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A Second Look at Fiber Type Differentiation in Porcine Skeletal Muscle^{1 ,2,}

Muscle Biology Laboratory, University of Wisconsin, Madison 53706

Abstract

The differentiation of fiber types was investigated by morphological and histochemical methods in the superficial and deep portions of the porcine semitendinosus. With morphological methods, the differentiation of primary and secondary fetal muscle fibers was shown to follow the same pattern in both portions of the muscle; differentiation of fiber types with histochemical methods showed a marked difference between muscle portions. Primary fibers exhibited a positive reaction for acid-preincubated ATPase (Type I) in the deep portion of the muscle but not in the superficial portion. Secondary fibers initially exhibited a negative reaction for acid-preincubated ATPase (Type II) throughout the muscle, but in the deep portion, fibers located adjacent to single Type I fibers exhibited a conversion from Type II to Type I ATPase histochemistry. This conversion commenced between 90 and 105 days of gestation and continued through the third week of postnatal development. It appears r.hat this pattern of histochemical conversion gives rise to the Type I grouping observed in porcine skeletal muscle. Induction of acid ATPase differentiation preceded alkaline ATPase differentiation in both portions of the muscle.

These observations suggest that prenatal and postnatal histochemical differentiation of porcine skeletal muscle fibers is not determined by prenatal structural differentiation. Primary and secondary fibers were innervated shortly after their formation and secondary fibers were innervated prior to histochemical conversion. We suggest, therefore, that fiber type differentiation in the pig is neurally regulated. The hypothesis that collateral sprouting of first arrived axons occurs to innervate several nearby fibers is discredited by the low incidence of subterminal axon branching observed in postnatal pigs examined in this study.

¹ Supported by the College of Agricultural and Life Sciences, University of Wisconsin-Madison, and by a grant from the Muscular Dystrophy Association of America, Inc. Muscle Biology Manuscript No. 112.

² The technical assistance of T. Moen is gratefully acknowledged.

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