Muscle Fatigue: The Role of Intracellular Calcium Stores

Force declines when muscles are used repeatedly and intensively and a variety of intracellular mechanisms appear to contribute to this muscle fatigue. Intracellular calcium release declines during fatigue and has been shown to contribute to the reduction in force. Three new approaches have helped to...

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Bibliographic Details
Published in:Canadian journal of applied physiology 2002-02, Vol.27 (1), p.83-96
Main Authors: Allen, David G, Kabbara, Akram A, Westerblad, Håkau
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Calcium - metabolism
Calcium - physiology
Calcium channels
Causes of
Creatine Kinase - metabolism
Fatigue
Fundamental and applied biological sciences. Psychology
Humans
Medicin och hälsovetenskap
Muscle diseases
Muscle Fatigue - physiology
Muscle, Skeletal - metabolism
Muscle, Skeletal - physiology
Muscles
Phosphates - metabolism
Phosphates - physiology
Physiological aspects
Sarcoplasmic Reticulum - metabolism
Sarcoplasmic Reticulum - physiology
Striated muscle. Tendons
Vertebrates: osteoarticular system, musculoskeletal system
Citations: Items that cite this one
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Summary:Force declines when muscles are used repeatedly and intensively and a variety of intracellular mechanisms appear to contribute to this muscle fatigue. Intracellular calcium release declines during fatigue and has been shown to contribute to the reduction in force. Three new approaches have helped to define the role of calcium stores to this decline in calcium release. Skinned fibre experiments show that when intracellular phosphate is increased the amount of Ca 2+ released from the sarcoplasmic reticulum (SR) declines. Intact fibre experiments show that the size of the calcium store declines during fatigue and recovers on rest. Intact muscles which lack the enzyme creatine kinase, do not exhibit the usual rise of phosphate during fatigue and, under these conditions, the decline of Ca 2+ release is absent or delayed. These results can be explained by the "calcium phosphate precipitation" hypothesis. This proposes that if phosphate in the myoplasm rises, it enters the SR and binds to Ca 2+ as Ca 2+ phosphate. The resultant reduction in free Ca 2+ within the SR contributes to the reduced Ca 2+ release during fatigue. Key words: sarcoplasmic reticulum, myoplasmic phosphate, calcium phosphate precipitation, creatine kinase, glycogen
ISSN:1066-7814
1543-2718
DOI:10.1139/h02-006