Autonomic Activity Assessed by Heart Rate Spectral Analysis Varies with Fat Distribution in Obese Women

Gao, Young Y.; Lovejoy, Jennifer C.; Sparti, Andrea; Bray, George A.; Keys, L.K.; Partington, Curtis R.

doi:10.1002/j.1550-8528.1996.tb00512.x

Cited by 61 publications

(44 citation statements)

References 32 publications

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“…1,2 Such alterations are also found in non-diabetic obese patients and suggest a parasympathetic dysfunction. 3,4 In these patients, a reduction in peripheral vasoconstrictive response to sympathetic stimuli is also found 5 and might be indicative of a sympathetic disorder consisting of a defect in sympathetic nerve activation or in peripheral adrenoreceptors.…”

Section: Introductionmentioning

confidence: 82%

“…5,36,37,41 In particular, changes in parasympathetic and sympathetic heart control, evaluated by spectral analysis of heart rate variations, may occur in the same way and magnitude in obese and diabetic patients. 4,36,42 Moreover we have shown that the heart rate and blood pressure responses to sympathetic activation, induced by a handgrip, is reduced in the obese patients with a parasympathetic dysfunction. 43 The peripheral vasoconstrictive response to sympathetic activation also appears reduced in these patients.…”

Section: Group1mentioning

confidence: 90%

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Glucose-induced thermogenesis, inhibition of lipid oxidation rate and autonomic dysfunction in non-diabetic obese women

et al. 1998

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OBJECTIVE: The aim of this study was to look for a relationship between autonomic dysfunction and alterations in glucose-induced thermogenesis (GIT) and lipid oxidation rate in obese non-diabetic women. SUBJECTS: 37 obese women, 20 with impaired cardiac autonomic function tests (group 1) were matched with 17 women with normal tests (group 2) according to age, weight, body mass index (BMI), waist-to-hip ratio (WHR), fat mass (FM) and fat free mass (FFM). MEASUREMENTS: A series of ®ve standardized tests was carried out, three of which were based mainly on cardiac parasympathetic control (heart rate response to Valsalva, deep breathing and lying-to-standing) and two on cardiovascular sympathetic function (blood pressure response to standing and to handgrip). Energy expenditure (EE), lipid and glucose oxidation rate were determined by indirect calorimetry at fasting and after an oral glucose load (75 g). Blood glucose, insulin and catecholamines responses to glucose were examined. RESULTS: There was no signi®cant difference in plasma glucose, insulin, catecholamines, metabolic rate, glucose and lipid oxidation rate at fasting and plasma glucose, insulin and catecholamine responses to glucose. GIT was slightly but not signi®cantly lower in group 1 (24.7 AE 10.4 kJ) than in group 2 (46.8 AE 9.0 kJ). The cumulative glucose oxidation rate did not differ signi®cantly in the two groups. The cumulative lipid oxidation rate was signi®cantly lower in group 1 than in group 2 (749.4 AE 4.1 vs 730.8 AE 8.0, respectively, P 0.033). It correlated negatively with the area under the curve of insulin response (r 70.37, P 0.04). In the multivariate analysis, both autonomic dysfunction and the area under the curve of insulin response correlated signi®cantly with the cumulative lipid oxidation rate. CONCLUSION: This study suggests that 1) the glucose-induced inhibition of the lipid oxidation rate in obese women is greater in the patients with autonomic dysfunction; 2) a decrease in sympathetic activity is likely to be involved in this phenomenon.

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Section: Introductionmentioning

confidence: 82%

Section: Group1mentioning

confidence: 90%

Glucose-induced thermogenesis, inhibition of lipid oxidation rate and autonomic dysfunction in non-diabetic obese women

et al. 1998

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“…7 Possible mechanisms of the prolonged QTc interval in obesity include cardiac autonomic nervous system dysfunction, electrolyte abnormalities, left ventricular hypertrophy (LVH), hyperinsulinemia and CHD. 5,7,12,30±33 Obesity and UBO have been associated with autonomic nervous system dysfunction 34,35 which may result in prolongation of the QTc interval. 5,7,27,30,31 An imbalance in cardiac sympathetic enervation has been shown to prolong the QTc interval in men and women.…”

Section: Discussionmentioning

confidence: 99%

Effect of obesity and regional adiposity on the QTc interval in women

Park

Swan

1997

Int J Obes

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OBJECTIVES: To determine whether differences in body fat composition and body fat distribution patterns are associated with a prolongation of the corrected QT interval for heart rate (QTc) on the electrocardiogram (EKG) during rest and exercise. DESIGN: Cross-sectional evaluation of the QTc interval in three groups of premenopausal women during rest and two exercise conditions (50% VO 2 max and VO 2 max). SUBJECTS: Thirty-one healthy women with a mean age of 35 y (27±44 y) were classi®ed as either obese (n 22; percent body fat [%BF] b 30%) or nonobese (NO; n 9; %BF 27%) by hydrostatic weighing. Obese subjects matched for age and %BF were grouped by waist to hip ratio (WHR) into two groups: upper body obesity (UBO; n 11; WHR ! 0.85) and lower body obesity (LBO; n 11; WHR 0.75). MEASUREMENTS: RR and QT intervals were measured in a double-blind design with the aid of calipers and magnifying lens for seven consecutive beats in lead II from a 12-lead EKG at a paper speed of 25 mm/sec. Five consecutive cardiac cycles excluding the longest and shortest RR and QT intervals were averaged and calculated for QTc interval using Bazett's formula. RESULTS: Mean QTc intervals were signi®cantly different (P`0.001) across the groups for each condition. For all conditions, UBO had the longest QTc interval as compared to LBO and NO respectively (i.e., Rest: 0.426; 0.413; 0.399 sec 1/2 ; Mid50%: 0.447; 0.426; 0.409 sec 1/2 ; Max: 0.390; 0.374; 0.357 sec 1/2 ). CONCLUSIONS: The QTc interval is positively associated with UBO even at the same level of body fat in moderately obese women. It is clear that abdominal obesity may be one of the risk factors for a prolonged QTc interval in premenopausal women.

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“…Three studies reported an association between VAT and sympathetic activation (31)(32)(33). Two of these papers also investigated SAT and reported that VAT was stronger associated with sympathetic activation than SAT (32,33).…”

Section: Tablementioning

confidence: 99%

Body fat, especially visceral fat, is associated with electrocardiographic measures of sympathetic activation

Hillebrand

Mutsert

Christen

et al. 2014

Obesity

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Objective: Obesity is associated with sympathetic activation, but the role of different fat depots is unclear. The association between body fat, specifically visceral fat, and electrocardiographic measures of sympathetic activation in a population with structurally normal hearts was investigated. Methods: In this cross-sectional baseline analysis of the Netherlands Epidemiology of Obesity study, body fat percentage was assessed with BIA and abdominal subcutaneous (SAT) and visceral adipose tissue (VAT) with magnetic resonance (MR) imaging. Mean heart rate (HR) and five other electrocardiographic measures of sympathetic activation were calculated. We performed multivariate linear regression analyses. Results: In 868 participants with a mean age(SD) of 55(6) years, BMI of 26(4) kg/m 2 , 47% men, body fat was associated with HR and two other measures of sympathetic activation. Per sex-specific SD total body fat, the difference in HR was 1.9 beats/min (95% CI: 1.0, 2.9; P < 0.001) and per SD waist circumference 2.1 beats/min (95% CI: 1.3, 2.9; P < 0.001). The difference in HR per SD VAT was 2.1 beats/min (95% CI: 1.3, 3.0; P < 0.001). Conclusions: Body fat, especially visceral fat, was associated with electrocardiographic measures of sympathetic activation. Our study implies that already before the onset of cardiovascular disease, excess (visceral) body fat is associated with sympathetic activation.

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Autonomic Activity Assessed by Heart Rate Spectral Analysis Varies with Fat Distribution in Obese Women

Cited by 61 publications

References 32 publications

Glucose-induced thermogenesis, inhibition of lipid oxidation rate and autonomic dysfunction in non-diabetic obese women

Glucose-induced thermogenesis, inhibition of lipid oxidation rate and autonomic dysfunction in non-diabetic obese women

Effect of obesity and regional adiposity on the QTc interval in women

Body fat, especially visceral fat, is associated with electrocardiographic measures of sympathetic activation

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