ArticleThe Journal of physiology2002
Development of T-tubular vacuoles in eccentrically damaged mouse muscle fibres.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 69 citations in OpenAlex.
- Beyond the first bout: Adaptations to repeated injuries across physiological and pathological conditions.Physiological reports · 2026Review
- Eccentric Exercise and Muscle Damage: An Introductory Guide.Journal of functional morphology and kinesiology · 2026Review
- MCARE enhances SERCA1 activity in fast-twitch muscle to maintain calcium handling and muscle integrity.Nature communications · 2025Article
- Myofiber structure, sarcoplasmic reticulum CaPhysiological reports · 2025Article
- Pathophysiology of exercise-induced muscle damage and its structural, functional, metabolic, and clinical consequences.Physiological research · 2020Review
- The effects of fatigue and oxidation on contractile function of intact muscle fibers and myofibrils isolated from the mouse diaphragm.Scientific reports · 2019Article
- Human skeletal muscle plasmalemma alters its structure to change its CaNature communications · 2017Article
- Revealing T-Tubules in Striated Muscle with New Optical Super-Resolution Microscopy Techniquess.European journal of translational myology · 2015Review
- Cellular mechanism of eccentric-induced muscle injury and its relationship with sarcomere heterogeneity.Journal of exercise rehabilitation · 2014Review
- Eccentric contractions disrupt FKBP12 content in mouse skeletal muscle.Physiological reports · 2014Article
- Unaccustomed eccentric contractions impair plasma K+ regulation in the absence of changes in muscle Na+,K+-ATPase content.PloS one · 2014Article
- Dysferlin stabilizes stress-induced Ca2+ signaling in the transverse tubule membrane.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Low-frequency fatigue as an indicator of eccentric exercise-induced muscle injury: the role of vitamin E.Oxidative medicine and cellular longevity · 2012Article
- Dimethyl sulphoxide addition or withdrawal causes biphasic volume changes and its withdrawal causes t-system vacuolation in skeletal muscle.The Journal of physiology · 2011Article
- Dysferlin, annexin A1, and mitsugumin 53 are upregulated in muscular dystrophy and localize to longitudinal tubules of the T-system with stretch.Journal of neuropathology and experimental neurology · 2011Article
- The accessibility and interconnectivity of the tubular system network in toad skeletal muscle.The Journal of physiology · 2008Article
- FKBP12 deficiency reduces strength deficits after eccentric contraction-induced muscle injury.Journal of applied physiology (Bethesda, Md. : 1985) · 2008Article
- Mechanisms of stretch-induced muscle damage in normal and dystrophic muscle: role of ionic changes.The Journal of physiology · 2005Review
- Effects of stretch-activated channel blockers on [Ca2+]i and muscle damage in the mdx mouse.The Journal of physiology · 2005Article
- Osmotic properties of the sealed tubular system of toad and rat skeletal muscle.The Journal of general physiology · 2004Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Single fibres were dissected from mouse flexor digitorum brevis muscles and subjected to a protocol of eccentric stretches consisting of ten tetani each with a 40 % stretch. Ten minutes later the fibres showed a reduced force, a shift in the peak of the force-length relation and a steepening of the force-frequency relation. Addition of the fluorescent dye sulforhodamine B to the extracellular space enabled the T-tubular system to be visualized. In unstimulated fibres and fibres subjected to 10 isometric tetani, the T-tubules were clearly delineated. Sulforhodamine B diffused out of the T-tubules with a half-time of 18 +/- 1 s. Following the eccentric protocol, vacuoles connected to the T-tubules were detected in six out of seven fibres. Sulforhodamine B diffused out of the vacuoles of eccentrically damaged fibres extremely slowly with a half-time of 6.3 +/- 2.4 min and diffused out of the T-tubules with a half-time of 39 +/- 4 s. Vacuole production was eliminated by application of 1 mM ouabain to the muscle during the eccentric protocol. On removal of the ouabain, vacuoles appeared over a period of 1 h and were more numerous and more widely distributed than in the absence of ouabain. We propose that T-tubules are liable to rupture during eccentric contraction probably because of the relative movement associated with the inhomogeneity of sarcomere lengths. Such rupture raises intracellular sodium and when the sodium is pumped from the cell by the sodium pump, the volume load of Na(+) and water exceeds the capacity of the T-tubules and causes vacuole production. The damage to the T-tubules may underlie a number of the functional changes that occur in eccentrically damaged muscle fibres.
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