ArticleJournal of muscle research and cell motility2022
Mechanisms of weakness in Mdx muscle following in vivo eccentric contractions.
Article in Journal of muscle research and cell motility, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 12 citations in OpenAlex.
- Open-Source Tools for Neuromuscular Electrical Stimulation in Mouse Models: A Methodological Validation Study.Muscles (Basel, Switzerland) · 2026Article
- CORP: In vivo muscle strength-perspectives on the design and interpretation of preclinical animal studies.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Review
- Polyplex Nanomicelle-Mediated Pgc-1α4 mRNA Delivery Via Hydrodynamic Limb Vein Injection Enhances Damage Resistance in Duchenne Muscular Dystrophy Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Ablation of satellite cell-specific clock gene, Bmal1, alters force production, muscle damage, and repair following contractile-induced injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Traumatic Skeletal Muscle Injury and Recovery.Advances in experimental medicine and biology · 2025Review
- Transcriptional and morphological responses following distinct muscle contraction protocols for Snell dwarf (Pit1Physiological reports · 2024Article
- Time-of-day effects on ex vivo muscle contractility following short-term satellite cell ablation.American journal of physiology. Cell physiology · 2024Article
- Acute microtubule changes linked to DMD pathology are insufficient to impair contractile function or enhance contraction-induced injury in healthy muscle.bioRxiv : the preprint server for biology · 2024Article
- Ablation of skeletal muscle estrogen receptor alpha impairs contractility in male mice.Journal of applied physiology (Bethesda, Md. : 1985) · 2024Article
- Mechanism of static loading injury in human skeletal muscle cells.American journal of translational research · 2024Article
- Eccentric contraction-induced strength loss in dystrophin-deficient muscle: Preparations, protocols, and mechanisms.The Journal of general physiology · 2023Article
- Proteomic profiling of impaired excitation-contraction coupling and abnormal calcium handling in muscular dystrophy.Proteomics · 2022Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Skeletal muscle of the dystrophin-deficient mdx mouse is hypersensitive to eccentric (ECC) contraction-induced strength loss due to plasmalemmal electrical dysfunction. Despite plasmalemmal inexcitability being a logical mechanism responsible for weakness, it remains unclear if processes up- and/or down-stream remain functionally intact in injured mdx muscle. The purpose of this study was to analyze additional processes necessary for excitation-contraction coupling that are potentially disrupted by ECC contractions. Anterior crural muscles (tibialis anterior, extensor digitorum longus [EDL], and extensor hallucis muscles) of wildtype (WT) and mdx mice were injured in vivo with 50 ECC contractions and torque was measured immediately before and after the contraction bout. Following the in vivo assessment, EDL ex vivo isometric and caffeine forces were analyzed. In vivo isometric torque and ex vivo force in WT muscle were reduced 38 and 30% (p < 0.001), while caffeine force was also reduced (p = 0.021), albeit to a lesser degree (9%). In contrast, in vivo isometric torque, ex vivo isometric force and ex vivo caffeine-induced force were all reduced 56-67% (p < 0.001) in mdx muscle and did not differ from one another (p = 0.114). Disproportional reductions in isometric strength and caffeine-induced force confirm that ECC contractions uncoupled the plasmalemma from the ryanodine receptors (RyRs) in WT muscle. In mdx muscle, the proportional reductions in isometric strength and caffeine-induced force following ECC contractions reveal that dysfunction occurs at and/or distal to the RyRs immediately post-injury. Thus, weakness in injured mdx muscle cannot be isolated to one mechanism, rather several steps of muscle contraction are disrupted.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.