[beta]1-adrenoreceptors regulate resting metabolic rate

This was a randomized, cross-over experiment designed to determine whichβ-adrenergic receptors, β1, β2, or both, regulate metabolic rate in humans. All subjects (3 women, 4 men) were administered a 7-d therapeutic dose of a selective β1-antagonist (atenolol 50 mg BID), a combined β1,β2-antagonist (propranolol 80 mg BID), and a placebo control (BID). Indirect calorimetry was determined before and after 1 h of submaximal exercise. Exercise was performed at 50% of the trial specific˙VO_2peak because maximal exercise was significantly decreased in the presence of the nonselective β1, β2-antagonist(˙VO_2peak placebo: 44.90 ± 4.40 mL·kg^-1·min^-1 vs β1, β2-antagonism: 39.20 ± 3.00 mL·kg^-1·min^-1; P< 0.05). Both the β1 and the combined β1, β2-adrenoreceptor antagonists reduced resting oxygen consumption to a similar extent (0.247± 0.007 L·min^-1 placebo, vs 0.218 ± 0.007 L·min^-1 β1-antagonism, vs 0.226 ± 0.007 L·min^-1 β1,β2-antagonism; P < 0.05). However, the 30-min and 60-min excess post-exercise oxygen consumption (mean EPOC) remained unchanged. It is concluded that the β1-receptors are regulating the effects of the sympathetic nervous system on resting but not exercise recovery metabolic rate. These metabolic side effects may suggest that changes need to be made in the nutritional requirements of patients usingβ-adrenergic antagonists.