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Department of Biology, University of Portland, Portland, 97203; and Department of Physics, Portland State University, Portland, Oregon 97207
Efforts to examine the relevant mechanisms involved in skeletal muscle fatigue are focusing on Ca2+ handling within the active muscle cell. It has been demonstrated time and again that reductions in sarcoplasmic reticulum (SR) Ca2+ release resulting from increased or intense muscle contraction will compromise tension development. This review seeks to accomplish two related goals: 1) to provide an up-to-date molecular understanding of the Ca2+-release process, with considerable attention devoted to the SR Ca2+ channel, including its associated proteins and their regulation by endogenous compounds; and 2) to examine several putative mechanisms by which cellular alterations resulting from intense and/or prolonged contractile activity will modify SR Ca2+ release. The mechanisms that are likely candidates to explain the reductions in SR Ca2+ channel function following contractile activity include elevated Ca2+ concentrations, alterations in metabolic homeostasis within the "microcompartmentalized" triadic space, and modification by reactive oxygen species.
excitation-contraction coupling; muscle; calcium; exercise
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