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Obstructive sleep apnea-dependent and -independent adrenergic activation in obesity

Clinica Medica, Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie Sanitarie, Università Milano-Bicocca, Ospedale San Gerardo, Monza, Milan, Italy.
Hypertension (Impact Factor: 7.63). 08/2005; 46(2):321-5. DOI: 10.1161/01.HYP.0000174243.39897.6c
Source: PubMed

ABSTRACT No agreement exists as to the mechanisms responsible for the sympathetic hyperactivity characterizing human obesity, which has been ascribed recently to a chemoreflex stimulation brought about by obstructive sleep apnea rather than to an increase in body weight, per se. In 86 middle-age normotensive subjects classified according to body mass index, waist-to-hip ratio, and apnea/hypopnea index (overnight polysomnographic evaluation) as lean and obese subjects without or with obstructive sleep apnea, we assessed via microneurography muscle sympathetic nerve traffic. The 4 groups were matched for age, gender, and blood pressure values, the 2 obese groups with and without obstructive sleep apnea showing a similar increase in body mass index (32.4 versus 32.0 kg/m2, respectively) and waist-to-hip ratio (0.96 versus 0.95, respectively) compared with the 2 lean groups with or without obstructive sleep apnea (body mass index 24.3 versus 23.8 kg/m2 and waist-to-hip ratio 0.77 versus 0.76, respectively; P<0.01). Compared with the nonobstructive sleep apnea lean group, muscle sympathetic nerve activity showed a similar increase in the obstructive sleep apnea lean group and in the nonobstructive sleep apnea obese group (60.4+/-2.3 and 59.3+/-2.0 versus 40.9+/-1.8 bs/100 hb, respectively; P<0.01), a further increase being detected in obstructive sleep apnea subjects (73.1+/-2.5 bursts/100 heart beats; P<0.01). Our data demonstrate that the sympathetic activation of obesity occurs independently in obstructive sleep apnea. They also show that this condition exerts sympathostimulating effects independent of body weight, and that the obstructive sleep apnea-dependent and -independent sympathostimulation contribute to the overall adrenergic activation of the obese state.

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    • "Espino et al. (2011) showed that melatonin could reduce insulin secretion during sleep, preventing the development of obesity . Human obesity is also characterized by marked sympathetic activation (Grassi et al. 2005). Cardiac sympathetic activity was increased by weight gain during wakefulness and sleep (Adachi et al. 2011). "
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    ABSTRACT: During the past several decades, obesity has been increasing globally. In Japan, obesity is defined by a BMI of 25 kg/m(2) or over; 28.6 % of men and 20.6 % of women are obese. Obese people have an increased incidence of developing cardiovascular, renal, and hormonal diseases and sleep disorders. Obese people also have shortened sleep durations. We investigated seasonal differences in melatonin concentrations, heart rates, and heart rate variability during sleep in obese subjects in Japan. Five obese (BMI, 32.0 ± 4.9 kg/m(2)) and five non-obese (BMI, 23.2 ± 2.9 kg/m(2)) men participated in this study in the summer and winter. Electrocardiograms were measured continuously overnight in a climatic chamber at 26 °C with a relative humidity of 50 %. Saliva samples for melatonin were collected at 2300 hours, 0200 hours, and 0600 hours. We found that melatonin concentrations during sleep in obese subjects were significantly lower than those in non-obese subjects in the winter. Heart rate during sleep in winter was significantly higher than that in summer in both obese and non-obese subjects. Heart rate variability was not significantly different in the summer and winter in both obese and non-obese subjects. Our results show that decreased nocturnal melatonin concentrations during winter in obese men may be related to higher heart rates, and this may suggest that obese men are at an increased risk of a cardiovascular incident during sleep, especially in the winter.
    International Journal of Biometeorology 10/2012; 57(5). DOI:10.1007/s00484-012-0601-3 · 2.10 Impact Factor
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    • "There is a significant gender distribution, with males more affected than females. The more severe and untreated is sleep apnea syndrome, the less likely is blood pressure controlled despite the use of polymedications (Grote et al., 2000; Lavie & Hoffstein, 2001) Sleep apnea seems to create and maintain hypertension by increasing sympathetic nervous system (SNS) activity generated by intermittent hypoxemia; the SNS hyperactivation increases cardiac output, peripheral vascular resistances and fluid retention (Grassi et al., 2005). "
    Genetics and Pathophysiology of Essential Hypertension, 03/2012; , ISBN: 978-953-51-0282-3
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    • "Sympathetic activation is a hallmark in obesity. While uncomplicated obesity is accompanied by an increase in muscle sympathetic nerve activity (MSNA; Lambert et al., 2010b), sympathetic activation is more pronounced in obese subjects with central fat accumulation (Alvarez et al., 2002; Grassi et al., 2004), hypertension (Grassi et al., 2000; Lambert et al., 2007), obstructive sleep apnoea (Grassi et al., 2005b), and when associated with the metabolic syndrome (MS; Grassi et al., 2005a). Such sympathoexcitation is most likely involved in the generation and aggravation of the hemodynamic and metabolic profile of obese individuals as it has been shown to favor blood pressure (BP) elevation (Grassi et al., 2004), reduced insulin sensitivity and increased serum triglycerides (Landsberg, 2001) and to be associated with left ventricular hypertrophy (Schlaich et al., 2003) and dysfunction (Grassi et al., 2009). "
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    ABSTRACT: Sympathetic activation in subjects with the metabolic syndrome (MS) plays a role in the pathogenesis of cardiovascular disease development. Diet-induced weight loss decreases sympathetic outflow. However the mechanisms that account for sympathetic inhibition are not known. We sought to provide a detailed description of the sympathetic response to diet by analyzing the firing behavior of single-unit sympathetic nerve fibers. Fourteen subjects (57 ± 2 years, nine men, five females) fulfilling ATP III criteria for the MS underwent a 3-month low calorie diet. Metabolic profile, hemodynamic parameters, and multi-unit and single-unit muscle sympathetic nerve activity (MSNA, microneurography) were assessed prior to and at the end of the diet. Patients' weight dropped from 96 ± 4 to 88 ± 3 kg (P < 0.001). This was associated with a decrease in systolic and diastolic blood pressure (-12 ± 3 and -5 ± 2 mmHg, P < 0.05), and in heart rate (-7 ± 2 bpm, P < 0.01) and an improvement in all metabolic parameters (fasting glucose: -0.302.1 ± 0.118 mmol/l, total cholesterol: -0.564 ± 0.164 mmol/l, triglycerides: -0.414 ± 0.137 mmol/l, P < 0.05). Multi-unit MSNA decreased from 68 ± 4 to 59 ± 5 bursts/100 heartbeats (P < 0.05). Single-unit MSNA indicated that the firing rate of individual vasoconstrictor fibers decreased from 59 ± 10 to 32 ± 4 spikes/100 heart beats (P < 0.05). The probability of firing decreased from 34 ± 5 to 23 ± 3% of heartbeats (P < 0.05), and the incidence of multiple firing decreased from 14 ± 4 to 6 ± 1% of heartbeats (P < 0.05). Cardiac and sympathetic baroreflex function were significantly improved (cardiac slope: 6.57 ± 0.69 to 9.57 ± 1.20 ms·mmHg(-1); sympathetic slope: -3.86 ± 0.34 to -5.05 ± 0.47 bursts/100 heartbeats·mmHg(-1), P < 0.05 for both). Hypocaloric diet decreased sympathetic activity and improved hemodynamic and metabolic parameters. The sympathoinhibition associated with weight loss involves marked changes, not only in the rate but also in the firing pattern of active vasoconstrictive fibers.
    Frontiers in Physiology 08/2011; 2:52. DOI:10.3389/fphys.2011.00052 · 3.50 Impact Factor

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