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This Article Full Text Full Text (PDF) All Versions of this Article: 560/1/137    most recent jphysiol.2004.067322v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Payne, A. M. Articles by Delbono, O. Search for Related Content PubMed PubMed Citation Articles by Payne, A. M. Articles by Delbono, O.

¹ Department of Physiology and Pharmacology
² Department of Internal Medicine, Section on Gerontology
³ Neuroscience Program, Wake Forest University School of Medicine, Winston-Salem, NC 21757, USA

In the present work, we investigate whether changes in excitation–contraction (EC) coupling mode occur in skeletal muscles from ageing mammals by examining the dependence of EC coupling on extracellular Ca²⁺. Single intact muscle fibres from flexor digitorum brevis muscles from young (2–6 months) and old (23–30 months) mice were subjected to tetanic contractile protocols in the presence and absence of external Ca²⁺. Contractile experiments in the absence of external Ca²⁺ show that about half of muscle fibres from old mice are dependent upon external Ca²⁺ for maintaining maximal tetanic force output, while young fibres are not. Decreased force in the absence of external Ca²⁺ was not due to changes in charge movement as revealed by whole-cell patch-clamp experiments. Ca²⁺ transients, measured by fluo-4 fluorescence, declined in voltage-clamped fibres from old mice in the absence of external Ca²⁺. Similarly, Ca²⁺ transients declined in parallel with tetanic contractile force in single intact fibres. Examination of inward Ca²⁺ current and of mRNA and protein assays suggest that these changes in EC coupling mode are not due to shifts in dihydropyridine receptor (DHPR) and/or ryanodine receptor (RyR) isoforms. These results indicate that a change in EC coupling mode occurs in a population of fibres in ageing skeletal muscle, and is responsible for the age-related dependence on extracellular Ca²⁺.

(Received 28 April 2004; accepted after revision 3 August 2004; first published online 5 August 2004)
Corresponding author O. Delbono: Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA. Email: odelbono{at}wfubmc.edu

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