Cortical Adaptation to Muscle Fatigue Does Not Alter Early Proprioceptive Processing in Primary Sensorimotor Cortex
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Updated: Nov 4, 2026

Intracortical Inhibition Within the Primary Motor Cortex Can Be Modulated by Changing the Focus of Attention
Published on: September 11, 2017
Junru Chen1,2, Toni Mujunen3, Feiyue Li1,2
1Faculty of Sport and Health Sciences, University of Jyväskylä, Jyväskylä, Finland.
Abstract:
Muscle fatigue potentially interferes with proprioceptive afference from peripheral "movement sensors"-the proprioceptors, which may hinder crucial sensorimotor integration and thus movement performance. However, little is known about how muscle fatigue affects cortical processing of proprioceptive afference. Twenty-four healthy volunteers (30.7 ± 6.5 years) participated in the experiment, which included magnetoencephalography (MEG) recordings during 2-Hz passive ankle-joint rotations, and fatigue tasks comprised of isometric ankle plantarflexion. Corticokinematic coherence (CKC) between linear foot acceleration and MEG signals was examined before (PRE) and ~3 min after (POST) the fatigue tasks to compare the cortical proprioceptive processing. CKC peaked in the gradiometer pairs above the foot region of the primary sensorimotor (SM1) cortex in each participant. CKC strength did not show significant difference between PRE and POST at 2 Hz (0.30 ± 0.12 vs. 0.30 ± 0.14, p = 0.981) or its first harmonic at 4 Hz (0.38 ± 0.14 vs. 0.37 ± 0.13, p = 0.724). However, 4-Hz MEG power was ~30% lower in POST than in PRE. Surprisingly, fatigue-induced increase of alpha and beta power was observed bilaterally in SM1 hand regions during the ankle movements. Our results indicate that the early processing of proprioceptive afference from the ankle joint was negligibly affected by muscle fatigue or the effect recovered rapidly. The fatigue elevated alpha and beta power while diminishing neuronal activity at the 4-Hz harmonic frequency, which may reflect a compensatory mechanism for asynchronous proprioceptive afference by enhancing cortical inhibitory control.
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