Serum enzymes and lactic dehydrogenase isoenzymes after exercise and training in rats

¹ Laboratory of Experimental Pathology and Laboratory of Physical Biology, National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Maryland

After 16 hr exercise, untrained rats, in contrast to exercise-trained rats, show a marked rise in serum lactic dehydrogenase, aldolase, glutamic oxalacetic transaminase, glutamic pyruvic transaminase, and urea nitrogen. Electrophoretic studies reveal abnormal serum isoenzyme patterns indicating that excess lactic dehydrogenase is derived not only from muscle, but also from heart and probably other organs. Histopathologic studies and serum transaminase ratios support this conclusion. These findings are correlated with necrosis in muscle fibers and fatty changes in muscle, heart, and other organs of untrained rats after prolonged exercise and the absence of such changes in similarly exercise-trained animals. Alterations in cellular permeability best explain the rise in serum enzymes. However, exercise training does not prevent pathologic and serum enzyme and isoenzyme changes induced by epinephrine in oil. Moreover, the adrenergic blocking agent, Dibenamine, which ameliorates such changes induced by epinephrine or hypoxia, does not mitigate the effects of prolonged exercise in untrained rats. These findings suggest that the permeability changes induced by prolonged exercise are not due merely to the effects of hypoxia or of catecholamines released from the adrenal medulla, but are different and perhaps specific.

Key Words: serum aldolase • serum transaminases • exercise histopathology • epinephrine • Dibenamine • zymosan stress; muscle necrosis • fatty changes

Submitted on December 26, 1963