Evidence suggests that the nervous system controls motor tasks using a low-dimensional modular organization of muscle activation. However, it is not clear if such an organization applies to coordination of human walking, nor how nervous system injury may alter the organization of motor modules and their biomechanical outputs. We first tested the hypothesis that muscle activation patterns during walking are produced through the variable activation of a small set of motor modules. In 20 healthy control subjects, EMG signals from eight leg muscles were measured across a range of walking speeds. Four motor modules identified through nonnegative matrix factorization were sufficient to account for variability of muscle activation from step to step and across speeds. Next, consistent with the clinical notion of abnormal limb flexion-extension synergies post-stroke, we tested the hypothesis that subjects with post-stroke hemiparesis would have altered motor modules, leading to impaired walking performance. In post-stroke subjects (n = 55), a less complex coordination pattern was shown. Fewer modules were needed to account for muscle activation during walking at preferred speed compared with controls. Fewer modules resulted from merging of the modules observed in healthy controls, suggesting reduced independence of neural control signals. The number of modules was correlated to preferred walking speed, speed modulation, step length asymmetry, and propulsive asymmetry. Our results suggest a common modular organization of muscle coordination underlying walking in both healthy and post-stroke subjects. Identification of motor modules may lead to new insight into impaired locomotor coordination and the underlying neural systems.

Recent evidence suggests that performance of complex locomotor tasks such as walking may be accomplished using a simple underlying organization of co-active muscles, or “modules”, which have been assumed to be structured to perform task-specific biomechanical functions. However, no study has explicitly tested whether the modules would actually produce the biomechanical functions associated with them or even produce a well-coordinated movement. In this study, we generated muscle-actuated forward dynamics simulations of normal walking using muscle activation modules (identified using non-negative matrix factorization) as the muscle control inputs to identify the contributions of each module to the biomechanical sub-tasks of walking (i.e., body support, forward propulsion and leg swing). The simulation analysis showed a simple neural control strategy involving five muscle activation modules was sufficient to perform the basic sub-tasks of walking. Module 1 (gluteus medius, vasti and rectus femoris) primarily contributed to body support in early stance while Module 2 (soleus and gastrocnemius) contributed to both body support and propulsion in late stance. Module 3 (rectus femoris and tibialis anterior) acted to decelerate the leg in early and late swing while generating energy to the trunk throughout swing. Module 4 (hamstrings) acted to absorb leg energy (i.e., decelerate it) in late swing while increasing the leg energy in early stance. Post-hoc analysis revealed an additional module (Module 5: iliopsoas) acted to accelerate the leg forward in pre- and early swing. These results provide evidence that the identified modules can act as basic neural control elements that generate task-specific biomechanical functions to produce well-coordinated walking.

Automaticity is a hallmark feature of walking in adults who are healthy and well-functioning. In the context of walking, “automaticity” refers to the ability of the nervous system to successfully control typical steady state walking with minimal use of attention-demanding executive control resources. Converging lines of evidence indicate that walking deficits and disorders are characterized in part by a shift in the locomotor control strategy from healthy automaticity to compensatory executive control. This is potentially detrimental to walking performance, as an executive control strategy is not optimized for locomotor control. Furthermore, it places excessive demands on a limited pool of executive reserves. The result is compromised ability to perform basic and complex walking tasks and heightened risk for adverse mobility outcomes including falls. Strategies for rehabilitation of automaticity are not well defined, which is due to both a lack of systematic research into the causes of impaired automaticity and to a lack of robust neurophysiological assessments by which to gauge automaticity. These gaps in knowledge are concerning given the serious functional implications of compromised automaticity. Therefore, the objective of this article is to advance the science of automaticity of walking by consolidating evidence and identifying gaps in knowledge regarding: (a) functional significance of automaticity; (b) neurophysiology of automaticity; (c) measurement of automaticity; (d) mechanistic factors that compromise automaticity; and (e) strategies for rehabilitation of automaticity.