Initial events in exercise-induced muscular injury

Immediately following unaccustomed exercise, particularly that with eccentric contractions, there is evidence of injury to skeletal muscle fibers: a) disruption of the normal myofilament structures in some sarcomeres, observable with both light and electron microscope and b) loss of intramuscular pr...

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Bibliographic Details
Published in:Medicine and science in sports and exercise 1990-08, Vol.22 (4), p.429-435
Main Author: Armstrong, R B
Format: Article
Language:English
Subjects:
Calcium - metabolism
Exercise
Free Radicals
Homeostasis
Humans
Hydrogen-Ion Concentration
Mechanoreceptors - physiology
Mitochondria, Muscle - metabolism
Muscle Contraction
Muscles - metabolism
Muscles - physiopathology
Muscles - ultrastructure
Sarcolemma - ultrastructure
Space life sciences
Sprains and Strains - metabolism
Sprains and Strains - physiopathology
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Summary:Immediately following unaccustomed exercise, particularly that with eccentric contractions, there is evidence of injury to skeletal muscle fibers: a) disruption of the normal myofilament structures in some sarcomeres, observable with both light and electron microscope and b) loss of intramuscular proteins (e.g., creatine kinase enzymes) into the plasma, indicating damage to sarcolemma. This pathology is probably responsible for the temporary reductions in muscle force and delayed-onset soreness that can occur following eccentric exercise. The mechanisms underlying this injury are not known, although loss of intracellular Ca2+ homeostasis could play a primary role. In other experimental muscle injury models, elevated [Ca2+]i appears to cause release of muscle enzymes through activation of phospholipase A2, which in turn could induce injury to sarcolemma through production of leukotrienes and prostaglandins, through free O2 radical formation (in the subsequent lipoxygenase and cyclooxygenase reactions), and/or through release of detergent lysophospholipids. On the other hand, the mechanism responsible for the rapid damage to myofibrils caused by increased [Ca2+]i is unknown. Regardless of the cause(s), the initial and early events in the injury process are autogenetic; i.e., they are indigenous to the muscle cells and occur before phagocytic cells enter the injury site.
ISSN:0195-9131
DOI:10.1249/00005768-199008000-00002