Abstract
The control of normal motor behaviors involves sublime interactions between excitatory, inhibitory and neuromodulatory commands to motoneurons. The effects of altered inhibition on neuromodulatory commands has not received much attention in humans. Yet, motoneuron firing patterns can be readily measured from the muscle fibers they innervate, collectively known as motor units (MUs), due to their one‐to‐one spike ratio. Persistent inward currents (PICs) are reduced with activation of Ia fibers from the antagonist muscle in the decerebrate cat. Here, we set out to explore whether estimated PICs are affected by a tonic vibratory input to antagonist tendons in humans. MU firing patterns of the tibialis anterior (TA), soleus (SOL) and medial gastrocnemius (MG) were discriminated using high‐density surface electromyography array electrodes and a convolutive blind source separation algorithm. PICs were estimated using the paired MU analysis technique, which quantifies discharge rate hysteresis (ΔF) by comparing the onset and offset of a high‐threshold MU with respect to a low‐threshold MU, providing an estimate of neuromodulatory drive to the MU. Participants performed isometric plantarflexion and dorsiflexion triangular ramp contractions to 30% of maximal voluntary contraction with 10 s ascending and descending phases. In half of the trials, we applied vibration (128 Hz) to the distal TA tendon (plantarflexion) or Achilles tendon (dorsiflexion) with a constant force of 15 ± 2 N. There were large decreases in ΔF for both the SOL (31.3 ± 7.94%, p = 0.006, d = 0.81) and MG (31.4 ± 10.36%, p = 0.008, d = 0.9) during plantarflexion contractions with vibration applied to the distal TA tendon, and there was a moderate decrease in ΔF for the TA (10.9 ± 8.79%, p = 0.009, d = 0.63) during dorsiflexion with vibration to the Achilles tendon. These findings suggest that Ia reciprocal inhibition from the antagonist muscle can reduce the discharge rate hysteresis, providing insights about the interactions that occur to produce normal human motor behaviors.Support or Funding InformationThis work was supported by National Institute of Health (NIH) grants R01NS098509‐01 and T32HD007418‐23, and a Natural Sciences and Engineering Research Council of Canada (NSERC) Postdoctoral Fellowship.
Published Version
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