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Extracellular matrix disruption and pain after eccentric muscle action
W T Stauber1, P M Clarkson, V K Fritz
1Department of Physiology, West Virginia University Health Science Center, Morgantown 26506.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|September 1, 1990
Summary
Delayed muscle soreness after exercise is linked to inflammation. Eccentric muscle actions cause muscle damage, leading to inflammation and pain sensations 48 hours post-exercise.
Area of Science:
- Exercise Physiology
- Muscle Biology
- Cellular Biology
Background:
- Eccentric muscle actions, involving muscle lengthening under load, can cause delayed-onset muscle soreness (DOMS).
- The precise cellular mechanisms triggering DOMS remain incompletely understood.
Purpose of the Study:
- To investigate the temporal relationship between muscle damage indicators, pain perception, and cellular changes following eccentric exercise.
- To elucidate the cellular events contributing to delayed muscle soreness.
Main Methods:
- Maximal resisted lengthening of elbow flexor muscles was performed in a single bout.
- Measurements included elbow joint position, pain perception, and muscle biopsy analysis at various time points post-exercise.
- Biopsies were analyzed for mast cell degranulation, extracellular matrix integrity, and plasma constituent presence.
Main Results:
- A decrease in resting muscle length was observed immediately post-exercise, persisting for 48 hours.
- Significant muscle soreness was reported at 48 hours post-exercise.
- Muscle biopsies revealed mast cell degranulation, myofiber-extracellular matrix separation, and increased extracellular plasma constituents at 48 hours.
Conclusions:
- Myofiber disruption allows intracellular proteins to leak out and extracellular components to enter, leading to swelling.
- Disruption of the extracellular matrix initiates an inflammatory response, including mast cell degranulation.
- Delayed muscle soreness after eccentric exercise is likely caused by inflammation resulting from extracellular matrix disruption.