The recovery of functional continuity after crush injury was measured by a simple electrophsiological technique in semitendinosus muscles of normal and dystrophic mice of the C57BL6J(dy2Jdy2J) strain. In contrast to virtually complete restitution in normal muscles, only one-third of fibers regained continuity in dystrophic muscles. The study also confirmed the lower resting membrane potentials of dystrophic fibers and the presence of “functional” denervation in some of them.

The possibility was examined that fibrillation potentials may occur in those parts of muscle fibers which become functionally denervated following segmental necrosis. Focal necrotic lesions were induced in rat semitendinosus muscles by crushing, ligating, or cutting muscle fibers. When the treated muscles were examined microscopically and recordings made with intracellular or extracellular electrodes, fibrillations were found to be either completely absent or extremely infrequent. Fibrillation potentials were also absent in the brachioradialis muscle of a human subject after myotomy. In contrast to these negative results, surgical denervation of the rat semitendinosus induced fibrillation activity within 3 days; when fully developed, fibrillations occurred in approximately one-half of the fibers at any time. The findings are considered to have significance for an understanding of the pathogenesis of those “myopathic” disorders in which fibrillations are found.

Extracellular and intracellular recordings of directly evoked action potentials were used to detect the restoration of functional continuity in regenerating rat semitendinosus muscle fibers. After a crush lesion, muscle fibers became almost fully depolarized at the site of injury and some decrease in resting potential could be detected several millimeters on either side of the lesion. Functional continuity was reestablished in some fibers by the 5th day and in all fibers by the 30th day after crushing. At first, impulse propagation was delayed in the regenerating segments of fibers but normal response latencies were attained by the 30th day.