Mechanisms of stretch-induced muscle damage in normal and dystrophic muscle: Role of ionic changes

Davida G. Allen, N. P. Whitehead, Wai Ella Yeung

Research output: Journal article publicationReview articleAcademic researchpeer-review

137 Citations (Scopus)

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 Ca2+ 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.
Original languageEnglish
Pages (from-to)723-735
Number of pages13
JournalJournal of Physiology
Volume567
Issue number3
DOIs
Publication statusPublished - 15 Sep 2005

ASJC Scopus subject areas

  • Physiology

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