Abstract
The effect of intravenous administration of propranolol and/or epinephrine on glycogen stores in the dog gastrocnemius-plantaris muscle group was assessed at rest and following 30 min of contractions. In resting muscle, glycogen stores were not altered 60 min following propranolol (0.5 mg/kg) nor did a 10 min infusion of epinephrine (1 μg/kg/min) induce glycogenolysis. Following 30 min of contractions at 5 twitches/s, about 30% of the muscle glycogen stores were depleted. This rate of glycogenolysis was unaffected by prior administration of propranolol, suggesting that the breakdown of glycogen during electrical stimulation of the muscle group is not mediated through activation of beta receptors. When epinephrine was infused during the last 10 min of the contraction period, about 50% of the initial glycogen stores was depleted. This epinephrine-induced glycogenolysis was mediated through activation of beta receptors as it was abolished by pretreatment of the animals with propranolol. These data suggest that the relatively small breakdown of glycogen stores in the gastrocnemius-plantaris during electrical stimulation of the muscle group may reflect the lack of an increase in circulating catecholamines.
Publisher
Canadian Science Publishing
Subject
Physiology (medical),Pharmacology,General Medicine,Physiology
Cited by
13 articles.
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