Fig 1.
Neural pathways likely involved in the generation of the SLCR.
SLCRs are elicited in the contralateral gastrocnemius medialis (cGM) and lateralis (cGL) following stimulation of the tibial nerve (iTN) in the ipsilateral leg during human walking. The current study was designed to investigate whether the activity of contralateral afferents (dashed gray lines) contributes to the SLCR. The gray and black full lines represent the ipsilateral afferent pathways and contralateral efferent pathways involved in the generation of the SLCR, respectively. Supraspinal contribution to the SLCR is not excluded (dashed black line). All other dashed lines in the spinal cord represent unknown pathways.
Fig 2.
Overview of the experiment and the analysis performed.
The aim of experiment 1 was to estimate muscle afferent output for the two heads of the contralateral gastrocnemius. In experiment 1a, kinematic and kinetic data was collected from 8 subjects during normal and hybrid walking. In experiment 1b, muscle activation during normal and hybrid walking was recorded from the triceps surae of 6 subjects to evaluate muscle relative activation. Data from Experiments 1a and 1b was combined to estimate, using an inverse dynamics model modified from [17], muscle fascicles length changes and muscle force for the two heads of the gastrocnemius. A mathematical model modified from [18,19] was then used to estimate group Ia, Ib and II afferent outputs. The estimated contralateral afferent activity was compared between these normal (80% gait cycle) and hybrid walking (50% gait cycle) conditions to assess whether a different afferent activity is accountable for the reversal in the response. In experiment 2, the modulation of the SLCR was quantified in 12 subjects during normal walking. The modulation of the response was then compared with the estimated activity of the different afferents to evaluate whether contralateral afferent activity contributes to the generation of the SLCR.
Fig 3.
A: The subjects walked on a split belt treadmill. The vertical component of the GRF was recorded through 8 force transducers placed at the corners under each belt. Subjects wore a safety harness that did not alter the subjects’ body weight support. Retroreflective ball-shaped markers were placed on the skin of the subject’s over the ipsilateral calcaneus (iCalc) and on contralateral leg over the following anatomical landmarks: fifth metatarsal joint (c5met), on the lateral malleolus (cMall), on the lateral epicondyle of the femur (cCond), on the great trochanter (cTroc) and on the sacral bone (sacr). B: Crossed responses in cGM were investigated after iTN stimulation. Bilateral SOL and cGL sEMG signal were also collected in order to evaluate the correct stimulation location and intensity (iSOL) and the relative activation of triceps surae muscles for the estimation of the force produced by the individual muscles (cSOL, cGM and cGL).
Fig 4.
Kinetic and kinematic data used to calculate the net ankle moment during normal walking.
All data represent an average gait cycle for one subject. A. Ankle joint (black) and knee joint (gray) kinematics. B. Vertical component of the GRF for the contralateral foot. C. Estimated net ankle moment for the contralateral leg.
Fig 5.
Differences in estimated afferent activity between normal and hybrid walking.
Estimated ensemble activity for group Ia (A), Ib (B) and II (C) cGL’s afferent fibers at 80% of the normal walking ipsilateral gait cycle (left) and at 50% of the hybrid walking ipsilateral gait cycle (right). The data, collected from 8 subjects, are displayed as mean ± SD. * indicates significant differences.
Fig 6.
Modulation of estimated afferent feedback activity and SLCR in cGM during walking.
Estimated muscle fascicles length changes (A) muscle force (B), and ensemble group Ia (C), Ib (D) and II (E) afferent activity estimated for cGM (data form 8 subjects) are shown to allow a comparison with the modulation of the short-latency crossed responses in cGM (F, data from 12 subjects) during a normal ipsilateral walking gait cycle. The full gray line and the dashed lines in A represent respectively the average and the standard deviation of the estimated values across all subjects. The state of stretch of the muscle are indicated by the gray areas. The thick black line and gray dashed lines in B, C, D and E represent respectively the mean estimated value of cGM muscle force (B) and ensemble afferent activity across all subjects (C, D, E). In F, the magnitude of the response elicited at different timings during the walking cycle is expressed (mean and SD) as a percentage of the control (no stimulation). Positive values indicate a facilitation and negative values indicate an inhibition of the muscle activation.
Fig 7.
Modulation of cGL estimated afferent feedback activity and SLCR in cGM during walking.
Estimated muscle fascicles length changes (A) muscle force (B), and ensemble group Ia (C), Ib (D) and II (E) afferent activity estimated for cGL (data form 8 subjects) are shown to allow a comparison with the modulation of the short-latency crossed responses in cGM (F, data from 12 subjects) during a normal ipsilateral walking gait cycle. The full gray line and the dashed lines in A represent respectively the average and the standard deviation of the estimated values across all subjects. The state of stretch of the muscle is indicated by the gray areas. The thick black line and gray dashed lines in B, C, D and E represent respectively the mean estimated value of cGM muscle force (B) and ensemble afferent activity across all subjects (C, D, E). In F, the magnitude of the response elicited at different timings during the walking cycle is expressed (mean and SD) as a percentage of the control (no stimulation). Positive values indicate a facilitation and negative values indicate an inhibition of the muscle activation.
Fig 8.
Correlations between the estimated ensemble afferent activity of cGM and cGL and the magnitude of the crossed responses elicited in cGM during the state of stretch of the muscle.
No significant correlation was found between the magnitude of the cGM responses and group Ia afferent output of the same muscle (A) (P = 0.78, r = 0.14) and of cGL (B) (P = 0.71, r = -0.18). Similarly, no significant correlation (in both cases P = 0.11, r = 0.70) was observed between the magnitude of the responses and the ensemble group Ib activity of cGM (C) or of cGL (D). A significant correlation was instead observed between the magnitude of the cGM responses and ensemble group II afferent activity of cGM (E) and of cGL (F) (in both cases P = 0.03, r = 0.82).