Group II muscle afferents probably contribute to the medium latency soleus stretch reflex during walking in humans

Abstract

1. The objective of this study was to determine which afferents contribute to the medium latency response of the soleus stretch reflex resulting from an unexpected perturbation during human walking. 2. Fourteen healthy subjects walked on a treadmill at approximately 3.5 km h(-1) with the left ankle attached to a portable stretching device. The soleus stretch reflex was elicited by applying small amplitude (approximately 8 deg) dorsiflexion perturbations 200 ms after heel contact. 3. Short and medium latency responses were observed with latencies of 55 +/- 5 and 78 +/- 6 ms, respectively. The short latency response was velocity sensitive (P < 0.001), while the medium latency response was not (P = 0.725). 4. Nerve cooling increased the delay of the medium latency component to a greater extent than that of the short latency component (P < 0.005). 5. Ischaemia strongly decreased the short latency component (P = 0.004), whereas the medium latency component was unchanged (P = 0.437). 6. Two hours after the ingestion of tizanidine, an alpha(2)-adrenergic receptor agonist known to selectively depress the transmission in the group II afferent pathway, the medium latency reflex was strongly depressed (P = 0.007), whereas the short latency component was unchanged (P = 0.653). 7. An ankle block with lidocaine hydrochloride was performed to suppress the cutaneous afferents of the foot and ankle. Neither the short (P = 0.453) nor medium (P = 0.310) latency reflexes were changed. 8. Our results support the hypothesis that, during walking the medium latency component of the stretch reflex resulting from an unexpected perturbation is contributed to by group II muscle afferents.

Figure 1. Determination of windows defining the short and medium latency muscle responses to a stretch in the soleus EMG

The beginning of the short latency response (SLR) window was placed coincidental with the onset of the stretch reflex response. Each window was 20 ms wide. The beginning of the medium latency response (MLR) window was placed 10 ms after the end of the short latency window. The reflex responses were defined by the area between the perturbed record (thick line) and control record (thin line). The time base in this figure is presented such that zero corresponds with the stretch onset.

Figure 2. Example of an averaged data record for one subject with the perturbed trials and control trials superimposed

A full step cycle for the left leg is shown. The perturbed (thick line) and control (thin line) records are shown superimposed. The time base is shifted so that zero corresponds with the stretch onset. A, ankle angular position with an offset such that 0 deg corresponds to the position at the time of stretch onset. B, soleus (SOL) EMG. C, tibialis anterior (TA) EMG.

Figure 3. Area increments from the muscle responses resulting from ankle stretches at various relative perturbation velocities for a single subject

A, area increment for a reflex response over a 50 ms window (▪). In this case the slope was 0.26 ± 0.08 and significantly different from zero (P = 0.008). B, comparison of the short (•) and medium (○) latency muscle responses. The slopes were 0.54 ± 0.06 (P < 0.001) and -0.04 ± 0.12 (P = 0.725), respectively.

Figure 4. Comparison of the slope of the stretch velocity-stretch reflex relationship for the short and medium latency responses

The slopes are shown for the short and medium latency reflex responses. Although both responses show positive velocity sensitivity, only the short latency response is statistically different from zero (P < 0.001).

Figure 5. The effect of nerve cooling, ischaemia, tizanidine and an ankle block on the short and medium latency muscle responses

The left side of each panel shows a soleus (SOL) EMG and ankle angular position recording from a single subject during perturbed steps. Control steps have been omitted for clarity. Averaged data across all subjects are shown on the right side of each panel. A, left side, data records before (thin line) and after (thick line) nerve cooling. The arrows shown above the soleus EMG highlight the latency differences before and after cooling. Right side, short (•) and medium (○) latency responses averaged across all subjects (n = 8). Both responses were delayed although the medium response is delayed to a greater extent than the short latency response (P < 0.005). B, during ischaemia the short latency response was reduced to the level of the background EMG determined just prior to the stretch (P < 0.001). The medium response decreased but the decrease was not significant (P = 0.437). Left side, data records before (thin line) and after (thick line) the ischaemic block. Right side, average across all subjects (n = 4) before (▪) and after (□) ischaemia. C, 2 h after the ingestion of tizanidine the medium latency response was significantly depressed (P = 0.007). The short latency response decreased, although the change was not statistically significant (P = 0.653). Left side, data records before (thin line) and after (thick line) tizanidine. Right side, average across all subjects (n = 3) before (▪) and after (□) the ingestion of tizanidine. D, after an ankle block with subcutaneously administered lidocaine, there were no significant changes in either the short (P = 0.453) or medium (P = 0.310) latency components of the stretch reflex. Left side, data records before (thin line) and after (thick line) the ankle block. Right side, average across all subjects (n = 3) before (▪) and after (□) the ankle block. The filled and open rectangles shown immediately below the soleus EMG records in panels B, C and D represent the 20 ms windows for the short and medium latency responses, respectively.