Author:
Trudeau F.,Péronnet F.,Béliveau L.,Brisson G.
Abstract
The respective roles of allosteric regulators and catecholamines in the control of muscle glycogen breakdown during exercise remain a matter of controversy. This study was designed to reassess the role of the sympathoadrenal system during prolonged exercise in rats. Animals were studied at rest or after treadmill exercise (28 m∙min−1; 8% slope) to exhaustion in a control situation or following administration of a specific β2-adrenergic receptor antagonist (ICI 118,551, 1 mg∙kg−1, i.v.). Running times to exhaustion were 54 and 36 min in control and treated rats, respectively. For the purpose of comparison, another group of control rats was studied after a 36-min exercise bout. The reduction in endurance in treated rats was associated with an impairment in glycogen utilization, as measured by muscle glycogen stores, in soleus muscle but not in superficial vastus lateralis or gastrocnemius lateralis muscles. Utilization of liver glycogen stores was similar in the two groups of animals, but plasma glucose (7 vs. 13 mM) and lactate (4 vs. 7 mM) levels were significantly lower in rats under β-blockade than in control rats run for 36 min. Plasma free fatty acid and glycerol concentrations were not significantly different between groups. On the other hand, plasma epinephrine concentration was significantly higher in treated rats (13 vs. 5 mM), which might reflect a compensatory increase in adrenal activity. These results suggest that glycogen breakdown during prolonged exercise is under the control of the sympathoadrenal system in predominantly slow-twitch but not in predominantly fast-twitch muscles. Epinephrine appears to play an important role in the maintenance of blood glucose level during prolonged exercise by (i) promoting muscle glycogen breakdown and thus reducing peripheral glucose utilization, and (ii) possibly increasing lactate availability for hepatic gluconeogenesis.Key words: glycogen, catecholamines, sympathoadrenal system, fiber type.
Publisher
Canadian Science Publishing
Subject
Physiology (medical),Pharmacology,General Medicine,Physiology
Cited by
8 articles.
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