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Am J Physiol Endocrinol Metab 280: E740-E744, 2001;
0193-1849/01 $5.00
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Vol. 280, Issue 5, E740-E744, May 2001

Direct evidence for tonic sympathetic support of resting metabolic rate in healthy adult humans

Mary Beth Monroe1, Douglas R. Seals1,2, Linda F. Shapiro1,2, Christopher Bell1, David Johnson3, and Pamela Parker Jones1

1 Department of Kinesiology and Applied Physiology, University of Colorado at Boulder, Boulder 80309; 2 Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado 80262; and 3 Department of Medicine, University of Arizona Health Sciences Center, Tucson, Arizona 85724

The sympathetic nervous system (SNS) plays an important role in the regulation of energy expenditure. However, whether tonic SNS activity contributes to resting metabolic rate (RMR) in healthy adult humans is controversial, with the majority of studies showing no effect. We hypothesized that an intravenous propranolol infusion designed to achieve complete beta -adrenergic blockade would result in a significant acute decrease in RMR in healthy adults. RMR (ventilated hood, indirect calorimetry) was measured in 29 healthy adults (15 males, 14 females) before and during complete beta -adrenergic blockade documented by plasma propranolol concentrations >= 100 ng/ml, lack of heart rate response to isoproterenol, and a plateau in RMR with increased doses of propranolol. Propranolol infusion evoked an acute decrease in RMR (-71 ± 11 kcal/day; -5 ± 0.7%, P < 0.0001), whereas RMR was unchanged from baseline levels during a saline control infusion (P > 0.05). The response to propranolol differed from the response to saline control (P < 0.01). The absolute and percent decreases in RMR with propranolol were modestly related to baseline plasma concentration of norepinephrine (r = 0.38, P = 0.05; r = 0.44, P = 0.02, respectively). These findings provide direct evidence for the concept of tonic sympathetic beta -adrenergic support of RMR in healthy nonobese adults.

sympathetic nervous system; resting energy metabolism; beta -adrenergic blockade


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