Exploring Neuromuscular Fatigue in Stroke Survivors: Understanding Central-Peripheral Interaction

Stroke is a leading cause of long-term disability worldwide. Although many stroke survivors can initiate movement, sustaining motor performance during everyday activities often becomes progressively difficult, suggesting abnormal development of neuromuscular fatigue. Neuromuscular fatigue, defined as an exercise-induced reduction in force-generating capacity, arises through interactions between central neural and peripheral muscular mechanisms. However, despite extensive investigation in healthy populations, the neurophysiological mechanisms underlying neuromuscular fatigue after stroke remain poorly understood. Existing studies have focused predominantly on peripheral manifestations of fatigue, with limited investigation of cortical oscillatory dynamics and brain-muscle communication. Here, we propose a multimodal neurophysiological study combining electroencephalography (EEG), electromyography (EMG), and corticomuscular coherence analyses to determine whether fatigability after stroke is driven predominantly by altered central neural processes rather than peripheral muscle failure. Stroke survivors and age-matched healthy controls will perform sustained isometric contractions while neural and muscular activity are recorded across progressive fatigue stages. We hypothesize that stroke survivors will exhibit earlier and greater fatigability, accompanied by altered cortical oscillatory activity, peripheral muscular changes, and disrupted corticomuscular coherence, consistent with a predominant contribution of central oscillatory dysfunction.