Mechanisms within the human spinal cord suppress fast reflexes to control the movement of the legs.

Passive locomotor-like movement induces depression of the gain of a fast conducting spinal sensorimotor path in humans. It was hypothesized that this gain control is mediated through a spinal circuit. In the first experiment, passive pedalling motion was rapidly initiated in eight able bodied subjects. Soleus H-reflexes (used to reveal the gain of the short latency stretch reflex) were recorded over the first 250 ms after the movement started. Significant depression in H-reflex magnitude was observed by 50 ms after the onset of movement. On the basis of the timing, this gain attenuation was likely mediated through a spinal circuit. In a second experiment we tested chronic quadriplegics with clinically complete lesions of the spinal cord. Of five subjects tested, three expressed the reflex and all three showed significant inhibition with passive pedalling movement (mean depression was to 39% of controls). Both the rapid onset of the gain change (Expt. 1) and the presence of movement-induced inhibition in individuals with spinal lesions (Expt. 2) provide evidence that this component of human locomotor control is located in the spinal cord. The initiating source is probably somatosensory receptor discharge due to the movement.