The effects of muscle coactivation patterns on gait, muscle strength and symptoms in different stages of knee osteoarthritis

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Abstract

Objective This study aimed to investigate the neuromuscular adaptive mechanisms across different stages of knee osteoarthritis (KOA) by comprehensively evaluating the relationships between symptoms, muscle activation patterns, muscle strength, and gait parameters. Methods In this cross-sectional study, 197 unilateral KOA patients (Kellgren-Lawrence grades I-IV; 55.2% females) and 32 healthy controls underwent synchronized gait analysis, isokinetic strength testing, surface electromyography (sEMG), and knee joint symptoms (WOMAC scores). Spatiotemporal, kinematic, kinetic parameters, muscle strength, and muscle activation cocontraction ratios were measured and compared. Group comparisons were conducted using one-way ANOVA or Kruskal-Wallis tests, with post-hoc analyses (Tukey's post-hoc or Bonferroni correction). Spearman correlation and multiple linear regression models​were employed to examine relationships between muscle activation, biomechanical parameters, and WOMAC scores. Results Compared to controls, KOA patients exhibited progressively deteriorating gait patterns and strength performance with increasing disease severity (p < 0.05). A distinct compensatory neuromuscular strategy, characterized by excessive coactivation of the hamstrings, particularly the lateral hamstring, and vastus lateralis, was identified (p = 0.002–0.048). This adaptive pattern was strongly associated with reduced knee flexion moment (KFM), elevated knee adduction moment (KAM) impulse, and increased joint loading (p = 0.004–0.038). Notably, these changes were evident from early stages (K-L II) and intensified significantly in advanced KOA (K-L ≥ III), correlating with higher WOMAC pain, stiffness and functional scores (p = < 0.001–0.046). Significant asymmetry was observed between the affected and contralateral limbs (ASI = 1.72–13.84; LSI = 56.3–92.7%). Conclusion The progression of KOA is characterized by a maladaptive neuromuscular compensatory strategy. While aiming to stabilize the joint, this strategy ultimately leads to biomechanical inefficiency, exacerbating symptoms and functional decline. Targeting these abnormal activation patterns through neuromodulatory rehabilitation could be a promising strategy for mitigating disease progression.

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