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Muscle coordination retraining inspired by musculoskeletal simulations reduces knee contact force.

ABSTRACT: Humans typically coordinate their muscles to meet movement objectives like minimizing energy expenditure. In the presence of pathology, new objectives gain importance, like reducing loading in an osteoarthritic joint, but people often do not change their muscle coordination patterns to meet these new objectives. Here we use musculoskeletal simulations to identify simple changes in coordination that can be taught using electromyographic biofeedback, achieving the therapeutic goal of reducing joint loading. Our simulations predicted that changing the relative activation of two redundant ankle plantarflexor muscles-the gastrocnemius and soleus-could reduce knee contact force during walking, but it was unclear whether humans could re-coordinate redundant muscles during a complex task like walking. Our experiments showed that after a single session of walking with biofeedback of summary measures of plantarflexor muscle activation, healthy individuals reduced the ratio of gastrocnemius-to-soleus muscle activation by 25 ± 15% (p = 0.004, paired t test, n = 10). Participants who walked with this "gastrocnemius avoidance" gait pattern reduced late-stance knee contact force by 12 ± 12% (p = 0.029, paired t test, n = 8). Simulation-informed coordination retraining could be a promising treatment for knee osteoarthritis and a powerful tool for optimizing coordination for a variety of rehabilitation and performance applications.

SUBMITTER: Uhlrich SD

PROVIDER: S-EPMC9262899 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Deficits in the ankle plantarflexor muscles, such as weakness and contracture, occur commonly in conditions such as cerebral palsy, stroke, muscular dystrophy, Charcot-Marie-Tooth disease, and sarcopenia. While these deficits likely contribute to observed gait pathologies, determining cause-effect relationships is difficult due to the often co-occurring biomechanical and neural deficits. To elucidate the effects of weakness and contracture, we systematically introduced isolated deficits into a musculoskeletal model and generated simulations of walking to predict gait adaptations due to these deficits. We trained a planar model containing 9 degrees of freedom and 18 musculotendon actuators to walk using a custom optimization framework through which we imposed simple objectives, such as minimizing cost of transport while avoiding falling and injury, and maintaining head stability. We first generated gaits at prescribed speeds between 0.50 m/s and 2.00 m/s that reproduced experimentally observed kinematic, kinetic, and metabolic trends for walking. We then generated a gait at self-selected walking speed; quantitative comparisons between our simulation and experimental data for joint angles, joint moments, and ground reaction forces showed root-mean-squared errors of less than 1.6 standard deviations and normalized cross-correlations above 0.8 except for knee joint moment trajectories. Finally, we applied mild, moderate, and severe levels of muscle weakness or contracture to either the soleus (SOL) or gastrocnemius (GAS) or both of these major plantarflexors (PF) and retrained the model to walk at a self-selected speed. The model was robust to all deficits, finding a stable gait in all cases. Severe PF weakness caused the model to adopt a slower, "heel-walking" gait. Severe contracture of only SOL or both PF yielded similar results: the model adopted a "toe-walking" gait with excessive hip and knee flexion during stance. These results highlight how plantarflexor weakness and contracture may contribute to observed gait patterns.

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Muscle coordination retraining inspired by musculoskeletal simulations reduces knee contact force.

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