Adiposity-independent sympathetic activity in black men
ABSTRACT Obesity is thought to lead to sympathetic overactivity as a compensatory adjustment to weight gain. However, most of the experimental support for the hypothesis has been derived from white cohorts. Our previous study in blacks indicated that sympathetic nerve activity (SNA) is closely correlated with body mass index only in women, whereas, in black men, SNA is elevated and dissociated from adiposity (Abate et al., Hypertension 38: 379-383, 2001). To further determine whether total and regional adiposity are determinants of SNA in blacks, we performed a prospective weight loss study in 12 normotensive obese black men and 9 obese black women. SNA, body mass index, and abdominal fat mass were measured before and 16 wk after hypocaloric diet. The major new findings are that, in obese black men, the dietary-induced weight loss of 11.3+/-0.8 kg resulted in reduction in plasma leptin, insulin, and visceral abdominal fat but had no effect on SNA (from baseline of 26+/-4 to 28+/-3 bursts/min, P=not significant). In contrast, in black women, weight loss of 8.0+/-0.9 kg caused similar reductions in plasma leptin, insulin, and visceral abdominal fat and led to a reduction in SNA by 40% (from baseline of 22+/-2 to 13+/-3 bursts/min, P<0.05). In conclusion, these new data from this prospective study provide strong support for a major adiposity-independent sympathetic activity in black men and adiposity-related sympathetic activity in black women.
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ABSTRACT: The hemodynamic responses to exercise have been studied to a great extent over the past decades, and an exaggerated blood pressure response during an acute exercise bout has been considered as an indicator of cardiovascular risk. Obesity is a major factor influencing the blood pressure response to exercise since evidence indicates that the arterial pressure response to exercise is exacerbated in obese compared with lean adults. Signs of augmented responses (such as an exaggerated blood pressure response) to physical exertion appear early in life (from the prepubertal years) in obese individuals. Understanding the mechanisms that drive the altered hemodynamic responses during exercise in obese individuals and prevent the progression to hypertension is vitally important. This paper focuses on the evidence linking obesity with alterations of the autonomic nervous system and discusses the potential mechanisms and consequences of the altered sympathetic nervous system behavior in obese individuals at rest and during exercise. Furthermore, this paper presents the alterations in the reflex regulatory mechanisms ("exercise pressor reflex" and baroreflex) in obese children and adults and addresses the effects of training on obesity-related disturbances.Journal of obesity 05/2012; 2012:147385. DOI:10.1155/2012/147385
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ABSTRACT: Metabolic syndrome is associated with adverse health outcomes and is a growing problem worldwide. Although efforts to harmonise the definition of metabolic syndrome have helped to better understand the prevalence and the adverse outcomes associated with the disorder on a global scale, the mechanisms underpinning the metabolic changes that define it are incompletely understood. Accumulating evidence from laboratory and human studies suggests that activation of the sympathetic nervous system has an important role in metabolic syndrome. Indeed, treatment strategies commonly recommended for patients with metabolic syndrome, such as diet and exercise to induce weight loss, are associated with sympathetic inhibition. Pharmacological and device-based approaches to target activation of the sympathetic nervous system directly are available and have provided evidence to support the important part played by sympathetic regulation, particularly for blood pressure and glucose control. Preliminary evidence is encouraging, but whether therapeutically targeting sympathetic overactivity could help to prevent metabolic syndrome and attenuate its adverse outcomes remains to be determined.04/2014; 3(2). DOI:10.1016/S2213-8587(14)70033-6