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This Article Full Text Full Text (PDF) All Versions of this Article: 91/4/781    most recent expphysiol.2005.033043v1 Alert me when this article is cited Alert me if a correction is posted 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 Google Scholar Google Scholar Articles by Rader, E. P. Articles by Faulkner, J. A. Search for Related Content PubMed PubMed Citation Articles by Rader, E. P. Articles by Faulkner, J. A. Related Collections Muscle

¹ Department of Biomedical Engineering² Institute of Gerontology, University of Michigan, Ann Arbor, MI 48109, USA ³ Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA

A protocol of 75 lengthening contractions (LCP) administered to skeletal muscles of mice causes an initial force deficit owing to the mechanical disruption of sarcomeres and a reduction in calcium release from the sarcoplasmic reticulum. During the 3 days following the LCP, a ‘sealing off process’ and inflammatory response occurs. The reactive oxygen species (ROS) released by invading inflammatory cells produce a secondary force deficit that is more severe than the initial deficit. The timing of the infiltration of inflammatory cells and increase in force deficit relative to the sealing off process is not well documented. We tested the null hypothesis that following a lifetime of overexpression of the genes for the intracellular antioxidants manganese superoxide dismutase, copper zinc superoxide dismutase or catalase in transgenic mice, the force deficits 3 days following the administration of a 75 LCP to in situ extensor digitorum longus muscles are not different from those of wild-type mice. Following the LCP, the force deficits ranged from 39 to 59% for the muscles of transgenic mice that overexpressed the genes for intracellular antioxidants and were not different from the force deficit of 44% observed for muscles of wild-type mice. The results provide evidence that the ROS damage does not occur within the cytosol of the injured fibres. Apparently, the hypercontraction of sarcomeres and accumulation of vesicles seal off and protect the intact portions of damaged fibres, such that the ROS damage and repair occurs in the milieu of the necrotic segments that are continuous with the extracellular matrix.

(Received 9 December 2005; accepted after revision 2 May 2006; first published online 4 May 2006)
Corresponding author J. A. Faulkner: Institute of Gerontology, University of Michigan, Ann Arbor, MI 48109-2007, USA. Email: jafaulk{at}umich.edu