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• W2000225993 abstract "After strenuous exercise there is a sustained increase in resting O2 consumption. The magnitude and duration of the excess post-exercise O2 consumption (EPOC) is a function of exercise intensity and exercise duration. Some of the mechanisms underlying the rapid EPOC component (<1 h) are well defined, while the mechanisms causing the prolonged EPOC component (>1 h) are not fully understood. It has been suggested that beta-adrenergic stimulation is of importance for the prolonged component. There is an increased level of plasma adrenaline and noradrenaline during exercise, and it is shown that catecholamines stimulate energy expenditure through beta-adrenoceptors. After exercise an increased fat oxidation and an increased rate of triglyceride fatty acid (TG-FA) cycling may account for a significant part of the prolonged EPOC component. These processes may be stimulated by catecholamines. However, the return of plasma concentration of catecholamines to resting levels after exercise is more rapid than the return of O2 uptake. But plasma concentration of catecholamines may be an insensitive indicator of sympathetic activity, since the clearance rate of catecholamines is high. Also, the sensitivity to catecholamines may be increased after exercise. A decreased post-exercise O2 uptake has been shown when beta-blockade is administered in dogs before the exercise bout. In a pilot study in humans, administration of beta-antagonist after exercise did not seem to change EPOC." @default.
• W2000225993 created "2016-06-24" @default.
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• W2000225993 date "1998-02-01" @default.
• W2000225993 modified "2023-10-17" @default.
• W2000225993 title "Adrenergic control of post-exercise metabolism" @default.
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• W2000225993 doi "https://doi.org/10.1046/j.1365-201x.1998.0321e.x" @default.
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