Differential modulation of reciprocal inhibition in ankle muscles during rhythmic arm cycling.

Interlimb neural linkages relay activity related to rhythmic arm movement to the lumbar spinal cord. This is detected by modulated reflex amplitudes in muscles remote from the rhythmic movement. Improved understanding of modulation in ankle flexor and extensor muscles due to rhythmic arm movement can be gained using modulation of spinal excitability as a probe. The modulatory effect of rhythmic arm movement on Ia reciprocal inhibition (RI) between functional antagonists at the ankle has not been studied. We investigated the influence of rhythmic arm cycling on short latency (∼55ms post-stimulus) RI between ankle flexor (tibialis anterior, TA) and extensor (soleus, SOL) muscles at varying (0.9, 1.0, 1.2, 1.5 and 2.0× motor threshold (MT)) stimulus intensities. We hypothesized that arm cycling would increase RI between antagonists, but that movement conditioning would vary depending on stimulus intensity used to evoke the RI response. Amplitude of RI deduced from suppression of ongoing EMG activity was compared in static and arm cycling conditions. Arm cycling significantly (p<0.05) increased RI in SOL at 1.0×MT, but had no effect in TA at any stimulus intensity (p>0.05). Descending signals arising from rhythmic arm movement significantly alter transmission in RI pathways between ankle flexor and extensor muscles differentially. This may be due to differences in descending supraspinal inputs to ankle flexors vs. extensors, and could be related to functional requirements during locomotion.