Cited by 94Muscle Physiology and DisordersMuscle activation and electromyography studiesExercise and Physiological Responses

Uncoupling of in vivo torque production from EMG in mouse muscles injured by eccentric contractions

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Warren, Gordon L., Ingalls, Christopher P., Shah, Shree J., Armstrong, R. B.·1999·The Journal of Physiology

Abstract

1. The main objective of this study was to determine whether eccentric contraction-induced muscle injury causes impaired plasmalemmal action potential conduction, which could explain the injury-induced excitation-contraction coupling failure. Mice were chronically implanted with stimulating electrodes on the left common peroneal nerve and with electromyographic (EMG) electrodes on the left tibialis anterior (TA) muscle. The left anterior crural muscles of anaesthetized mice were stimulated to perform 150 eccentric (ECC) (n = 12 mice) or 150 concentric (CON) (n = 11 mice) contractions. Isometric torque, EMG root mean square (RMS) and M-wave mean and median frequencies were measured before, immediately after, and at 1, 3, 5 and 14 days after the protocols. In parallel experiments, nicotinic acetylcholine receptor (AChR) concentration was measured in TA muscles to determine whether the excitation failure elicited a denervation-like response. 2. Immediately after the ECC protocol, torque was reduced by 47-89 %, while RMS was reduced by 9-21 %; the RMS decrement was not different from that observed for the CON protocol, which did not elicit large torque deficits. One day later, both ECC and CON RMS had returned to baseline values and did not change over the next 2 weeks. However, torque production by the ECC group showed a slow recovery over that time and was still depressed by 12-30 % after 2 weeks. M-wave mean and median frequencies were not affected by performance of either protocol. 3. AChR concentration was elevated by 79 and 368 % at 3 and 5 days, respectively, after the ECC protocol; AChR concentration had returned to control levels 2 weeks after the protocol. At the time of peak AChR concentration in the ECC protocol muscles (i.e. 5 days), AChR concentration in CON protocol muscles was not different from the control level. 4. In conclusion, these data demonstrate no major role for impaired plasmalemmal action potential conduction in the excitation-contraction coupling failure induced by eccentric contractions. Additionally, a muscle injured by eccentric contractions shows a response in AChR concentration similar to a transiently denervated muscle.

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Registry

Crossref · 10.1111/j.1469-7793.1999.609ac.x

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Authors
Warren, G. L., Ingalls, C. P., Shah, S. J., & Armstrong, R. B.
Affiliations
Texas A&M University (US)
Venue
The Journal of Physiology
Publisher
Wiley
Published
1999-03
Volume
515
Issue
2
Pages
609-619
ISSN
  • 0022-3751 (ISSN-L)
  • 1469-7793
OpenAlex
W2116809283
Cited by
94
References
28
Citations by year
2025: 2 · 2024: 2 · 2023: 1 · 2022: 3 · 2021: 2 · 2019: 3 · 2018: 4 · 2016: 7 · 2015: 3 · 2014: 5 · 2013: 7 · 2012: 4
FWCI
1.61
Type
journal article
Language
en
Open access
Locations
  • The Journal of Physiology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Physical Sciences › Engineering › Biomedical Engineering › Muscle activation and electromyography studies
  • Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
Keywords
eccentric contraction, muscle damage, excitation-contraction coupling, tibialis anterior, nicotinic acetylcholine receptors, M-wave, isometric torque, muscle recovery
MeSH terms
Animals, Electromyography, Female, Hindlimb, Mice, Inbred ICR, Muscle Contraction, Osmolar Concentration, Receptors, Cholinergic, Muscle, Skeletal, Torque, Mice

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