Rhythmic arm cycling differentially modulates stretch and H-reflex amplitudes in soleus muscle

During rhythmic arm cycling, soleus H-reflex amplitudes are reduced by modulation of group Ia presynaptic inhibition. This suppression of reflex amplitude is graded to the frequency of arm cycling with a threshold of 0.8 Hz. Despite the data on modulation of the soleus H-reflex amplitude induced by rhythmic arm cycling, comparatively little is known about the modulation of stretch reflexes due to remote limb movement. Therefore, the present study was intended to explore the effect of arm cycling on stretch and H-reflex amplitudes in the soleus muscle. In so doing, additional information on the mechanism of action during rhythmic arm cycling would be revealed. Although both reflexes share the same afferent pathway, we hypothesized that stretch reflex amplitudes would be less suppressed by arm cycling because they are less inhibited by presynaptic inhibition. Failure to reject this hypothesis would add additional strength to the argument that Ia presynaptic inhibition is the mechanism modulating soleus H-reflex amplitude during rhythmic arm cycling. Participants were seated in a customized chair with feet strapped to footplates. Three motor tasks were performed: static control trials and arm cycling at 1 and 2 Hz. Soleus H-reflexes were evoked using single 1 ms pulses of electrical stimulation delivered to the tibial nerve at the popliteal fossa. A constant M-wave and ~6% MVC activation of soleus were maintained across conditions. Stretch reflexes were evoked using a single sinusoidal pulse at 100 Hz given by a vibratory shaker placed over the triceps surae tendon and controlled by a custom-written LabView program. Results demonstrated that rhythmic arm cycling that was effective for conditioning soleus H-reflexes did not show a suppressive effect on the amplitude of the soleus stretch reflex. We suggest this indicates that stretch reflexes are less sensitive to conditioning by rhythmic arm movement, as compared to H-reflexes, due to the relative insensitivity to Ia presynaptic inhibition.