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Strength loss induced by lengthening contractions is typically attributed to damaged force‐bearing structures within skeletal muscle. Muscle lacking the structural protein dystrophin, as in Duchenne muscular dystrophy, is particularly susceptible to contraction‐induced injury.

We tested the hypothesis that changes in neuromuscular junctions (NMJs) contribute to strength loss following lengthening contractions in wild‐type and in dystrophic skeletal muscle.

NMJs in dystrophic (mdx) mice, the murine model of Duchenne muscular dystrophy, show discontinuous and dispersed motor end‐plate morphology. Following lengthening contractions, mdx quadriceps muscles show a greater loss in force, increased neuromuscular transmission failure and decreased electromyographic measures compared to wild‐type.

Consistent with NMJ disruption as a mechanism contributing to this force loss, only …