Effects of a complex balance task on soleus H-reflex and presynaptic inhibition in humans

Spinal modulation of motoneuron excitability has been extensively investigated during various tasks in humans. Previous studies have revealed that balance tasks induce a decrease in Ia-motoneuron communication which has been attributed to increased levels of presynaptic inhibition (PI). Moreover, this depression in Ia-motoneuron connectivity takes place subsequent to the elevation of muscle activity. Therefore, it is hypothesized that motor learning has inhibitory effects on the spinal mechanisms in spite of the increased muscle activity during a motor task. The purpose of this study was to explore the effects of a complex balance task on the H-reflex. Soleus H-reflexes were measured from 11 healthy adult subjects both before and after 20 minutes of a complex balance task. A commonly reported H-reflex conditioning technique was applied in order to measure changes in spinal PI: an electrical volley to the heteronymous Ia (common peroneal nerve conditioning, CPN). Subjects stood on a custom designed balance board and performed a continuous series of plantar and dorsiflexion. To ensure that the task was performed similarly between subjects, auditory cues for movement were given by a metronome with a frequency of 1 Hz. The initial amplitude of the unconditioned soleus H-reflex was set at 50% of H-max, and unconditioned and conditioned (PI) reflexes were recorded before, during, and after the balance task. The unconditioned soleus H-reflex was significantly decreased 59% after the balance task and PI was increased by 50%. Further, during a period of rest following the task (20 minutes) the unconditioned H-reflex returned to near baseline levels whereas the PI conditioned H-reflex was not altered The results suggest that the initial depression in motoneuron excitability immediately after the balance task is accompanied by an increase in PI, but also that the recovery of the depressed H-reflex after the task appears to be independent of PI.