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The response of cortical alpha activity to pain and neuromuscular changes caused by exercise-induced muscle damage

Authors

  • K. Plattner,

    Corresponding author
    1. UCT/MRC Research Unit for Exercise Science and Sports Medicine, Department of Human Biology, Faculty of Health Sciences, University of Cape Town, The Sport Science Institute of South Africa, Newlands, South Africa
    • Corresponding author: Kristina Plattner, PhD, Exercise Science, UCT/MRC Research Unit for Exercise Science and Sports Medicine, Sport Science Institute of South Africa, PO Box 115, Newlands, 7725, South Africa. Tel: +270 21 65 04572, Fax: +270 21 68 67530, E-mail address: kristina.plattner@gmail.com

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  • M. I. Lambert,

    1. UCT/MRC Research Unit for Exercise Science and Sports Medicine, Department of Human Biology, Faculty of Health Sciences, University of Cape Town, The Sport Science Institute of South Africa, Newlands, South Africa
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  • N. Tam,

    1. UCT/MRC Research Unit for Exercise Science and Sports Medicine, Department of Human Biology, Faculty of Health Sciences, University of Cape Town, The Sport Science Institute of South Africa, Newlands, South Africa
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  • J. Baumeister

    1. Exercise & Brain Laboratory, Institute of Sports Medicine, Department of Exercise and Health, University of Paderborn, Paderborn, Germany
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Abstract

Exercise-induced muscle damage (EIMD) is characterized by pain, swelling, and shortening of the muscle; increased serum creatine kinase; decreased force output; and altered neuromuscular function. The aim of this study was to investigate the effects of EIMD to determine the relationship between the peripheral symptoms, neuromuscular changes, and delayed pain sensation during a submaximal movement of the biceps brachii on cortical alpha (α) activity. In contrast to the control (n = 12) group, the experimental (n = 16) group participated in an EIMD protocol, and both groups were monitored for 132 h post-EIMD protocol. At 12 h, neuromuscular functioning was already disturbed while the sensation of pain was perceived, but not fully developed. Muscle pain scores in the experimental group peaked after 36 h with the lowest torque reported at 12 h. α-1 activity increased significantly in the motor and somatosensory area 12 h post-EIMD while α-2 activity increased in the contralateral fronto-central area. At 36 h, pain had further increased and neuromuscular function improved while α-1 and α-2 activities had decreased. We hypothesize that α-1 activity over the motor and somatosensory cortex of the experimental group displays a compensatory increase in response to the changes in neuromuscular function during movement, while an increase in α-2 activity is related to the suppression of pain experienced within the first 12 h.

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