Effects of terbutaline on basal thermogenesis of human skeletal muscle and Na‐K pump after 1 week of oral use—a placebo controlled comparison with propranolol.

1. A double‐blind placebo‐controlled study was conducted on the effects of oral terbutaline (beta 2‐adrenoceptor agonist) and propranolol (beta 1 beta 2‐adrenoceptor antagonist) on basal heat production of skeletal muscle, measured ex vivo by direct microcalorimetry. Terbutaline slow‐ release 7.5 mg, propranolol 80 mg, and matching placebo were randomly administered twice daily for 1 week to 15 healthy males, using a cross‐ over design. 2. Resting heat production in biopsied vastus lateralis was lowered by median 27% (P < 0.01) after terbutaline medication as compared with placebo. The cause of this hypometabolism at the cellular level is obscure but may possibly be explained by desensitization of beta 2‐receptors. 3. Propranolol decreased the metabolic rate by 17% (P > 0.3); this might imply that the sympathetic nervous system is playing only a minor role in the regulation of basal metabolic rate in muscle, or that up‐regulation of beta‐receptors had influenced the decline. 4. The muscle utilized about 6% of its total energy for the Na‐K pump as assessed after inhibition by ouabain. 5. Serum potassium was significantly lowered by terbutaline and slightly increased by propranolol with no relationship between changes in extracellular levels and muscle content of potassium under resting conditions. Energy values for the Na‐K pump in muscle after 1 week of terbutaline or propranolol medication were similar to placebo. The results are not consistent with the hypothesis that decreased serum potassium during continuous beta 2‐adrenoceptor agonist treatment is due to a chronically activated Na‐K pump, at least not in resting muscle.