Sympathetic Activity in Obese Subjects With and Without Obstructive Sleep Apnea

Narkiewicz, Krzysztof; Borne, Philippe J. H. van de; Cooley, Ryan; Dyken, Mark Eric; Somers, Virend K.

doi:10.1161/01.cir.98.8.772

Cited by 461 publications

(329 citation statements)

References 37 publications

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“…The fact that excessive obesity [47] and increased visceral fat [48] have previously been associated with sympathetic nerve hyperactivity could indicate that the sympathetic hyperactivity in our diabetic group was even greater than that observed. However, there have been other reports showing that normal obese subjects without obstructive sleep apnoea have normal levels of sympathetic nerve activity [49] and that any increase in this activity over a wide range of body mass index can be attributed to a coexisting increase in age, hormonal levels and abdominal obesity [40,50,51]. Our findings are consistent with these reports, in that the normal-weight control group had a similar level of sympathetic nerve activity as the overweight group, at a time when both groups had no hormonal abnormality or obs- tructive sleep apnoea.…”

Section: Discussionmentioning

confidence: 94%

Disparity of autonomic control in type 2 diabetes mellitus

et al. 2004

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Aims/hypothesis: Acute insulinaemia activates the sympathetic drive in a nonuniform manner. The extent and nature of such activation in type 2 diabetic patients who do not have neuropathy have not yet been addressed despite evidence relating sympathetic activation to cardiovascular risk. We planned to determine the magnitude and extent of the sympathetic drive and its reflex responses in patients with type 2 diabetes and fasting hyperinsulinaemia. Methods: We measured resting muscle sympathetic nerve activity (MSNA) as the mean frequency of multiunit bursts and single unit muscle sympathetic nerve activity (s-MSNA) in 17 overweight patients with type 2 diabetes and two matched normal control groups comprising 17 overweight and 16 normal-weight subjects. We also tested the MSNA and s-MSNA responses to cold pressor and isometric hand-grip tests, along with the effect of sympatho-vagal balance on heart period variability. Results: Both MSNA and s-MSNA in the group with type 2 diabetes (66±3.5 bursts/100 beats and 78±4.5 impulses/100 beats) were greater (at least p<0.0001) than in the overweight control group (42±2.6 bursts/100 beats and 48±3.4 impulses/100 beats) and normal-weight control group (43±6.2 bursts/100 beats and 51±7.1 impulses/100 beats), though the three groups had similar reflex responses, baroreflex sensitivity and sympathovagal balance controlling the heart period. Conclusions/ interpretation: The patients with type 2 diabetes had no evidence of impaired reflex or autonomic control of heart period variability at a time when there was central sympathetic activation to the periphery. Furthermore, being overweight itself was not associated with sympathetic activation.

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Section: Discussionmentioning

confidence: 94%

Disparity of autonomic control in type 2 diabetes mellitus

et al. 2004

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“…It has been suggested, however, that an elevated efferent sympathetic activity in the peroneal nerves may not characterize all obese patients, but only those concomitantly affected by obstructive sleep apnea, an issue, which is still a matter of debate. 11,12 There has been one reported exception in the findings of high SNS activity with increasing adiposity. Pima Indians have the highest reported prevalence of obesity and hyperinsulinemia in the world, but a relatively low presence of hypertension and atherosclerotic disease.…”

Section: Sympathetic Activation In Obesitymentioning

confidence: 99%

Mechanisms of obesity-induced hypertension

et al. 2010

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The relationship between obesity and hypertension is well established both in children and adults. The mechanisms through which obesity directly causes hypertension are still an area of research. Activation of the sympathetic nervous system has been considered to have an important function in the pathogenesis of obesity-related hypertension. The arterial-pressure control mechanism of diuresis and natriuresis, according to the principle of infinite feedback gain, seems to be shifted toward higher blood-pressure levels in obese individuals. During the early phases of obesity, primary sodium retention exists as a result of increase in renal tubular reabsorption. Extracellular-fluid volume is expanded and the kidney-fluid apparatus is resetted to a hypertensive level, consistent with a model of hypertension because of volume overload. Plasma renin activity, angiotensinogen, angiotensin II and aldosterone values display significant increase during obesity. Insulin resistance and inflammation may promote an altered profile of vascular function and consequently hypertension. Leptin and other neuropeptides are possible links between obesity and the development of hypertension. Obesity should be considered as a chronic medical condition, which is likely to require long-term treatment. Understanding of the mechanisms associated with obesity-related hypertension is essential for successful treatment strategies. Hypertension Research (2010) 33, 386-393; doi:10.1038/hr.2010.9Keywords: leptin; obesity; pressure natriuresis; rennin-angiotensin-aldosterone system; sympathetic nervous system INTRODUCTION Obesity is a common disorder that develops from the interaction between the genotype and the environment and involves social, behavioral, cultural, physiological, metabolic and genetic factors. A large number of studies have shown that obesity has an important negative impact on health in a population, leading to the recommendation for general practitioners to have an important function in the management of this condition and of its associated comorbidities such as hypertension, hyperlipidemia and hyperinsulinemia/insulin resistance. The relationship between obesity and hypertension is well established both in adults and children. 1,2 Obese individuals exhibit higher levels of office as well as ambulatory blood pressure (BP) from childhood to old age. Obese subjects display higher BP levels than non-obese individuals even in the normotensive range. The combination of obesity, hypertension and other cardiovascular risk factors significantly increases the probability of adverse cardiovascular outcomes, and raises considerations for aggressive treatment strategies. 3 The mechanisms through which obesity directly causes hypertension are still an area of research. Human and animal studies have elucidated the function of adipose tissue derivatives (adipokines and cytokines), neurohumoral pathways, metabolic functions and modulation of pressor/depressor mechanisms. Although obesity-related hypertension may be the result of a combinatio...

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“…36 This effect depends on the marked adrenergic overdrive caused by abnormalities in the apnea/hypopnea index as measured by nighttime polysomnographic evaluation. 37,38 BLOOD PRESSURE VARIABILITY AND SYMPATHETIC NEURAL FACTORS Blood pressure variability is influenced by sympathetic factors. Originally documented in experimental animals, 39 this finding has also been confirmed in humans by spectral analysis of heart rate 40 and more recently by the direct microneurographic approach.…”

Section: Mechanisms Involved In Diurnal Blood Pressure Variationsmentioning

confidence: 99%

Diurnal blood pressure variation and sympathetic activity

et al. 2010

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Blood pressure changes occurring over a 24-h period are under behavioral, humoral and reflex regulation. The sympathetic nervous system modulates blood pressure variation by affecting cardiac output and peripheral vascular resistance. This paper reviews evidence for the relationship between adrenergic neural drive and blood pressure as measured by direct and indirect approaches. This paper also reviews the sympathetic activity associated with increased 'in-office' and 'out-of-office' blood pressure, that is, the white-coat and the masked-hypertensive states. Finally, this paper examines altered neuroadrenergic influences on nocturnal blood pressure reduction and blood pressure variability.

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Sympathetic Activity in Obese Subjects With and Without Obstructive Sleep Apnea

Abstract: Obesity alone, in the absence of OSA, is not accompanied by increased sympathetic activity to muscle blood vessels.

Cited by 461 publications

References 37 publications

Disparity of autonomic control in type 2 diabetes mellitus

Disparity of autonomic control in type 2 diabetes mellitus

Mechanisms of obesity-induced hypertension

Diurnal blood pressure variation and sympathetic activity

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