Abstract
PURPOSE: Muscle that lacks dystrophin, as in the mdx mouse, has a heightened sensitivity to eccentric (ECC) contraction-induced strength loss but an enhanced rate of recovery. However, the timeline and mechanisms underlying why mdx muscle recovers quicker have yet to be determined. We used an EMG approach to analyze plasmalemma electrophysiological function during and after ECC contraction-induced injury to test the hypothesis that loss of plasmalemmal excitability is a transient event in mdx muscle. METHODS: Mice were implanted with stimulating electrodes on the common peroneal nerve and EMG electrodes on the tibialis anterior muscle. Anterior crural muscles of anesthetized mice performed one or two bouts of 50 injurious ECC contractions, and recovery of maximal isometric torque and M-wave root mean square (RMS) were assessed after each bout. RESULTS: Maximal isometric torque and M-wave RMS were equally reduced 62% (P < 0.001) in mdx mice immediately after the initial ECC injury. For these mdx mice, M-wave RMS was still reduced at 2 d postinjury (P = 0.034) but was not different from preinjury values by 6 d (P = 0.106), whereas torque took up to 9 d to recover (P = 0.333). M-wave RMS did not change (P = 0.390) in wild-type mice in response to ECC injury, whereas torque decreased 35% (P < 0.001) and recovered by day 2 (P = 0.311). Results from the second bout of ECC contractions were similar to those observed during and after the initial injury. CONCLUSION: Functional dystrophin is necessary for excitation to occur at the plasmalemma during ECC contractions but is not essential for the complete recovery of plasmalemma electrophysiological function or maximal isometric strength.