Effect of β-Adrenoceptor Blockade on Exercise Performance and Metabolism

Abstract

1. Carbohydrate and lipid metabolism and the capacity to perform prolonged submaximal physical exercise were studied in six young healthy subjects treated in a randomized double-blind fashion for 2 days with either placebo, the non-selective beta-adrenoceptor antagonist propranolol (80 mg b.i.d.) or the cardioselective agent metoprolol (100 mg b.i.d.). On day 3, 1 h after the last dose, the subjects exercised for 30 min periods followed up 10 min rest up to the point of exhaustion. 2. The capacity to perform exercise was decreased with both beta-adrenoceptor antagonists. However, at an equal degree of beta 1-adrenoceptor blockade, all subjects could exercise for a longer period of time on the cardioselective agent as compared with the non-selective drug. 3. Blood glucose levels decreased during exercise irrespective of the type of treatment, but the attenuation occurred most rapidly on propranolol. At exhaustion the average non-esterified fatty acid levels had increased 256% on placebo, 148% on metoprolol and 65% on propranolol. A significant positive correlation was found between changes in non-esterified fatty acid levels during exercise and total working time. It is concluded that beta-adrenoceptor blockade diminishes the capacity for prolonged sub-maximal exercise at least in part by reducing the availability of substrates to the working muscles.

Beta‐adrenoceptor blocking agents and lipolysis.

“…The relatively weak antilipolytic effect of cardioselective 3-adrenoceptor blocking agents has been found in studies using either isoprenaline or adrenaline as the agonist and was also reported in a study using exercise induced sympathetic activation as the agonist (Harms et al, 1978;William-Olsson et al, 1979;Lundborg et al, 1981;Raptis et al, 1981).…”

“…(1981) and Lundborg et al (1981), who reported that the cardioselective agent metoprolol, after a normal therapeutic dose of 100 mg p.o., significantly reduced both basal and exercise induced increases of free fatty acid plasma levels, under conditions where noradrenergic rather than adrenergic activation is operant. At these dose levels, there is no or only minimal P2-adrenoceptor blockade, as judged by effects on respiration (Thiringer & Svedmyr, 1976).…”

Effects of beta‐adrenoceptor blockade on exercise performance and respiratory response in healthy, physically untrained humans.

“…One such mechanism may be the change in the balance between free fatty acids and carbohydrates as an energy source for exercise. It is known that propranolol inhibits either lipolysis or glycolysis (Lundborg et al, 1981;Deacon, 1978;Issekutz, 1978), but it is also likely that the utilization of free fatty acids as a fuel is more compromised than that of glucose (Lundborg et al, 1981). Under these circumstances V0, must be reduced, since the caloric value of 1 1 Of 02 iS greater for carbohydrates than fat metabolism, whereas tissue respiratory quotient (RQ) increases (Christensen & Hansen, 1939;Douglas & Priestly, 1948).…”

Effects of selective beta 2‐adrenoceptor blockade on serum potassium and exercise performance in normal men.

“…Exercise performance ,B-adrenoceptor antagonists are known to cause muscle fatigue and reduced exercise performance in hypertensive and healthy subjects (Epstein et al, 1965;Gullestad et al, 1988Gullestad et al, , 1989aLundborg et al, 1981;Pearson et al, 1979;Sklar et al, 1982), more pronounced with non-selective than with 1l-selective agents (Gullestad et al, 1988;Lundborg et al, 1981). The present study demonstrates that the reduction in exercise performance with each of the 1l-and P2-adrenoceptor blockers amounted to 50% of that obtained with the non-selective agent.…”

“…The rise in potassium during exercise is potentiated by non-selective and to a lesser extent by selective 13l-adrenoceptor antagonists (Carlsson et al, 1978;Gullestad et al, 1988Gullestad et al, , 1989aLundborg et al, 1981;McDonald et al, 1984), which has led to the assumption that the exercise-induced increase in potassium by ,B-adrenoceptor antagonists is 32-adrenoceptor dependent.…”