Fatigue induces altered spatial myoelectric activation patterns in the medial gastrocnemius during locomotion
Author(s) -
Bryan R. Schlink,
Andrew D. Nordin,
Christi. Brooks,
Daniel P. Ferris
Publication year - 2021
Publication title -
journal of neurophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.302
H-Index - 245
eISSN - 1522-1598
pISSN - 0022-3077
DOI - 10.1152/jn.00602.2020
Subject(s) - physical medicine and rehabilitation , gastrocnemius muscle , electromyography , muscle fatigue , neuroscience , leg muscle , medicine , anatomy , psychology , skeletal muscle
Sustained voluntary muscle contractions can lead to fatigue, which diminishes the muscle's ability to absorb energy and produce force at a desired level. Prolonged fatigue can lead to a decline in human performance and increase the muscle's susceptibility to injury. In this study, we investigated how localized muscle fatigue affected spatial EMG patterns during locomotion. We recorded high-density electromyography (EMG) from the medial gastrocnemius of 11 healthy subjects while they walked (1.2 m/s) and ran (3.0 m/s) on a treadmill before and after performing a task that locally fatigued their ankle plantarflexor muscles. We applied multivariate signal cleaning methods to remove motion artifacts from the recorded signals. From these data, we computed the peak EMG amplitude, spatial entropy, peak EMG barycenter, and mean power frequency content during walking and running before and after subjects fatigued. We also calculated sagittal plane lower limb joint kinematics and kinetics in each condition. We found that peak EMG activity significantly decreased during walking and running after the fatigue task, and the location of the peak EMG barycenter had shifted proximally compared to its pre-fatigue location. We also observed an increase in the EMG mean power frequency during locomotion post-fatigue. Despite the changes in spatial EMG activation, lower limb biomechanics were similar before and after fatigue. These results suggest that motor unit recruitment was altered to sustain force production and forward propulsion. This may be a protective mechanism to more broadly distribute muscle loads and avoid myotendinous injury.
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