Changes in gait asymmetry may be caused by adaptation of spinal reflexes

In a recent human study, we found that adaptive changes in step length asymmetry (SLA) are correlated with similar changes in the H-reflex gains of the leg muscles during split-belt treadmill locomotion. Although this observation indicated a closer link between gait asymmetry and spinal reflex adaptation, it did not reveal their causal relationship. To better understand this relationship, here we use a neuromuscular model of human walking whose control relies primarily on spinal reflexes. Subjecting the model to split-belt treadmill locomotion with different combinations of belt speed and reflex gain patterns, we find that belt speed changes increase the variability in SLA but do not result in consistent SLA patterns as observed in human experiments, whereas reflex gain changes do. Furthermore, we find that the model produces SLA patterns similar to healthy adults when its reflex gains are adapted in a way similar to the H-reflex changes we observed in our previous study. The model also predicts SLA patterns similar to the ones observed for cerebellar degeneration patients when the reflexes do not adapt beyond a sudden dip at the time the ipsilateral belt speed is lowered. Our results suggest that SLA does not arise from imposing belt speed changes but requires the change of the reflex gains and that the dynamic adjustment of these gains may be an essential part of human gait control when encountering unexpected environmental changes such as uneven speed changes in split-belt treadmill locomotion.<b>NEW & NOTEWORTHY</b> This work uses computational modeling to investigate the role of spinal reflex tuning during locomotor adaptation. We show, in simulation, that tuning spinal reflex gains leads to gait asymmetry adaptation, not vice versa, and that patterns of gait adaptation on a split-belt treadmill are mostly driven by tuning of spinal reflexes, and not by biomechanical disturbances triggered by belt changes. The model further hints at the cerebellum as the source of spinal reflex modulation.