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Calcium exchange hypothesis of skeletal muscle fatigue: A brief review
Author(s) -
Williams Jay H.,
Klug Gary A.
Publication year - 1995
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.880180409
Subject(s) - muscle fatigue , calcium , endoplasmic reticulum , skeletal muscle , intracellular , myocyte , chemistry , calcium in biology , muscle contraction , endocrinology , medicine , biophysics , biology , neuroscience , biochemistry , electromyography
Skeletal muscle fatigue is often associated with diminished athletic performance and work productivity as well as increased susceptibility to injury. The exact cause of muscle fatigue probably involves a number of factors which influence force production in a manner dependent on muscle fiber type and activation pattern. However, a growing body of evidence implicates alterations in intracellular Ca 2+ exchange as a major role in the fatigue process. These changes are thought to occur secondary to reductions in the rates of Ca 2+ uptake and release by the sarcoplasmic reticulum (SR). This hypothesis is based on the finding that peak myoplasmic Ca 2+ concentration ([Ca 2+ ] i ) is reduced as force declines during fatigue. In addition, direct measurements of Ca 2+ uptake and release show that fatiguing activity causes intrinsic alterations in the functional properties of the SR. We also propose that fatigue‐induced alterations in Ca 2+ exchange may be beneficial, reducing the rate of energy utilization by the muscle fiber and preventing irreversible damage to the cell. © 1995 John Wiley & Sons, Inc.