TitleShort-term sympathoadrenal inhibition augments the thermogenic response to beta-adrenergic receptor stimulation.
Publication TypeJournal Article
Year of Publication2010
AuthorsNewsom, SA, Richards, JC, Johnson, TK, Kuzma, JN, Lonac, MC, Paxton, RJ, Rynn, GM, Voyles, WF, Bell, C
JournalJ Endocrinol
Volume206
Issue3
Pagination307-15
Date Published09/2010
ISSN1479-6805
KeywordsAdrenergic alpha-Agonists, Adrenergic beta-Agonists, Adult, Analysis of Variance, Body Mass Index, Body Temperature Regulation, Calorimetry, Indirect, Clonidine, Energy Metabolism, Female, Humans, Isoproterenol, Male, Norepinephrine, Receptors, Adrenergic, beta, Sedentary behavior, Sex Factors, Sympathetic Nervous System
Abstract
 

Sedentary behavior is associated with an attenuated thermogenic response to beta-adrenergic receptor (beta-AR) stimulation, an important regulator of energy expenditure (EE) in humans. Chronic stimulation of beta-ARs, via heightened activity of the sympathoadrenal system, leads to diminished beta-AR function. We have investigated the hypothesis that the thermogenic response of sedentary adults to beta-AR stimulation will be increased during short-term sympathoadrenal inhibition. Using a randomly ordered, repeated measures study design, resting EE (REE; indirect calorimetry, ventilated hood technique) and the % increase in EE above REE (%DeltaEE) during acute i.v. isoproterenol administration (nonselective beta-AR agonist; 6, 12, and 24 ng/kg fat-free mass per min) were determined in 16 sedentary adults (nine females and seven males, 25+/-1 years, body mass index: 26.1+/-0.9 kg/m(2), maximal oxygen uptake: 40+/-2 ml/kg per min (mean+/-s.e.m.)) in the basal state and on the 6th day of transdermal clonidine administration (centrally acting alpha2-AR agonist; 0.2 mg/day). Relative to baseline, clonidine inhibited sympathoadrenal activity, as evidenced by decreased plasma norepinephrine concentration (1.04+/-0.13 vs 0.34+/-0.03 nmol/l; P<0.001), skeletal muscle sympathetic nerve activity (22.5+/-3.8 vs 8.5+/-1.9 bursts/min; P=0.003), and resting heart rate (63+/-2 vs 49+/-1 beats/min; P<0.001). Sympathoadrenal inhibition decreased REE (6510+/-243 vs 5857+/-218 kJ/day; P<0.001), increased respiratory exchange ratio (0.84+/-0.01 vs 0.86+/-0.01; P=0.03), and augmented the thermogenic response to beta-AR stimulation (%DeltaEE: 11+/-2, 16+/-2, and 24+/-2 vs 14+/-1, 20+/-2, and 31+/-2; P=0.04). These data demonstrate that in sedentary humans, short-term inhibition of sympathoadrenal activity increases the thermogenic response to beta-AR stimulation, an important determinant of EE and hence energy balance.

DOI10.1677/JOE-10-0152
Alternate JournalJ. Endocrinol.
PubMed ID20603265
Grant ListAG022053 / AG / NIA NIH HHS / United States