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  • Title: Haemodynamic and metabolic responses to prolonged exercise after chronic beta 1-adrenoceptor blockade in hypertensive man.
    Author: Frisk-Holmberg M, Juhlin-Dannfelt A, Aström H.
    Journal: Clin Physiol; 1985 Jun; 5(3):231-42. PubMed ID: 2860992.
    Abstract:
    The influence of chronic beta 1-adrenoceptor blockade on haemodynamic and metabolic responses was examined in eight young hypertensive subjects during a 40 min submaximal bicycle test at 50% of maximal capacity. The patients were randomly allocated to one placebo and one treatment period of 6 weeks. During treatment atenolol (Tenormin, 100 mg) was given twice daily. Arterial pressure, cardiac output, leg blood flow, oxygen uptake and different metabolites in the blood were determined. The heart rate was reduced by beta 1-adrenoceptor blockade by 30% during exercise, and the decrease was related to plasma concentration of the drug. Cardiac output was decreased by approximately 10%, but the negative chronotropic effect was partly compensated for by a higher stroke volume. Blockade leg blood flow was reduced by 10%, but more oxygen was extracted, giving an unchanged oxygen uptake. Blood concentration and leg uptake of glucose were not influenced by the treatment, but plasma free fatty acids were reduced by 30-40%. Leg lactate release was decreased to half the value in the unblocked situation. Plasma renin activity did not increase at the beginning of exercise, but after 40 min an increase was seen, though only to half of the pretreatment value. It is concluded that beta 1-adrenoceptor blockade during submaximal exercise reduces blood flow to the working muscles and that this reduction is the result of a lower cardiac output. Aerobic metabolism is unchanged as a result of increased oxygen extraction, but less fat is used as lipolysis is inhibited. Glucose uptake by the working muscles is unchanged by beta 1-blockade, but there is evidence for an increased carbohydrate metabolism. As for non-selective blockade, atenolol decreases lactate release but this could be the result of non-specific action on the beta 1-receptor and/or increased carbohydrate oxidation. Furthermore, the beta 1-adrenoceptors seem to have a major influence on the renin release during exercise.
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