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Cited by 196

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Mechanisms of stretch‐induced muscle damage in normal and dystrophic muscle: role of ionic changes

Allen, D. G., Whitehead, N. P., Yeung, E. W.·2005·The Journal of Physiology
DOI 10.1113/jphysiol.2005.091694
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Abstract

Muscle damage, characterized by prolonged weakness and delayed onset of stiffness and soreness, is common following contractions in which the muscles are stretched. Stretch‐induced damage of this sort is more pronounced in the muscular dystrophies and the profound muscle damage observed in these conditions may involve similar pathways. It has been known for many years that damaged muscles accumulate calcium and that elevating calcium in normal muscles simulates many aspects of muscle damage. The changes in intracellular calcium, sodium and pH following stretched contractions are reviewed and the various pathways which have been proposed to allow ion entry are discussed. One possibility is that TRPC1 (transient receptor potential, canonical), a protein which seems to form both a stretch‐activated channel and a store‐operated channel, is the main source of Ca 2+ entry. The mechanisms by which the changes in intracellular ions contribute to reduced force production, to increased protein breakdown and to increased membrane permeability are considered. A hypothetical scheme for muscle damage which incorporates these ideas is presented.

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Metadata

Authors
Allen, D. G., Whitehead, N. P., & Yeung, E. W.
Venue
The Journal of Physiology
Publisher
Wiley
Published
2005-09
Volume
567
Issue
3
Pages
723-735
ISSN
  • 0022-3751 (ISSN-L)
  • 1469-7793
DOI
10.1113/jphysiol.2005.091694
OpenAlex
W2162646067
Cited by
196
References
6
FWCI
4.38
Type
journal article
Language
en
Open access
closed

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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