The Journal of Neurophysiology Vol. 83 No. 5 May 2000, pp. 2881-2890
Copyright ©2000 by the American Physiological Society

On the Origin of the Soleus H-Reflex Modulation Pattern During Human Walking and Its Task-Dependent Differences

Department of Anatomy and Physiology, Centre de Recherche Université Laval-Robert Giffard, Quebec G1J 2G3, Canada

Schneider, Cyril, Brigitte A. Lavoie, and Charles Capaday. On the Origin of the Soleus H-Reflex Modulation Pattern During Human Walking and Its Task-Dependent Differences. J. Neurophysiol. 83: 2881-2890, 2000. Recently, Brooke and colleagues have suggested "that the strong inhibition arising from passive movement about the knee and hip joints, lays down the base for the soleus H-reflex gain modulation seen during human gait." In particular stretch-evoked afferent activity from the quadriceps muscle was emphasized as the most important source of movement-induced inhibition of the H-reflex. To test this hypothesis we examined the kinematics and electromyographic (EMG) activity of the leg during human walking and correlated these with the modulation pattern of the soleus H-reflex. To further test the possible contribution of stretch-evoked quadriceps afferent activity to the soleus H-reflex modulation pattern during walking different walking gaits were studied. In one condition subjects were asked to walk with their knee locked in full extension by a rigid knee brace. In a second condition subjects were asked to walk backwards. During normal walking, the soleus H-reflex modulation pattern is strongly correlated with the EMG events of the soleus and tibialis anterior (TA), but not with hip, knee, or ankle angular displacement or velocity. When subjects walked with the knee locked in full extension, the amplitude of the H-reflex, its modulation pattern, and the task-dependent changes of its amplitude were the same as during normal walking. During backward walking, the H-reflex increases in late swing before activity of the soleus has begun and while the knee is flexing, an observation that highlights central control of the H-reflex amplitude. The effects of imposed flexion of the knee in passive subjects were also reexamined. The knee flexion imposed by the experimenter followed the same trajectory as that which occurred during the swing phase of the subject's step cycle. It was found that imposed knee flexions elicited a burst of TA EMG activity with an average latency of 81.6 ms (SD = 21 ms) in six out of eight subjects. Inhibition of the H-reflex, when it occurred, was associated with the occurrence of this burst. When subjects voluntarily flexed their right knee from an initial quiet standing posture, the inhibition of the soleus H-reflex began before flexion of the knee or that of any other leg segment. Once again the onset of inhibition was closely associated with the onset of activity in the TA. In the discussion section the present observations are examined in light of the predictions made by the movement-induced inhibition hypothesis of Brooke et al. It will be concluded that none of the predictions of this hypothesis were corroborated by present tests done during human walking. In consequence, we suggest that the modulation pattern of the H-reflex observed during normal human walking is centrally determined, as are the task-dependent differences of its amplitude (e.g., standing versus the stance phase of human walking).