Figure 1: Mice lacking dystrophin are more susceptible to injury. Producing the injury, the fibular (aka peroneal) nerve was used to stimulate the dorsiflexor muscles supramaximally while moving the plate forced the foot into plantar flexion. Injury was induced by 10 large strain lengthening (“eccentric”) contractions through a 70° arc of motion. Maximal isometric torque was measured before and after injury in wild type (WT) and mice lacking dystrophin (mdx). The dorsiflexors were maximally activated isometrically for 200 ms prior to movement and then forcibly stretched through a 70° arc of plantarflexion at 900°/s. (a) Trace recordings of torque lengthening contractions (superimposed on a maximal lengthening contraction for 200 ms) for repetitions 1, 5, and 10 (black, pink, and red lines, resp.). (b) Maximal isometric torque was recorded at optimal length ( ) before (black line) and after (red line) injury. Note that mdx muscles generate at least the same absolute force, but they consistently showed a significant drop in torque (yellow arrow) compared to the wild-type muscles, with an average loss of 85% compared to 32% ( ) in normal mice. Not only do the mdx muscles sustain more force loss, but this usually occurs very early in the protocol (after the first few, resp.). = .