Effects of beta-adrenergic receptor blockade on glycogenolysis during exercise.
The purpose of this study was to determine whether beta-adrenergic receptor blockade inhibits glycogen utilization in rats during exercise. Propranolol (1 mg/kg body wt) completely blocked the glycogenolytic effect of a large dose of epinephrine given by injection but did not prevent glycogen breakdown in skeletal muscle or liver during a bout of treadmill exercise. On the contrary, exercise resulted in greater glycogen depletion in plantaris muscles of beta-blocked rats than in those of control rats, probably as a result of decreased availability of fatty acids. Increasing the availability of exogenous substrates slowed the rate of skeletal muscle glycogen depletion during exercise. However, even with increased availability of exogenous substrates, beta-blockade did not result in reduced utilization of skeletal muscle or liver glycogen. In contrast to its effect on skeletal muscle, beta-blockade markedly reduced glycogen depletion in the heart during exercise. We conclude that beta-adrenergic stimulation is of major importance in mediating glycogenolysis in the heart but is not necessary for glycogenolysis in skeletal muscle or liver during prolonged exercise.
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D004837:Epinephrine / Q000494:pharmacology; D005230:Fatty Acids, Nonesterified / Q000097:blood; D006003:Glycogen / Q000032:analysis / Q000378:metabolism*; D006801:Humans; D008297:Male; D009132:Muscles / Q000032:analysis / Q000378:metabolism; D005082:Physical Exertion; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013315:Stress, Psychological / Q000378:metabolism
D000319:Adrenergic beta-Antagonists; D005230:Fatty Acids, Nonesterified; D006003:Glycogen; D011433:Propranolol; D004837:Epinephrine