Received December 9, 2005
Revised December 15, 2005
Accepted after revision May 2, 2006

¹ University of Michigan
² University of Texas Health Science Center

^* To whom correspondence should be addressed. E-mail: jafaulk{at}umich.edu.

	Abstract

A protocol of 75 lengthening contractions (LCP) administered to skeletal muscles of mice causes an initial force deficit due to the mechanical disruption of sarcomeres and a reduction in calcium release from the sarcoplasmic reticulum. During the three 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 life-time of over-expression of the genes for the intracellular antioxidants manganese superoxide dismutase, copper zinc superoxide dismutase, or catalase in transgenic mice, the force deficits three 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 over-expressed 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 fibers. Apparently, the hypercontraction of sarcomeres and accumulation of vesicles seal off and protect the intact portions of damaged fibers, such that the ROS damage and repair occurs in the milieu of the necrotic segments that are continuous with the extracellular matrix.

Key Words: Muscle, Muscle contraction, Oxidation