Metabolic activity during the degenerative and early regenerative stages of minced skeletal muscle Supported by NIH grant 5 t01 GM 00312-10 and funds from Muscular Dystrophy Association of America. The material in this paper is taken from a dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy, University of Michigan, Ann Arbor, Michigan. Reported earlier in abstract form (Snow, '71).

Abstract

In the rat, autotransplanted minced skeletal muscle undergoes degenerative changes prior to the regeneration of a whole muscle. In this study, both the degenerative and early regenerative processes were examined using histochemical procedures for the localization of glycogen, neutral lipid, phosphorylase, lactate dehydrogenase, cytochrome oxidase, glucose-6-phosphate dehydrogenase and non-specific esterases. Glycogen and phosphorylase activity disappeared in all muscle fibers within 24 hours after mincing. Vascular injections of ink demonstrated that during the second to tenth days after mincing a central ischemic zone of degenerating minced muscle was surrounded by a vascularized zone of regenerating muscle. Lactate dehydrogenase staining persisted during the first week in the degenerating muscle fragments of the central zone. This latter histochemical observation was supported by quantitative evidence which showed that degenerating muscle isolated from the central zone of four day regenerates produced lactic acid in the presence of glucose. Cytochrome oxidase activity decreased rapidly in the degenerating muscle while succinic dehydrogenase persisted somewhat longer. Although non-specific esterases and glucose-6-phosphate dehydrogenase activities were not significant in normal muscle, they were histochemically detectable in degenerating muscle during the first week. The capacity for anaerobic metabolism apparently persists in the degenerating minced muscle for several days; this energy source may be sufficient to maintain the myogenic cells in an environment of degeneration and ischemia until they become reassociated with a vascular supply.