the reflex is mediated by smaller diameter afferents originating from the fatigued muscle.