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Updated: Jun 9, 2026
Assessing Functional Performance in the Mdx Mouse Model
Published on: March 27, 2014
Stretch-induced membrane damage in muscle: comparison of wild-type and mdx mice
David G Allen1, Bao-ting Zhang, Nicholas P Whitehead
1Bosch Institute and School of Medical Sciences, University of Sydney, F13, Sydney, NSW, 2006, Australia. david.allen@sydney.edu.au
Abstract:
One component of stretch-induced muscle damage is an increase in the permeability of the cell membrane. As a result soluble myoplasmic proteins leak out of the muscle into the plasma, extracellular proteins can enter the muscle, and extracellular ions, including calcium, are driven down their electrochemical gradient into the myoplasm. In Duchenne muscular dystrophy, caused by the absence of the cytoskeletal protein dystrophin, stretch-induced membrane damage is much more severe. The most popular theory to explain the occurrence of stretch-induced membrane damage is that stretched-contractions cause transient mechanically-induced defects in the membrane (tears or rips). Dystrophin, which is part of a mechanical link between the contractile machinery and the extracellular matrix, is thought to contribute to membrane strength so that in its absence mechanically-induced defects are worse. In our view the evidence that stretch-induced muscle damage causes increased membrane permeability is overwhelming but the evidence that the increased permeability is caused by mechanically-induced defects is weak. Instead we review the substantial evidence that the membrane permeability is a secondary consequence of the mechanical events in which elevated intracellular calcium and reactive oxygen species are important intermediaries.
Insights
Stretch-induced muscle damage increases cell membrane permeability. This study suggests elevated calcium and reactive oxygen species, not membrane tears, are the primary cause of this increased permeability in muscle damage.
Area of Science:
- Muscle physiology
- Cell membrane biology
- Biochemistry
Background:
- Stretch-induced muscle damage involves increased cell membrane permeability, leading to protein leakage and ion imbalance.
- Duchenne muscular dystrophy exhibits more severe stretch-induced damage due to the absence of dystrophin, a key cytoskeletal protein.
- The prevailing theory attributes this damage to mechanically-induced membrane defects (tears).
Purpose of the Study:
- To critically evaluate the evidence for mechanically-induced membrane defects as the cause of stretch-induced muscle damage.
- To present an alternative hypothesis implicating intracellular factors in membrane permeability changes.
- To explore the roles of elevated intracellular calcium and reactive oxygen species in muscle membrane damage.
Main Methods:
- Review of existing scientific literature on stretch-induced muscle damage.
- Analysis of evidence supporting and refuting the mechanically-induced defect theory.
- Examination of studies investigating intracellular calcium and reactive oxygen species in muscle damage.
Main Results:
- Overwhelming evidence supports increased membrane permeability during stretch-induced muscle damage.
- Evidence for mechanically-induced membrane defects as the primary cause is weak.
- Substantial evidence indicates that increased membrane permeability is a secondary consequence of mechanical events.
Conclusions:
- Mechanically-induced membrane defects are unlikely to be the primary cause of stretch-induced muscle damage.
- Elevated intracellular calcium and reactive oxygen species are significant intermediaries in the development of muscle membrane permeability.
- This revised understanding has implications for Duchenne muscular dystrophy and other muscle-damaging conditions.
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