E-C coupling failure in mouse EDL muscle after in vivo eccentric contractions
Abstract
The objectives of this research were to determine the contribution of excitation-contraction (E-C) coupling failure to the decrement in maximal isometric tetanic force (Po) in mouse extensor digitorum longus (EDL) muscles after eccentric contractions and to elucidate possible mechanisms. The left anterior crural muscles of female ICR mice (n = 164) were injured in vivo with 150 eccentric contractions. Po, caffeine-, 4-chloro-m-cresol-, and K+-induced contracture forces, sarcoplasmic reticulum (SR) Ca2+ release and uptake rates, and intracellular Ca2+ concentration ([Ca2+]i) were then measured in vitro in injured and contralateral control EDL muscles at various times after injury up to 14 days. On the basis of the disproportional reduction in Po (approximately 51%) compared with caffeine-induced force (approximately 11-21%), we estimate that E-C coupling failure can explain 57-75% of the Po decrement from 0 to 5 days postinjury. Comparable reductions in Po and K+-induced force (51%), and minor reductions (0-6%) in the maximal SR Ca2+ release rate, suggest that the E-C coupling defect site is located at the t tubule-SR interface immediately after injury. Confocal laser scanning microscopy indicated that resting [Ca2+]i was elevated and peak tetanic [Ca2+]i was reduced, whereas peak 4-chloro-m-cresol-induced [Ca2+]i was unchanged immediately after injury. By 3 days postinjury, 4-chloro-m-cresol-induced [Ca2+]i became depressed, probably because of decreased SR Ca2+ release and uptake rates (17-31%). These data indicate that the decrease in Po during the first several days after injury primarily stems from a failure in the E-C coupling process.
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Force-producing capabilities of muscle usually return to baseline between 2 and 4 weeks post-eccentric contraction-induced injury.
“The force-producing capabilities of the muscle usually return to baseline (pre-injury) levels between 2 and 4 weeks post-eccentric contraction-induced injury (34, 42, 44, 46, 47).”
From Phytoecdysteroids Accelerate Recovery of Skeletal Muscle Function Following in vivo Eccentric Contraction-Induced Injury in Adult and Old Mice (2021) · cites this paper as [47]
The greatest declines in muscle function occur immediately following eccentric contraction-induced injury, yet markers of muscle damage are not fully apparent until 1-2 days after injury.
“Recall that the greatest declines in muscle function occur immediately following eccentric contraction-induced injury, yet markers of muscle damage are not fully apparent until 1–2 days after injury (34, 47, 52).”
From Phytoecdysteroids Accelerate Recovery of Skeletal Muscle Function Following in vivo Eccentric Contraction-Induced Injury in Adult and Old Mice (2021) · cites this paper as [47]
There is a dissociation between muscle function and histological markers of muscle damage that disputes the causal relationship that disruption of sarcomeric structures causes loss of muscle function after eccentric damage.
“However, there is a dissociation between muscle function and histological markers of muscle damage that disputes the latter causal relationship.”
From Phytoecdysteroids Accelerate Recovery of Skeletal Muscle Function Following in vivo Eccentric Contraction-Induced Injury in Adult and Old Mice (2021) · cites this paper as [47]
The novel observation that 20E treatment fully recovers skeletal muscle function in just 7 days after eccentric damage is much earlier than other studies using similar eccentric damage protocols in mice.
“The novel observation that 20E treatment fully recovers skeletal muscle function in just 7 days after eccentric damage is much earlier than other studies using similar eccentric damage protocols in mice (34, 35, 42, 47).”
From Phytoecdysteroids Accelerate Recovery of Skeletal Muscle Function Following in vivo Eccentric Contraction-Induced Injury in Adult and Old Mice (2021) · cites this paper as [47]
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SERCA1 overexpression minimizes skeletal muscle damage in dystrophic mouse models
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Self-citationCompression-Induced Muscle Injury in Rats That Mimics Compartment Syndrome in Humans
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Is eccentric exercise-induced torque decrease contraction type dependent?
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Self-citationAdaptation to lengthening contraction-induced injury in mouse muscle
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Self-citationMuscle Fiber Types and Training
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- Authors
- Ingalls, C. P., Warren, G. L., Williams, J. H., Ward, C. W., & Armstrong, R. B.
- Affiliations
- Texas A&M University (US)
- Virginia Tech (US)
- Venue
- Journal of Applied Physiology
- Publisher
- American Physiological Society
- Published
- 1998-07-01
- Volume
- 85
- Issue
- 1
- Pages
- 58-67
- ISSN
- 0161-7567 (ISSN-L)
- 8750-7587
- 1522-1601
- OpenAlex
- W2123343796
- Cited by
- 262
- References
- 33
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 2 · 2023: 2 · 2022: 4 · 2021: 12 · 2020: 1 · 2019: 5 · 2018: 8 · 2017: 6 · 2016: 15 · 2015: 7 · 2014: 16 · 2013: 11 · 2012: 17
- FWCI
- 2.95
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Applied Physiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ar042761-03)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR-42761)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Surgery › Muscle and Compartmental Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Keywords
- extensor digitorum longus, skeletal muscle injury, isometric tetanic force, sarcoplasmic reticulum Ca2+ release, intracellular calcium, 4-chloro-m-cresol, muscle fatigue
- MeSH terms
- Animals, Caffeine, Calcium, Electric Stimulation, Female, Mice, Inbred ICR, Microtubules, Muscle Contraction, Phosphodiesterase Inhibitors, Potassium, Sarcoplasmic Reticulum, Stimulation, Chemical, Muscle, Skeletal, Microscopy, Confocal, Mice, Rats, In Vitro Techniques
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