Journal of Applied Physiology AJP: Gastrointestinal and Liver Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


J Appl Physiol (October 25, 2007). doi:10.1152/japplphysiol.00908.2007
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
104/1/296    most recent
00908.2007v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Allen, D. G.
Right arrow Articles by Westerblad, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Allen, D. G.
Right arrow Articles by Westerblad, H.
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.




This article has been cited by other articles:


Home page
J. Physiol.Home page
N. Place, T. Yamada, J. D. Bruton, and H. Westerblad
Interpolated twitches in fatiguing single mouse muscle fibres: implications for the assessment of central fatigue
J. Physiol., June 1, 2008; 586(11): 2799 - 2805.
[Abstract] [Full Text] [PDF]


Home page
J. Appl. Physiol.Home page
M. Amann, S. M. Marcora, L. Nybo, T. A. Duhamel, T. D. Noakes, V. Jaquinandi, J. L. Saumet, P. Abraham, B. T. Ameredes, M. Burnley, et al.
Viewpoint: Fatigue mechanisms determining exercise performance: integrative physiology is systems physiology.
J Appl Physiol, May 1, 2008; 104(5): 1543 - 1544.
[Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 1948 by the American Physiological Society.