ROLE OF EXCITATION-CONTRACTION COUPLING IN MUSCLE FATIGUE

被引：48

作者：

ALLEN, DG

WESTERBLAD, H

LEE, JA

LANNERGREN, J

机构：

[1] Muscle Cell Function Laboratory, Department of Physiology, University of Sydney, Sydney, New South Wales

[2] Division of Pathology, University of Newcastle Upon Tyne, Royal Victoria Infirmary, Newcastle Upon Tyne

[3] Department of Physiology, Karolinska Institutet, Stockholm

来源：

SPORTS MEDICINE | 1992年 / 13卷 / 02期

关键词：

D O I：

10.2165/00007256-199213020-00007

中图分类号：

G8 [体育];

学科分类号：

04 ; 0403 ;

摘要：

The force produced by muscles declines during prolonged activity and this decline arises largely from processes within the muscle. At a cellular level the reduced force could be caused by: (a) reduced intracellular calcium release during activity; (b) reduced sensitivity of the myofilaments to calcium; or (c) reduced maximal force development. Experiments involving intracellular calcium measurements in isolated single fibres show that all 3 of the above contribute to the decline of force during fatigue. Metabolic changes associated with fatigue are probably involved in each of the 3 factors. Thus the accumulation of phosphate and protons which occur during fatigue cause a reduction in calcium sensitivity and a decline in maximal force. The cause of the reduced intracellular calcium during contractions in fatigue is less clear. During prolonged tetani the conduction of the action potential in the T-tubules appears to fail leading to reduced intracellular calcium in the central part of the muscle fibre. However, during repeated tetani there is a uniform decline of intracellular calcium across the fibre and this remains one of the least understood processes which contribute to fatigue.

引用

页码：116 / 126

页数：11

共 27 条

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