METABOLIC AND HORMONAL RESPONSES TO ADRENOCEPTOR ANTAGONISTS IN EXERCISING RATS

alpha- and beta-adrenoceptors play a key role in the regulation of nutrient supply to working muscles during exercise. To assess their influence in the regulation of substrate utilization, rats were studied during alpha- or beta-adrenoceptor blockade. Energy metabolism was studied by means of indirect calorimetry before, during, and after moderate swimming exercise. Blood samples were taken far the determination of nutrient and hormone concentrations. In addition, central venous blood samples were withdrawn for determination of blood gases, pH, and total hemoglobin concentration (c/Hb). alpha- and beta-adrenoceptor blockade decreased the rates of energy expenditure (EE) and fat oxidation (fat-ox) during and after swimming in comparison to swimming without adrenoceptor blockade. The oxidation of carbohydrates (CHO-ox) was increased in both cases. alpha-Blockade prevented the exercise-induced increase in blood glucose, plasma free fatty acids (FFA) were not affected, and plasma insulin, norepinephrine (NOR), epinephrine (EPI), and lactate were markedly increased. beta-adrenoceptor blockade prevented the exercise-induced increases in blood glucose and FFA. EPI increased slightly more than and NOR less than in the control experiment. The exercise-induced decrease in insulin was more pronounced after beta-blockade. alpha-Blockade caused a less pronounced decrease in venous oxygen saturation (SO2) and tension (PO2) than in the control experiment. The exercise-induced increase in carbon dioxide tension (PCO2) was almost absent. After beta-blockade, venous SO2 and PO2 decreased more and PCO2 increased more than in the control experiment. It is concluded that both alpha- and beta-blockade restrict the rate of EE during exercise. In the case of beta-blockade, this may be due to an insufficient supply of nutrients, mainly FFA, although the oxygen supply to the muscles also seems to be diminished by inhibition of the exercise-induced increase in cardiac output and prevention of beta-adrenergically mediated vasodilatation in working muscles. In the case of alpha-blockade, the restriction of energy metabolism seems mainly to be due to an insufficient supply of oxygen caused by prevention of redistribution of cardiac output mainly resulting from insufficient vasoconstriction in the visceral vascular bed. Copyright (C) 1995 by W.B. Saunders Company