Major role for sensory feedback in soleus EMG activity in the stance phase of walking in man

Abstract

1. Sensory feedback plays a major role in the regulation of the spinal neural locomotor circuitry in cats. The present study investigated whether sensory feedback also plays an important role during walking in 20 healthy human subjects, by arresting or unloading the ankle extensors 6 deg for 210 ms in the stance phase of gait. 2. During the stance phase of walking, unloading of the ankle extensors significantly (P < 0.05) reduced the soleus activity by 50 % in early and mid-stance at an average onset latency of 64 ms. 3. The onset and amplitude of the decrease in soleus activity produced by the unloading were unchanged when the common peroneal nerve, which innervates the ankle dorsiflexors, was reversibly blocked by local injection of lidocaine (n = 3). This demonstrated that the effect could not be caused by a peripherally mediated reciprocal inhibition from afferents in the antagonist nerves. 4. The onset and amplitude of the decrease in soleus activity produced by the unloading were also unchanged when ischaemia was induced in the leg by inflating a cuff placed around the thigh. At the same time, the group Ia-mediated short latency stretch reflex was completely abolished. This demonstrated that group Ia afferents were probably not responsible for the decrease of soleus activity produced by the unloading. 5. The findings demonstrate that afferent feedback from ankle extensors is of significant importance for the activation of these muscles in the stance phase of human walking. Group II and/or group Ib afferents are suggested to constitute an important part of this sensory feedback.

Figure 1. Example of averaged recorded data during control steps and steps with unloading or a hold input to the ankle extensors in the stance phase

Control steps, thick lines; steps with an unloading, thin lines, left; steps during a hold input, thin lines, right. A, ankle angle positions. B, rectified and filtered soleus muscle EMG. The black, white and shaded areas represent the different time windows used to characterise the response. C, rectified and filtered tibialis anterior muscle EMG. 0 deg, standing position. Positive values represent plantar movement directions.

Figure 3. Example of unloading responses in the early stance phase of walking before (left) and after (right) reversible lidocaine block of the common peroneal nerve (CPN)

Thick lines are control steps and thin lines are perturbed steps. A, ankle angle positions. B, rectified and filtered soleus muscle EMG. C, rectified and filtered tibialis anterior muscle EMG. After CPN block, no TA EMG activity was present except crosstalk from other non-blocked muscles. Positive values represent plantar flexion movement direction. One subject.

Figure 2. The effect of unloading (left) and holding (right) the ankle extensor movement 100, 200, 300, 400 and 500 ms into the stance phase of walking

A, percentage decreases in soleus EMG 50 ms (▪), 200 ms (□) and 150 ms (×) from onset of the EMG response. B, onset latency of the unloading (left) and hold (right) responses. C, velocity of the ankle joint during the control steps. The decrease in background soleus EMG following unloading or a hold of the ankle extensors was calculated as the difference between the soleus EMG during the control steps and the perturbed steps, expressed as a percentage of the soleus EMG during the control steps. Responses are means ± 1 s.d.

Figure 4. Stretch and unloading responses before and after applying ischaemia to the thigh of the investigated leg

A shows the amplitude (left) and onset latency (right) of the short latency stretch reflex in a sitting subject. Time 0 is the onset of the ischaemia. B-E, examples of the ankle position (B and D) and soleus EMG (C and E) before (right) and during ischaemia (left) in two walking subjects. Thick lines are control steps and thin lines are perturbed steps.

Figure 5. The effect of ischaemia on the unloading responses during walking

The upper panel shows the change in soleus EMG over a 50 ms time window, and the lower panel illustrates the onset latency in response to unloading before (control) and during ischaemia. The unloading effect is calculated as in Fig. 2. Responses are means ± 1 s.d. from nine subjects.