Development and growth of extensor carpi radialis longus muscle in normal and dystrophic chickens.

The development and growth of the skeletal muscles in normal and dystrophic chickens were studied to obtain a clue to the mechanism of dystrophic pathogenesis. A relatively small and isolated muscle--the extensor carpi radialis longus (ECRL) muscle--was utilized to analyze quantitatively the histologic and physiologic parameters. Both normal and dystrophic chickens attained qualitatively the same parameters, but there were some quantitative differences. The first disorder to appear in the dystrophic muscle was a substantial retardation of muscle cell proliferation in the early postnatal development, and the fiber loss was fully compensated by hypertrophy of the remaining cells. The succeeding abnormalities in the dystrophic muscle, e.g., reduction of efficiency in the tension output per unit area, were interpreted as compensating reactions. Therefore, it is likely that the dystrophic lesions in avian muscular dystrophy are caused by retardation of muscle cell proliferation in the early postnatal period. Possible mechanisms for the retardation are discussed in terms of the nerve--muscle trophic interactions which could be greatly intensified in the early postnatal period.