Fatigue-induced modulation of human soleus Hoffmann reflex in conditions of ipsilateral common peroneal nerve stimulation
Introduction. The effect of triceps muscle of calf (m.m. gastrocnemius-soleus) fatigue on the soleus muscle H (Hoffmann) reflex amplitude was investigated in conditions of ipsilateral common peroneal nerve (n.peroneus communis) stimulation in group of healthy people, 18-34 years of age. It is known that after fatiguing contraction the soleus H-reflex is inhibited, probably due to the activation of the groups III and IV afferent nerves under the influence of mechanical and metabolic changes in the muscle. Different authors described H-reflex depression which was caused by conditioning peroneal nerve stimulation at rest, changes of visual control and upper limb movement. We supposed that investigation of presynaptic inhibition, connected with conditioning peroneal nerve stimulation at rest and after fatiguing contraction, might help to understand mechanisms of muscle movement regulation.
Purpose. The purpose of our work was to investigate in detail the influence of conditioning stimulation of ipsilateral common peroneal nerve (n.peroneus communis) on human soleus H-reflex amplitude at rest and after long-lasting voluntary contraction of m.m. gastrocnemius-soleus, which caused the fatigue of soleus muscle.
Methods. Fatigue was caused by voluntary tonic static contraction (6-9 min long) of triceps muscle of calf with a force egual to 75% of the maximal voluntary contraction. During the test, the person was sitting and pressing on fixed pedal with the foot, trying to realize sole flexion. The H-reflex was elicited by transcutaneous stimulation of tibial nerve (n. tibialis) and recorded from the soleus muscle (m. soleus). Testing impulses (by stimulation of n. tibialis) and conditioning impulses (by stimulation of n.peroneus and then n. tibialis) were used in turn. Registration of electromyographic signals, tibial and peroneal nerve stimulation were performed using neurodiagnostic complex (Nicolet Viking Select, USA-Germany).
Results. It was found that in the group of healthy people an amplitude of conditioned soleus H-reflex at rest egualed of about 75% of test H-reflex value. It means that stimulation of peroneal nerve before tibial nerve stimulation caused soleus H-reflex inhibition of about 25%. After voluntary static contraction an amplitude of test soleus H-reflex was significantly reduced, egualing immediately after fatigue period of about 64% of initial value. The amplitude of conditioned H-reflex was also reduced and egualed of about 50% of the initial value of test H-reflex. Then H-reflex amplitude subsequently recovered. In 2-3 minutes test H-reflex amplitude attained approximately 83%, while conditioned H-reflex amplitude attained 70% of the initial value of test H-reflex. This was followed by the period of slow recovery of the two types of reflexes, to 99% and 72% (test H-reflex and conditioned H-reflex, respectively) of test H-reflex initial value in 30 minutes after the fatigue period.
Originality. In this paper for the first time features of human soleus H-reflex inhibition and recovering after long-lasting fatiguing voluntary contraction in conditions of ipsilateral common peroneal nerve stimulation were investigated.
Conclusion. It was found that after fatiguing contraction amplitude changes of test soleus H-reflex were similar to changes of H-reflex, conditioning by stimulation of ipsilateral common peroneal nerve. Decreasing of the conditioned H-reflex amplitude just after standard fatiguing contraction was proportional to reduction of the test H-reflex. It was found that two types of presynaptic inhibition, namely connected with conditioning peroneal nerve stimulation and fatiguing contraction, proceed mainly through different nervous pathways, although partial convergence of inhibition influences is possible. Individual temporal pattern of conditioned soleus H-reflex recovery after fatiguing voluntary contraction might be the evidence of complex phenomena proceeding in the muscle, spinal cord segment and suprasegmental structures during fatigue and after the fatigue period.
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