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INVITED REVIEW

HIGHLIGHTED TOPIC
Fatigue Mechanisms Determining Exercise Performance

Impaired calcium release during fatigue

¹School of Medical Sciences and Bosch Institute, University of Sydney; ²Department of Zoology, La Trobe University, Melbourne, Victoria, Australia; and ³Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden

Impaired calcium release from the sarcoplasmic reticulum (SR) has been identified as a contributor to fatigue in isolated skeletal muscle fibers. The functional importance of this phenomenon can be quantified by the use of agents, such as caffeine, which can increase SR Ca²⁺ release during fatigue. A number of possible mechanisms for impaired calcium release have been proposed. These include reduction in the amplitude of the action potential, potentially caused by extracellular K⁺ accumulation, which may reduce voltage sensor activation but is counteracted by a number of mechanisms in intact animals. Reduced effectiveness of SR Ca²⁺ channel opening is caused by the fall in intracellular ATP and the rise in Mg²⁺ concentrations that occur during fatigue. Reduced Ca²⁺ available for release within the SR can occur if inorganic phosphate enters the SR and precipitates with Ca²⁺. Further progress requires the development of methods that can identify impaired SR Ca²⁺ release in intact, blood-perfused muscles and that can distinguish between the various mechanisms proposed.

calcium channel; isolated skeletal muscle fibers

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