Journal of Applied Physiology AJP: Gastrointestinal and Liver Physiology
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J Appl Physiol (October 25, 2007). doi:10.1152/japplphysiol.00908.2007
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Submitted on August 23, 2007
Accepted on October 24, 2007

Impaired calcium release during fatigue

David G. Allen1*, Graham D. Lamb2, and Hakan Westerblad3

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

* To whom correspondence should be addressed. E-mail: davida{at}physiol.usyd.edu.au.

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 which 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 which can identify impaired SR Ca2+ release in intact, blood-perfused muscles and which can distinguish between the various mechanisms proposed.




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