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Int J Obes (Lond). 1998 November ; 22(11): 1079–1083.

Central adiposity and hemodynamic functioning at rest and

during stress in adolescents
VA Barnes1,*, FA Treiber1,2,3, H Davis4, TR Kelley1, and WB Strong1,2
1Georgia Institute for Prevention of Human Disease and Accidents, Medical College of Georgia,

Augusta, GA 30912, USA

2Department of Pediatrics, Medical College of Georgia, Augusta, GA 30912, USA
3Department of Psychiatry, Medical College of Georgia, Augusta, GA 30912, USA
4Office of Biostatistics, Medical College of Georgia, Augusta, GA 30912, USA

Abstract
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OBJECTIVE—To examine the impact of central adiposity upon hemodynamic functioning at rest
and during stress in adolescents.
DESIGN—Cross-sectional, correlational study.
SUBJECTS—46 White and 49 Black normotensive adolescents with family histories of essential
hypertension.
MEASUREMENTS—Systolic and diastolic blood pressure (SBP, DBP), cardiac output and total
peripheral resistance responses were assessed at rest, during postural change, video game
challenge and forehead cold stimulation. Specific lower and higher waist-to-hip ratio (WHR)
tertiles were created for each gender and then integrated for analyses. This resulted in a lower
WHR tertile of 11 Whites and 21 Blacks and an upper WHR tertile of 15 Whites and 17 Blacks.
RESULTS—No differences in age, gender or ethnicity proportions were found between tertile
groups (all P > 0.21). The upper WHR group showed greater body weight, waist and hip
circumferences, body mass index (BMI), triceps skinfold and body surface area (all P < 0.001).
Controlling for peripheral (that is, triceps skinfold) and overall (that is, BMI) adiposity, the upper
WHR group exhibited greater SBP (that is, peak response minus mean pre-stressor level) to all
three stressors and greater DBP reactivity to postural change and cold pressor (all P < 0.05).
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CONCLUSION—Central adiposity appears to adversely influence hemodynamic functioning

during adolescence. Underlying mechanisms responsible for these associations require
exploration.

Keywords
central adiposity; obesity; stress response; adolescents; cardiovascular reactivity

Introduction
Obesity has long been recognized as a risk factor for numerous health problems including
cardiovascular diseases (CVD).1,2 Recent findings have indicated that specific fat deposition

© 1998 Stockton Press All rights reserved

*
Correspondence: Dr Vernon A. Barnes, Georgia Prevention Institute, Bldg. HS1640, Medical College of Georgia, Augusta, GA
30912, USA.
 Barnes et al. Page 2

sites confer differential risks for development of CVD. Specifically, central adiposity (for
example waist-to-hip ratio (WHR)) has been identified as a more powerful predictor of
essential hypertension (EH), CVD and premature death, than measures of peripheral (for
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example, triceps skin-folds) or general adiposity (for example, body mass index (BMI)).3–5
WHR has frequently been used in epidemiological research as a measure of central
obesity.4–6

Exaggerated sympathoadrenal responsivity to stress has been proposed as one mechanism

linking central adiposity to CVD.6,7 Moyer et al 8 found increased central adiposity, (that is,
high WHR) associated with exaggerated blood pressure reactivity and cortisol release to a
battery of acute psychological stressors in women. Other studies involving men and women
have found central adiposity, as measured by WHR, to be associated with endocrine
aberrations such as deranged steroid hormone secretion9 and elevated cortisol output due to
increased sensitivity along the hypothalamic-pituitary-adrenal (HPA) axis during stress.10
Recently, using a sample of normotensive young men, Jern et al 11 observed that increased
WHR was associated with increased total peripheral resistance reactivity to a psychological
stressor.

Longitudinal epidemiological studies and necropsy findings have shown that the
pathogenesis of CVD has its origins in childhood.12,13 Only a few studies have addressed
the relationship between general adiposity and CV responsivity to stress in youth and none
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have evaluated the role of central adiposity.14–16 The purpose of this study was to provide
an exploratory examination of the impact of central adiposity upon hemodynamic
functioning at rest and in response to stress in adolescents with family histories of EH.
Studies with such youth are particularly needed as they are at increased risk for development
of EH compared to negative family history cohorts.17–19

Methods
Subjects
From participants in a longitudinal study of the development of EH risk factors,20,21 95
adolescents with a mean age of 14.8 ± 1.4 y were selected, based upon age (≥13 y). All
subjects had a family history of EH defined as having at least one biological parent and one
biological grandparent with EH, verified by physician reports or hospital records. All
subjects were apparently healthy, normotensive, nondiabetic, nonsmokers and free from
chronic disease, based on examination by a pediatrician and parental report of the subject’s
medical history. The study was approved by the institutional human assurance committee.

Anthropometric assessments
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Informed written consent was obtained and anthropometric measures were collected using
established protocols. Weight and height were measured, without shoes, using a
Healthometer scale and standard stadiometer. Body mass index (BMI) was calculated as
weight/height2. Waist circumference was measured at the center of the umbilicus and hip
circumference was measured at the level of the greater trochanters (widest point of the
buttocks). Two sets of measurements were recorded and averaged, from which WHR was
determined. The triceps skinfold was measured three times on the right side of the body with
Lange calipers and the readings were averaged.

Hemodynamic assessments
After anthropometric measurements were completed, subjects were fitted with an
appropriate sized blood pressure (BP) cuff on the right arm. Systolic blood pressure (SBP)
and diastolic blood pressure (DBP) were monitored with a Dinamap Vital Signs Monitor

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(Model 1846SX: Critikon, Inc. Tampa, FL) which has been validated for use at rest and
during laboratory stressors.22,23 Subjects were instrumented with two sets of tetrapolar
electrodes (one current emitting and one sensing) interfaced with a noninvasive thoracic
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electrical bioimpedance system (NCCOM-3 Model 6; Bo-Med Medical Manufacturing Ltd,

Irvine, CA). This system has been validated via comparison with simultaneous cardiac
output (CO) values derived from oximetric measurements using the Fick equation.24,25
Cardiac output was calculated every successive 12 QRS complexes with the NCCOM, while
the Dina-map was inflating and calculating BPs. These values were averaged to provide one
measurement for each BP evaluation. Blood pressure and CO values were measured
simultaneously and used to calculate total peripheral resistance (TPR):

Following fitting of the hemodynamic monitoring equipment, the subject was placed in a
supine position with their head propped up on a pillow and instructed to relax as completely
as possible for 15 min. All hemodynamic responses were simultaneously measured at the
end of the 11th, 13th and 15th minute. Following this, three stressors were presented in the
following order: postural change, video game and forehead cold stimulation. A 5 min supine
prestressor period preceded each stressor with hemodynamic parameters assessed every
other minute. Details of the stressor protocols are presented elsewhere.20,21 Briefly, for the
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postural change stressor, the subject stood and placed the right arm at a 90° angle across the
trunk and hemodynamic responses were recorded at 1 min intervals for 3 min. The 5 min
video game challenge was based upon the protocol of Murphy et al.26 The subject remained
supine with a 68.5 cm color television positioned at an appropriate height and angle for
viewing the video game ‘Breakout’ (Atari, Inc.). Three sets of hemodynamic readings were
obtained during 1st, 3rd and 5th minute of the video game challenge, in which monetary
incentive was used to increase involvement. The forehead cold stressor consisted of having a
plastic bag of crushed ice and water (3–5°C) placed across the subject’s forehead for 1 min,
while the subject was in a supine position. One set of hemodynamic readings was obtained
during the last 30–40 s of stimulation, after which the ice pack was removed.

Hemodynamic data were reduced by computing mean scores for measures obtained during
the initial supine rest and for each prestressor period. Reactivity change scores were then
calculated by subtracting mean values obtained during the prestressor period immediately
preceding the stressor from the peak reading obtained during the stressor.

Results
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Anthropometric and demographic characteristics

Specific lower and higher WHR tertiles were created for each gender and then integrated for
analysis. This resulted in a lower WHR tertile of 11 Whites (five male) and 21 Blacks (11
male) and an upper WHR tertile of 15 Whites (nine male) and 17 Blacks (seven male).
Descriptive characteristics of the lower and upper WHR groups are presented in Table 1.
There were no significant differences between the two groups in age (P > 0.83) or height (P
> 0.79). The upper WHR group showed greater body weight, body surface area, BMI, waist
and hip circumferences, and triceps skinfolds (all P < 0.001). The use of integrated gender-
specific WHR tertiles, resulted in comparable distributions by gender between the two
groups. Although there was a higher proportion of Blacks in the lower WHR tertile than in
the upper tertile, differences in the proportions by WHR tertile group were not statistically
significant (P > 0.30). There were overall gender differences in adiposity, with males having
a greater WHR, lower triceps skinfold and lower hip measures (all P < 0.03). No race
differences were observed in any of the anthropometric measures (all P > 0.07).

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Hemodynamic characteristics
The means and standard deviations for the hemodynamic parameters at rest are presented in
Table 1. Reactivity change scores to the three stressors are presented in Table 2. Initially, a
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multivariate analysis of covariance was conducted comparing the two WHR groups on all
four hemodynamic parameters at initial supine rest and in response to the three stressors.
Since the two WHR groups differed in overall (that is, BMI) and peripheral (that is, triceps
skinfold) adiposity, these parameters were used as covariates in separate analyses. In this
way, any observed differences between the two groups could more readily be attributed to
differences in central adiposity, rather than to overall or peripheral adiposity. Significant
overall effects were observed for both multivariate analyses (all P < 0.001). A series of
univariate analyses of covariance were subsequently conducted covarying either triceps
skinfold or BMI.

No significant differences were observed between the groups in resting hemodynamics when
the triceps skinfold or BMI were statistically controlled (all P > 0.11). With regard to
hemodynamic reactivity, both covariate analyses revealed that the upper WHR group
exhibited significantly greater SBP reactivity to postural change and video game challenge
and greater DBP reactivity to postural change and cold stimulation (all P < 0.05). The upper
WHR group also exhibited greater SBP reactivity to forehead cold, when triceps skinfold
was covaried (P < 0.04), but a trend was only noted when BMI was controlled (P < 0.11). It
should be noted that when the above analyses were also conducted using the mean
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hemodynamic response rather than peak response in the calculation of reactivity change
scores, the same pattern of significant results were observed for each stressor.

Discussion
The present findings indicate that increased central fat deposition, as measured by WHR,
was associated with increased hemodynamic responsivity during stress in a group of
normotensive adolescents with family histories of essential hypertension. Specifically,
statistically controlling for peripheral (that is, triceps skinfold) or overall (that is, BMI)
adiposity, no significant differences were noted between the two WHR groups on any of the
resting hemodynamic parameters. However, the upper WHR group exhibited significantly
greater increases in SBP and/or DBP to postural change, video game challenge and forehead
cold stimulation. The BP reactivity differences appeared to be due to a combination of
changes in vascular (that is, TPR) and myocardial (that is, CO) activity among the upper
WHR group, although neither reached statistical significance.

A number of studies have been conducted with youth which examined relationships between
adiposity and resting hemodynamics. These studies have generally found various measures
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of general adiposity (for example, BMI, and summation of multiple skinfold sites) to be
positively associated with resting SBP and DBP.27–29 With regard to central adiposity,
Gillum2 reported that increased WHR was associated with higher resting SBP and DBP in
children aged 6–17 y. In the present study, prior to controlling for peripheral or general
adiposity, the upper WHR group exhibited significantly higher resting TPR and lower CO.
The latter finding is consistent with the work of Jern et al,11 who observed that central
adiposity, as measured by WHR without adjusting for peripheral or general adiposity, was
negatively associated with CO at rest in a sample of healthy normotensive men aged 18–22
y.

Of the few youth studies conducted, findings have been mixed with regard to relationships
between adiposity and stress reactivity. Alpert et al 14 found a positive relationship between
a measure of general adiposity (that is, BMI) and BP reactivity to dynamic exercise in
children aged 6–16 y. Other pediatric studies have not observed significant relationships

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between measures of body adiposity and various lab stressors including mental arithmetic,
handgrip exercise, video game challenge and cold pressor.15,16 Reasons for discrepancies
between these studies may be due, in part, to methodological differences, including the type
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of adiposity evaluated (for example, general vs central adiposity), subject characteristics (for
example pre- vs post-pubertal youth) and the type of stressors used (for example,
challenging psychological vs passive physical).

Recent studies in adults have indicated that sympathetic arousal to stress may be one
pathway by which central adiposity may be linked to CVD.8,10 Jern et al11 recently found
that central obesity, as measured by WHR, without adjustment for peripheral or general
adiposity, was associated with higher TPR responsivity to a psychological stressor in a
sample of young healthy normotensive men. Overreactivity of the sympathetic nervous
system has been implicated in the pathogenesis of hypertension.18,21,27 Collectively, our
findings involving adolescents and those of Jern et al11 with young adults, suggest that
various neuro-hormonal and growth-related changes associated with pubertal maturation
(which include significant WHR changes) may be necessary before consistent relationships
are observed between sympathetic arousal to stress and central adiposity.

Conclusion
Although the present findings are intriguing, they must be viewed as tentative for several
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reasons. First, the sample size comprised of youth with strong family histories of EH. Such
individuals are more prone to exhibit exaggerated sympathetic arousal to stress, compared to
the negative family history cohorts.21 Thus, whether the observed positive relationships
between central adiposity and BP reactivity would generalize to youth, without family
histories of cardiovascular disease, is unknown and deserves empirical evaluation. Second,
the WHR, a useful index of central adiposity, is influenced by both subcutaneous and
visceral adipose tissue in the abdominal region.30 It is unclear whether the observed
relationships are attributable more to visceral adiposity, which was recently identified as the
specific type of fat most strongly associated with numerous CVD risk factors.31,32 Future
studies would benefit from inclusion of computed tomography (CT) or magnetic resonance
imaging (MRI) of visceral adiposity. Finally, given the exploratory nature of the study,
underlying factors which might link hemodynamic stress reactivity with increased central
adiposity and eventually to the development of CVD, were not assessed. These include
lifestyle factors of sedentary behavior and augmented intake of carbohydrates and sodium,
all of which have been associated with increased hemodynamic stress reactivity15,27 and
obesity in youth.33–35 Likewise, possible imbalances in metabolic and endocrine activity
(for example, increased cortisol, decreased insulin sensitivity) were not assessed which have
been associated with increased sympathetic arousal to stress and susceptibility to visceral fat
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accumulation.8,10,36,37 Nevertheless, the current findings are provocative and support the
need for further research examining relationships between hemodynamic stress reactivity,
central adiposity and cardiovascular health.

Acknowledgments
This research was supported in part by the National Heart, Lung and Blood Institute (Grant number #HL41781).

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Table 1
Descriptive characteristics by central adiposity classification
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Characteristics Lower WHR tertile Upper WHR tertile P value

Anthropometric/demographic
Age (y) 14.8 ± 1.3 14.8 ± 1.5 > 0.83
Height (cm) 164.4 ± 9.7 163.8 ± 8.3 > 0.79
Weight (kg) 58.1 ± 14.0 77.7 ± 17.4 < 0.001
Body surface area (m2) 1.6 ± 0.2 1.8 ± 0.2 < 0.001

BMI (kg/m2) 21.4 ± 4.5 29.0 ± 6.3 < 0.001

Waist circumference (cm) 26.8 ± 3.1 36.0 ± 5.1 < 0.001
Hip circumference (cm) 36.7 ± 4.2 41.6 ± 5.1 < 0.001
WHK 0.7 ± 0.03 0.9 ± 0.06 < 0.001
Triceps skinfolds (mm) 13.5 ± 9.6 29.1 ± 13.3 < 0.001
Resting hemodynamics
SBP (mmHg) 118.6 ± 10.6 117.0 ± 10.8 > 0.98a
DBP (mmHg) 62.9 ± 7.8 61.9 ± 6.0 > 0.85a
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CO (L/min) 8.2 ± 2.1 6.3 ± 2.1 > 0.12a

TPR (mmHg/(L/min)) 10.5 ± 3.0 13.9 ± 4.2 > 0.11a

Values are means ± standard deviations. BMI = body mass index; WHR = Waist-to-hip ratio; SBP = systolic blood pressure; DBP = diastolic blood
pressure; CO = cardiac output; TPR = total peripheral resistance.
a
maximal P values after covarying triceps skinfolds or BMI.
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Table 2
Reactivity change score comparisons by central adiposity classification
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Hemodynamic reactivity Lower WHR tertile Upper WHR tertile P valuea

Postural change
SBP (mmHg) 5.9 ± 10.8 12.7 ± 9.8 < 0.03
DBP (mmHg) 8.1 ± 6.7 14.0 ± 9.6 < 0.01
CO (L/min) −0.22 ± 1.3 0.7 ± 1.0 > 0.058
TPR (mmHg/(L/min)) 0.9 ± 2.3 0.7 ± 2.7 > 0.69
Video game
SBP (mmHg) 7.8 ± 7.1 17.0 ± 11.0 < 0.002
DBP (mmHg) 8.6 ± 7.4 12.7 ± 8.5 > 0.08
CO (L/min) −0.1 ± 1.1 0.1 ± 0.8 > 0.22
TPR (mmHg/(L/min)) 3.6 ± 5.9 4.8 ± 3.8 > 0.80
Cold pressor
SBP (mmHg) 8.2 ± 8.1 14.0 ± 14.8 < 0.11
DBP (mmHg) 13.3 ± 8.9 17.7 ± 8.4 < 0.05
−0.94 ± 1.0 −0.34 ± 1.1
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CO (L/min) > 0.37

TPR (mmHg/(L/min)) 5.5 ± 4.4 7.0 ± 4.7 > 0.60

Values are means ± standard deviations. WHR = Waist-to-hip ratio; SBP = systolic blood pressure; DBP = diastolic blood pressure; CO = cardiac
output; TPR = total peripheral resistance.
a
Maximal P values after covarying triceps skinfolds or body mass index.
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