NDLI: Mechanisms of excitation-contraction uncoupling relevant to activity-induced muscle fatigue

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lamb, Graham D.
Description	Country affiliation: Australia Author Affiliation: Lamb GD ( Department of Zoology, La Trobe University, Melbourne, Victoria, 3086, Australia. g.lamb@latrobe.edu.au)
Abstract	If the free $[Ca^{2+}]$ in the cytoplasm of a skeletal muscle fiber is raised substantially for a period of seconds to minutes or to high levels just briefly, it leads to disruption of the normal excitation-contraction (E-C) coupling process and a consequent long-lasting decrease in force production. It appears that the disruption to the coupling occurs at the triad junction, where the voltage-sensor molecules (dihydropyridine receptors) normally interact with and open the $Ca^{2+}$ release channels (ryanodine receptors) in the adjacent sarcoplasmic reticulum (SR). This disruption results in inadequate release of SR $Ca^{2+}$ upon stimulation. Such E-C uncoupling may underlie the long-duration low-frequency fatigue that can occur after various types of exercise, as well as possibly being a contributing factor to the muscle weakness in certain muscle diseases. The process or processes causing the disruption of the coupling between the voltage sensors and the release channels is not known with certainty, but might be associated with structural changes at the triad junction, possibly caused by activation of the $Ca^{2+}-dependent$ protease, µ-calpain.
File Format	HTM / HTML
ISSN	17155312
Issue Number	3
Volume Number	34
e-ISSN	17155320
Journal	Applied Physiology, Nutrition, and Metabolism
Language	English
Publisher	Canadian Science Publishing
Publisher Date	2009-06-01
Publisher Place	Canada
Access Restriction	Subscribed
Subject Keyword	Discipline Physiology Discipline Metabolism Discipline Nutritional Sciences Discipline Sports Medicine Muscle Contraction Physiology Muscle Fatigue Calcium Metabolism Exercise Humans Muscle, Skeletal Journal Article Research Support, Non-u.s. Gov't Review
Content Type	Text
Resource Type	Article
Subject	Nutrition and Dietetics Physiology Endocrinology, Diabetes and Metabolism Physiology (medical) Sports Science

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