Abstract

Spinal plasticity has been known to occur during various motor tasks. In humans, the effect of down-training on the soleus H-reflex by balance training has been demonstrated. It has been suggested that extrinsic presynaptic inhibition (EPI) is one of the most plausible factors causing this depression in motoneuron excitability during a balance task. However, no study to date has investigated the effect of balance task training upon EPI to the soleus Ia afferents. PURPOSE To determine whether the depression in the soleus H-reflex during a balance task could be attributed to extrinsic presynaptic inhibition. METHOD Soleus H-reflex amplitudes were measured from 5 healthy adult subjects. Two commonly reported H-reflex conditioning techniques were applied in order to measure changes in spinal motoneuron excitability: 1) common peroneal nerve stimulation (EPI) and 2) paired tibial nerve stimulation (paired reflex depression, PRD). A custom balance board was used to perform the balance task. Subjects stood on the balance board and performed planter and dorsiflexion. Auditory cues for movement were given by a metronome with a frequency of 1 Hz. Stimulating electrodes were placed in the popliteal fossa for tibial nerve stimulation and just distal to the fibular head for common peroneal nerve stimulation. Stimulation was delivered at the initiation of the planter flexion movement. The initial amplitude of the soleus H-reflex was set at 50% of H-max, as a control value. Reflexes were elicited in 36 blocks, with 10 reflex measurements in each block for both PRD and EPI (approximately 720 trials per subject). Measurements were analyzed from 5 blocks: prior to, beginning, middle, end of training, and post balance training (C1, T1, T2, T3, and C2, respectively). The dependent measure was the peak-to-peak amplitude of the soleus H-reflex (unconditioned) and the conditioned H-reflex (PRD and EPI). Oneway ANOVA with repeated measures was applied for statistical analysis. RESULT Comparing pre- with post-training, unconditioned H amplitude significantly decreased by 48% (C1 vs C2, p <.05). EPI conditioned H amplitude was also significantly depressed by 51%. During training, unconditioned H and EPI conditioned H amplitude significantly declined by 26% and 48% (T1 vs T3). PRD conditioning, however, demonstrated no significant difference. CONCLUSION The effect of down-training on spinal plasticity was observed from the depression in the soleus H-reflex. This depression was accompanied by a decline of EPI conditioned H amplitude, suggesting that the observed depression in the unconditioned soleus H-reflex was due to extrinsic presynaptic mechanisms.

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