International Journal of Psychophysiology 90 (2013) 7379

Contents lists available at ScienceDirect

International Journal of Psychophysiology

journal homepage: www.elsevier.com/locate/ijpsycho

Abdominal obesity and chronic stress interact to predict blunted

cardiovascular reactivity
Kulwinder Singh a,, Biing-Jiun Shen b, 1
a
b

Department of Psychology, Seeley G. Mudd Building Room 501, University of Southern California, 3620 South McClintock Ave., 90089-1061, Los Angeles, CA, USA
Department of Psychology, Ohio University, 245 Porter Hall, 45701, Athens, OH, USA

a r t i c l e

i n f o

Article history:
Received 10 November 2012
Received in revised form 7 March 2013
Accepted 18 March 2013
Available online 25 March 2013
Keywords:
Cardiovascular reactivity
Blunting
Abdominal obesity
Chronic stress
Body-mass index

a b s t r a c t
Abdominal obesity and chronic stress have independent effects on cardiac autonomic regulation, and may
also interact to inuence cardiovascular reactivity. In addition to main effects, we hypothesized that abdominal obesity and chronic stress would interact and predict blunted cardiovascular reactivity. One hundred and
twenty-two undergraduate students engaged in two stressful laboratory tasks while cardiovascular activity
was assessed. Results indicated that higher abdominal obesity signicantly predicted blunted systolic blood
pressure (SBP) and mean arterial pressure (MAP) change, while chronic stress was not directly associated
with any measure of cardiovascular reactivity. Furthermore, there was a signicant interaction between abdominal obesity and chronic stress on SBP and MAP change such that among participants with higher chronic
stress, higher abdominal obesity was signicantly associated with reduced SBP and MAP reactivity. In addition, body-mass index (BMI), a measure of overall obesity, also had both main and interaction effects with
chronic stress to predict blunted cardiovascular reactivity. These results suggest that abdominally obese individuals may incur difculty in mounting appropriately-sized cardiovascular responses during acute stress,
particularly when under high levels of chronic stress.
2013 Elsevier B.V. All rights reserved.

1. Introduction
Rates of obesity have been increasing dramatically worldwide. Its
prevalence has doubled in the United States (Stein and Colditz, 2004)
and tripled in developing countries (Hossain et al., 2007) since the
1970s. As prevalence rates increase, the health and economic costs
of obesity continue to mount. In the United States, the direct and indirect cost of obesity is estimated to be over 215 billion dollars per
year (Hammond and Levine, 2010). Excessive weight gain is closely
tied to the rising prevalence of a number of chronic diseases, including cardiovascular disease, type 2 diabetes, stroke, and cancer
(Hossain et al., 2007).
Whereas generalized obesity is characterized by an overall accumulation of adipose tissue spread throughout the body, abdominal obesity
refers to high levels of fat accumulation centered primarily in the abdominal region. Although these two forms of adiposity have been demonstrated to be highly correlated (Goldbacher et al., 2005), they may
also exist independently of each other. For example, some evidence
suggests that being lean but having higher abdominal fat is especially

We would like to thank the following students and colleagues for their assistance
with data collection: Stacy Eisenburg, Uta Maeda, Emily Kamen, Jessica Matlock, Jon
Arrington, Kelsey Rupp, Farva Jafri, and Danny Liu.
Corresponding author. Tel.: +1 415 246 0394; fax: +1 213 746 9082.
E-mail addresses: Kulwinds@usc.edu (K. Singh), Shenb@ohio.edu (B.-J. Shen).
1
Tel.: +1 740 593 1086; fax: +1 740 593 0579.
0167-8760/$ see front matter 2013 Elsevier B.V. All rights reserved.
http://dx.doi.org/10.1016/j.ijpsycho.2013.03.010

associated with risk for earlier death (Larsson et al., 1984). Also, obese
individuals may possess high levels of adipose tissue throughout the entire body in the absence of a relatively high accumulation of centralized
abdominal fat. In addition, the measurement of both generalized and
abdominal obesity also differs. Generalized obesity is typically measured by body-mass index (BMI), a measure based on an individual's
weight and height, with obesity dened as a BMI of 30 kg/m2 or higher.
Abdominal obesity can be measured using a variety of methods that are
either invasive (e.g., DEXA scan) or non-invasive (e.g., measuring tape).
Non-invasive assessment of abdominal obesity typically includes either
the measurement of individuals' waist-circumference (WC) alone, or
the assessment of both WC and hip-circumference (HC) to calculate
the ratio of the circumference of the waist to the hips, commonly
known as waist-to-hip ratio (WHR).
Abdominal obesity confers additional health risks above and beyond those associated with generalized obesity, including an increased risk of hypertension, left ventricular dysfunction, coronary
heart disease, diabetes, lipoprotein alterations and overall cardiovascular disease morbidity (Ammar et al., 2008; Despres et al., 1990; Lee
et al., 2008). These associations are independent of other contributing
risk factors such as high cholesterol, smoking, education, race, age,
and obesity dened by BMI (Freedman et al., 1995).
Although abdominal obesity has been recognized as a signicant risk
factor for chronic disease, the mechanisms by which it may lead to negative health outcomes remain poorly understood. Cardiovascular reactivity has been suggested as a potential mechanism linking abdominal

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K. Singh, B.-J. Shen / International Journal of Psychophysiology 90 (2013) 7379

obesity and pathophysiological processes. For example, some studies

have demonstrated a positive association between abdominal obesity
and cardiovascular responses to mental stress (Barnes et al., 1998;
Davis et al., 1999; Goldbacher et al., 2005; Steptoe and Wardle, 2005;
Waldstein et al., 1999). An exaggerated cardiovascular stress response
has been shown to be associated with future negative health outcomes,
including clinical and sub-clinical cardiovascular disease (Treiber et al.,
2003), hypertension (Light et al., 1992), increased left-ventricular mass
(Allen et al., 1997), and carotid atherosclerosis (Barnett et al., 1997).
Thus, an exaggerated cardiovascular response to mental stress, which
has been associated with abdominal obesity, may be a contributing
factor linking abdominal obesity to pathophysiological processes. In
contrast, although seemingly counter-intuitive, emerging evidence suggests that blunted cardiovascular reactivity may also be a risk factor for
negative health outcomes, including immunological suppression, depression, and poor self-reported health (Phillips, 2011).
Abdominal obesity has been associated with both exaggerated
(Barnes et al., 1998; Davis et al., 1999; Goldbacher et al., 2005;
Steptoe and Wardle, 2005; Waldstein et al., 1999) and blunted
(Carroll et al., 2008; Hamer et al., 2007; Laederach-Hofmann et al.,
2000; Phillips, 2011; Phillips et al., 2012) cardiovascular reactivity.
There are a number of factors that may contribute to the mixed results.
First, existing studies differ vastly in sample characteristics, selection
criteria and statistical covariates included in their designs and analyses.
Participant characteristics, such as age, gender, smoking status, medications, oral contraceptive use, and baseline cardiovascular activity have
been found to signicantly impact cardiovascular reactivity (Lawler
et al., 1995; Mills and Dimsdale, 1991; Straneva et al., 2000; Uchino
et al., 1999) and are infrequently included as covariates across studies.
Carroll et al. (2008) found that when only controlling for baseline cardiovascular measures, generalized obesity was positively associated
with diastolic blood pressure (DBP) reactivity and negatively associated
with heart rate (HR) reactivity. In addition, abdominal obesity, measured with WHR, was positively associated with SBP and DBP reactivity
and negatively associated with HR reactivity. Interestingly, after controlling for the effects of age, cohort, sex, occupational group, Paced
Auditory Serial Addition Test performance scores (a test involving
working memory and divided attention), medication, smoking status,
and baseline cardiovascular levels, previously observed positive associations between cardiovascular reactivity, generalized obesity, and
abdominal obesity became non-signicant, while all negative associations remained. In general, studies with comprehensive statistical adjustment and stringent exclusion criteria mostly have reported
negative associations between cardiovascular reactivity and abdominal
obesity (Hamer et al., 2007; Laederach-Hofmann et al., 2000; Phillips,
2011), although some have continued to report positive associations
(Goldbacher et al., 2005; Steptoe and Wardle, 2005). The mixed ndings strongly suggest that additional factors may help explain the relationship between abdominal obesity and cardiovascular reactivity.
It has been suggested that chronic stress may be one of these factors, as it may have particularly strong physiological consequences
among individuals who are abdominally obese (Bjrntorp, 2001; De
Vriendt et al., 2009; Shen et al., 2010). Chronic stress has been consistently associated with impaired hypothalamicpituitaryadrenal axis
(HPA) and central sympathetic nervous system functioning (Miller
et al., 2007; Pike et al., 1997). Excessive fat in tissues is also associated
with elevations in glucocorticoids and catecholamines (Grassi et al.,
2004; Marin et al., 1992). Individuals with high levels of chronic stress
and excessive abdominal fat centralization demonstrate persistent elevations in glucocorticoid and catecholamine activity (Bjrntorp,
1996, 2001; McEwen, 1998), which may inuence the body's ability
to maintain allostasis. Under high allostatic load, the physiological
wear and tear from repeated activation of the stress response
(McEwen and Seeman, 1998), the individual's physiological stress systems may become burned out and less responsive to environmental
demands (Bjrntorp, 2001; McEwen, 1998). This burned out state

may be reected by a diminished cardiovascular response to stress

(McEwen and Seeman, 1998).
The primary goal of this study was to examine the relationship between abdominal obesity, chronic stress, and cardiovascular reactivity
in a sample of healthy young adults. We rst aimed to examine whether
these characteristics inuenced baseline cardiovascular activity. We
also aimed to examine whether chronic stress and abdominal obesity
would interact to predict blunted cardiovascular reactivity. We hypothesized that in addition to their main effects, abdominal obesity and
chronic stress would interact to predict a prole of blunted cardiovascular reactivity across multiple cardiovascular measures. In addition, we
examined patterns of cardiovascular responding across other measures
of obesity, and whether chronic stress interacted with these measures
to predict a blunted cardiovascular response.
2. Method
2.1. Participants
One hundred and twenty-two undergraduate students were
recruited for this study. Participants were 35 male and 87 female students between the ages of 18 and 28 (M = 19.9, SD = 1.68) who met
the study inclusion criteria. The exclusion criteria were selected on
the basis of factors known to impact cardiovascular reactivity (Mills
and Dimsdale, 1991; Straneva et al., 2000). These included: currently
consuming medications that affect the cardiovascular system, currently smoking or using nicotine products, use of oral contraceptives,
use of illicit substances, and current or past history of chronic illness.
Eligible participants were instructed to abstain from caffeine, alcohol
and strenuous physical exercise 24 h before their scheduled appointment. The study was approved by the University Institutional Review
Board. All participants provided informed consent before partaking in
the study.
2.2. Measures
2.2.1. Anthropometric measures
Height and weight were measured using a scale. BMI was calculated as weight in kilograms (kg) divided by height in meters squared
(kg/m 2). In addition, WC, used as the primary index of abdominal
obesity in the current study, is a noninvasive measure that is most
predictive of cardiovascular events (Maffeis et al., 2001) and strongly
correlated with DEXA scan measures of abdominal obesity (Daniels
et al., 2000; Pouliot et al., 1994). The WC was measured in centimeters (cm) at the level of the umbilicus with a exible tape. In addition,
HC was measured at the point of most intrusion on the hips, and WHR
was calculated as WC divided with HC. To reduce measurement error,
both WC and HC were measured twice, and the averaged values were
used.
2.2.2. Chronic stress
The Inventory of College Students' Recent Life Experiences Scale
(ICSRLE) was used to measure chronic stress (Kohn et al., 1990). This
49-item measure was designed to measure stress in multiple domains
most relevant to college life, including academic, social mistreatment,
time pressure, friendship, and romantic stress. It has been validated in
college students and demonstrated high internal consistency reliability
(Cronbach's = .89) (Kohn et al., 1990).
Stress currency, duration, and intensity each may have unique effects on cardiovascular reactivity (Lepore et al., 1997; Matthews et al.,
1997). Because the original ICSRLE does not measure currency and duration, it was modied to include these dimensions in addition to stress
intensity. For stressors endorsed as being currently experienced, participants were asked to indicate the number of months they had been
dealing with the event and the level of intensity of the stressor. Two
subscales, stress duration and intensity, were produced for the chronic

K. Singh, B.-J. Shen / International Journal of Psychophysiology 90 (2013) 7379

stress measure. The product of these two subscales represented the

total stress score.
2.2.3. Cardiovascular measures
The cardiovascular responses measured were heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), meanarterial pressure (MAP), pre-ejection period (PEP) and respiratory
sinus arrhythmia (RSA). Blood pressure was measured with an automated blood pressure machine (Dinamap Pro 400 V2, Critikon,
Tampa, FL) using an inatable cuff placed over the brachial artery of
the non-dominant arm. PEP was measured by impedance cardiography (ICG; Mindware Technologies, Gahanna, OH) using a four-spot
electrode conguration designed to improve signal-to-noise ratio
and reduce artifact (Qu et al., 1986). One current electrode was placed
on the back of the neck over the fourth cervical vertebra and the other
on the back over the ninth thoracic vertebra. One voltage electrode
was placed on the front of the neck, 4 cm above the clavicle and the
other over the sternum at the fourth rib. HR and RSA were measured
using the Lead II conguration for electrocardiogram (ECG). Electrodes were placed on the right collarbone and on the left side of
the abdomen below the thoracic cage with a ground electrode placed
adjacent to the navel. SilverSilver chloride electrodes (Tracerite,
Pawtucket, Rhode Island) were used for ECG and ICG measurement.
PEP represents the time between the onset of depolarization of the
left ventricle and the opening of the aortic valve, and serves as an indicator of cardiac sympathetic drive (Sherwood et al., 1990). It is dened as the time between the Q wave onset and the B point inection
on the dZ/dt waveform (Cacioppo et al., 2007). RSA is a rhythmical
uctuation in heart periods at the respiratory frequency that is characterized by a shortening and lengthening of heart periods in a phase
relationship with inspiration and expiration, and serves as a primary
indicator of cardiac vagal tone (Berntson et al., 1993). RSA was derived by spectral analysis of an interbeat interval series calculated
from ECG following published guidelines (Berntson et al., 1997).
RSA was quantied as the integral power within the respiratory frequency band (0.12 to 0.40 Hz).
ECG and ICG were sampled at a rate of 500-Hz for 60 second intervals. Waveforms were screened and artifacts were removed prior to
exportation of data. HR, PEP, and RSA were measured continuously,
while SBP, DBP, and MAP were measured on 90 second intervals during rest and 60 second intervals during stress. Readings were averaged to produce aggregate values for each baseline and stress period.
2.3. Procedure
2.3.1. Stress tasks
Acute psychological stress was elicited with two three-minute behavioral stress tasks adapted from the Trier Social Stress Test
(Kirschbaum et al., 1993). The rst task required participants to prepare a speech for a hypothetical job position and present it to two experimenters who they had not previously interacted with. To increase
perceptions of uncontrollability and social threat, characteristics associated with heightened endocrine reactivity to stress (Dickerson and
Kemeny, 2004), experimenters dressed in professional attire and
white lab coats. Experimenters were always one male and one female
to balance for experimenter gender effects. The second task, mental
arithmetic, required participants to perform calculations orally in
the presence of two experimenters. The combination of a public
speaking and cognitive task has been associated with greater physiological responses than any combination of stressors (Dickerson and
Kemeny, 2004), and produces reliable elevations in cardiovascular activity compared to rest (Al'Absi et al., 1997; Fechir et al., 2008).
2.3.2. Experimental protocol
Experiments were conducted between the hours of 9:00 AM and
2:00 PM in a well-lit, sound-proofed room. Experimenters were

75

stationed in an adjacent room to monitor participants by real-time

video feed. After consent was provided, participant's weight, height,
WC, and HC were measured. Subsequent to weight measurement, psychophysiological recording equipment was applied and participants
were seated in front of a computer monitor that presented computerized task instructions throughout the experiment (Eprime 2.0; Psychology Software Tools, Inc., Sharpsburg, Pennsylvania). Participants then
completed psychosocial questionnaires for a period of 30 min while
blood pressure was assessed every 4 min. During this time, participants
were allowed to become habituated to the instrumentation and blood
pressure measurements, thus reducing the likelihood that the equipment would be distracting during tasks (Valdimarsdottir et al., 2002).
Following the questionnaires, participants were instructed to rest
for 6 min in order to establish an initial baseline. After the baseline period, participants received instructions to prepare for the 3 min speech
task. Participants were given 4 min to prepare their speech and 3 min
to present it. A 6 min inter-task rest period followed speech presentation. Subsequent to the interim rest period, participants were instructed
to prepare for the 3 min arithmetic task. Study participation concluded
after the arithmetic task.
2.4. Statistical analyses
Statistical analyses were conducted using SPSS version 17.0 for Windows. Paired-samples t-tests were conducted to evaluate whether
stress tasks produced signicant elevations in cardiovascular activity.
Pearson correlations were computed to examine the nature of association between anthropometric (e.g., WC, BMI, WHR) and stress variables.
For primary analysis, multiple regression analysis was conducted to test
the independent effects of chronic stress and abdominal obesity on
baseline cardiovascular measures and cardiovascular reactivity. Analyses were conducted separately for each cardiovascular variable during
baseline and reactivity. Age, gender, and self-reported exercise were included in each model as covariates. For each cardiovascular measure,
change scores were computed by subtracting the average of the initial
baseline readings from the average of readings during both stress
tasks. In models testing cardiovascular reactivity, corresponding baseline cardiovascular measures were included as a covariate.
A series of hierarchical multiple regression analyses were conducted
for each cardiovascular measure to test whether chronic stress, abdominal obesity, and their interaction term were associated with cardiovascular reactivity. Each cardiovascular reactivity measure was regressed
on three blocks of predictors. Block one included all covariates.
Mean-centered chronic stress and abdominal obesity were entered in
block two. The interaction term, calculated as the product of centered
chronic stress and abdominal obesity, was entered in block three. Signicant interactions were followed by simple slope analysis to examine
the slope of abdominal obesity at different levels (mean and one standard deviation above and below the mean) of chronic stress in
predicting cardiovascular reactivity. Separate hierarchical multiple regression analyses were also conducted to test the effects of both generalized and abdominal obesity measured by WHR on cardiovascular
reactivity following the same analytic approach.
3. Results
3.1. Participant characteristics
Sample characteristics are presented in Table 1. The sample was ethnically diverse, with 22% Caucasian, 47% Asian American, 7% African
American, 12% Hispanic, and 11% reporting as others. The mean BMI
was 25.6. On the basis of BMI, 40 (32.7%) participants were overweight
(BMI 25) and 16 (13.1%) were obese (BMI 30). For abdominal obesity, ve (4.1%) male participants (WC 100 cm) and 18 (14.8%) female participants (WC 85 cm) met criteria for abdominal obesity. A

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K. Singh, B.-J. Shen / International Journal of Psychophysiology 90 (2013) 7379

strong association remained when both abdominal and generalized

obesity measures were dichotomized (2 = 36.38, p b .001).
3.2. Effectiveness of psychological stressors
Table 1 also presents the means of cardiovascular measures at baseline and the mean degree of change for two stress tasks. Paired samples
t-test revealed that the stress tasks signicantly increased cardiovascular
activity. HR and BP increased signicantly during the tasks, with a mean
increase of 13.8 beats-per-minute for HR (t(121) = 14.58, p b .001),
20.3 mm Hg for SBP (t(121) = 21.48, p b .001), 10.8 mm Hg for DBP
(t(121) = 23.36, p b .001), and 12.3 mm Hg for MAP (t(121) = 21.85,
p b .001). Stress tasks produced signicantly shorter PEP, with a mean
decrease of 6.6 ms (t(121) = 6.57, p b .001), and lower RSA, with a
mean decrease of 0.30 (t(121) = 3.63, p b .001), indicating a shift in
the sympathovagal balance to reect increased cardiac sympathetic
drive and parasympathetic withdrawal.
3.3. Associations between anthropometric and stress variables
Table 2 displays the associations between anthropometric and
stress characteristics. All anthropometric measurements were highly
correlated with each other, with WC correlated with BMI (r = .92,
p b .001) and WHR (r = .84, p b .001). There was also a high correlation between WC and HC (r = .91, p b .001). For chronic stress, total
chronic stress was highly correlated with stress duration (r = .92,

Table 2
Correlation matrix of obesity and chronic stress.

Waist-circumference
Body mass index
Waist-to-hip ratio
ICSRLE-M
ICSRLE-A
ICSRLE-TOT

WC

BMI

WHR

ICSRLE-M

ICSRLE-A

ICSRLE-TOT

.92
.84
.00
.12
.06

.66
.02
.11
.07

.06
.10
.03

.44
.92

.66

ICSRLE-M = Stress duration, ICSRLE-A = Stress intensity, ICSRLE-TOT = Total score

of chronic stress measure (ICSRLE-M ICSRLE-A).
p b .05.
p b .01.

p b .001) and intensity (r = .67, p b .001). Stress intensity and duration were also correlated (r = .44, p b .001). Chronic stress and anthropometric characteristics were not associated with each other.
3.4. Associations between baseline cardiovascular values and
change scores
Baseline HR (r = .21, p = .02), RSA (r = .56, p b .001), and
PEP (r = .36, p b .001) were signicantly and negatively associated
with their respective change scores. Baseline SBP, DBP, and MAP were
not associated with their corresponding change scores.
3.5. Abdominal obesity, chronic stress, and baseline cardiovascular
activity

Table 1
Sample characteristics and stress task effectiveness.
Total sample (N = 122)
Demographics
Gender
Female
Male
Age (years)
Ethnicity
Caucasian
Asian American
African American
Hispanic
Other

N (%)
87 (71%)
35 (29%)
20 1.70
27 (22%)
57 (47%)
9 (7%)
15 (12%)
14 (11%)

Anthropometric characteristics

Mean SD

Weight (kg)
Height (cm)
Body-mass index
Waist-to-hip ratio
Waist circumference (cm)
Hip circumference (cm)
Stressor characteristics
Baseline
HR (beats per minute)
SBP (mm Hg)
DBP (mm Hg)
MAP (mm Hg)
PEP (ms)
RSA
Change during stress tasks
HR
SBP
DBP
MAP
PEP
RSA

68.2 18.01
164.8 8.89
25.6 5.80
0.84 0.06
84.9 14.20
101.2 10.30

73.9 9.00
104.1 10.80
64.9 5.00
90.0 5.60
132.6 16.50
6.5 1.00
13.8 10.40
20.3 10.40
10.8 5.10
12.3 6.20
6.6 11.10
0.3 0.90

HR = Heart rate; SBP = Systolic blood pressure; DBP = Diastolic blood pressure;
MAP = Mean arterial pressure; PEP = Pre-ejection period; RSA = Respiratory sinus
arrhythmia.
p b .05.
p b .01.
p b .001.

As illustrated in Table 3, after statistically controlling for the effects

of age, gender, exercise, and total chronic stress, WC was signicantly
associated with higher baseline SBP ( = .34, s.e. = .06, p b .001)
and MAP ( = .24, s.e. = .04, p = .01), but not with baseline HR,
DBP, PEP, or RSA. Total chronic stress was not associated with any baseline cardiovascular variables. Regression analyses to test the effects of
stress intensity and stress duration on baseline cardiovascular measures

Table 3
Hierarchical regression testing main effects and interaction of abdominal obesity and
chronic stress.
Step 2a

Baseline
HR
SBP
DBP
MAP
PEP
RSA
Change
HR
SBP
DBP
MAP
PEP
RSA

Step 3b

WC

Chronic
stress

WC

Chronic
stress

WC chronic
stress

.03
.34

.05
.13
.13
.16
.09
.08

.02
.29
.09
.22
.05
.004

.02
.12
.12
.16
.09
.09

.02
.08
.01
.04
.02
.14

.16
.12
.05
.08
.10
.02

.23
.16
.02
.07
.01
.03

.17
.10
.02
.05
.11
.01

.08
.27
.29c
.29

.10
.24
.06
.08
.18
.32
.17
.25
.01
.02

.03
.07

R2 change

.000
.003
.000
.001
.000
.01
.003
.04
.05
.05
.000
.003

a
Step 1 was not included, as it only contained covariates. Variables in Step 2 included
gender, age, self-reported exercise, WC, and total chronic stress. For change, baseline
cardiovascular variables were also included as covariates.
b
Variables in Step 3 included gender, age, self-reported exercise, WC, total chronic
stress, and the WC Stress interaction. For change models, baseline cardiovascular variables were also included as covariates. HR = Heart rate; SBP = Systolic blood pressure;
DBP Diastolic blood pressure; MAP = Mean arterial pressure, PEP = Pre-ejection period;
RSA = Respiratory sinus arrhythmia; WC = Waist-circumference; ICSRLE-TOT = Total
score of chronic stress scale; WC ICSRLE-TOT = WC Stress interaction.
c
Overall F-test for ANOVA was not signicant; interaction term reached signicance.
p b .05.
p b .01.

K. Singh, B.-J. Shen / International Journal of Psychophysiology 90 (2013) 7379

77

revealed that stress intensity was signicantly associated with lower

baseline PEP ( = .24, s.e. = .05, p = .02), and that stress duration
was signicantly associated with higher baseline MAP ( = .21,
s.e. = .01, p = .04) and PEP ( = .25, s.e. = .01, p = .02). Each
model included statistical adjustment for the effects of age, gender,
and exercise. In addition, stress duration and intensity were simultaneously entered as predictors into each model. There were no interactions between chronic stress and abdominal obesity on baseline
cardiovascular activity.
3.6. Abdominal obesity, chronic stress, and cardiovascular reactivity
Hierarchical regression analysis was conducted to test the independent and interactive effects of abdominal obesity and chronic stress on
cardiovascular reactivity. Each cardiovascular reactivity measure was
regressed on three blocks of predictors. The variables in block one
were age, gender, exercise, and the respective baseline cardiovascular
level. Mean-centered total chronic stress and abdominal obesity were
entered in block two. The interaction term, calculated as the product
of centered chronic stress and abdominal obesity, was entered in
block three. As shown in Table 3, hierarchical multiple regressions demonstrated that WC signicantly predicted blunted SBP ( = .32,
s.e. = .08, p = .01) and MAP ( = .25, s.e. = .05, p = .02) change
from baseline to stress tasks. Total chronic stress did not predict change
across any cardiovascular measure. Separate regression analyses to test
the effects of stress intensity and stress duration on cardiovascular reactivity demonstrated that neither stress measure signicantly predicted
change in cardiovascular reactivity. Table 3 also presents results from
the hierarchical regression analyses that examined whether chronic
stress moderated the relationship between WC and cardiovascular reactivity. After adjusting for covariates, the WC Stress interaction signicantly predicted blunted SBP ( = .27, s.e. = .001, p = .02) and
MAP ( = .29, s.e. = .001, p = .02) change. The addition of the interaction term explained 4.1% of the variance in SBP change and 4.5%
in MAP change. The interaction did not predict signicant change in
HR, DBP, PEP, or RSA. For DBP, although the overall model was not signicant, the interaction was signicant and explained 4.9% of the
variance.
In order to understand the nature of the interaction between
chronic stress and abdominal obesity in their associations with SBP
and MAP reactivity, simple slopes analysis was conducted to examine
the relationship between abdominal obesity and cardiovascular reactivity at different levels of chronic stress. According to Fig. 1, higher abdominal obesity was signicantly associated with smaller SBP
reactivity at one standard deviation above the mean of chronic stress
(b = .63, s.e. = .18, p b .001), but not at the mean or one standard
deviation below the mean. As can be seen in Fig. 2, higher abdominal
obesity was also signicantly associated with decreased reactivity at
one standard deviation above the mean of chronic stress (b = .36,

Fig. 2. Simple slopes analysis for MAP reactivity. Simple slopes of the association between abdominal obesity and mean arterial pressure (MAP) reactivity at 1 standard
deviation above mean chronic stress (high), mean chronic stress, and 1 standard deviation below mean chronic stress (low).

s.e. = .11, p = .01), but not at the mean or one standard deviation
below the mean. These results indicate that there was a stronger link
between abdominal obesity and cardiovascular reactivity among
those who reported concurrently high chronic stress compared to
those reporting average or low chronic stress. In addition, abdominal
obesity and cardiovascular reactivity were not associated among individuals with either a normal or low level of chronic stress.
3.6.1. BMI, WHR, and cardiovascular reactivity
Additional analyses were conducted to examine the associations between generalized obesity, abdominal obesity measured by WHR,
chronic stress, and cardiovascular reactivity. The results showed that
BMI was signicantly associated with increased baseline SBP ( = .42,
s.e. = .14, p b .001) and MAP ( = .32, s.e. = .09, p b .001). WHR
was not associated with baseline values across any cardiovascular
outcome variable. For cardiovascular reactivity, BMI signicantly predicted blunted SBP ( = .33, s.e. = .19, p = .01) and MAP change
( = .25, s.e. = .11, p = .02), but did not predict changes in other
cardiovascular variables. In addition, the BMI Stress interaction signicantly predicted blunted SBP ( = .29, s.e. = .001, p = .01) and
MAP change ( = .31, s.e. = .001, p = .01), but was nonsignicant
for HR, DBP, PEP, and RSA change. The WHR main effect and
WHR Stress interaction did not predict change across any cardiovascular variable.
The simple slopes analysis indicated that higher generalized obesity was signicantly associated with decreased SBP reactivity at one
standard deviation above the mean of chronic stress (b = .93,
s.e. = .37, p = .01), but not at the mean or one standard deviation
below the mean. For MAP reactivity, it was found that high generalized obesity was also signicantly associated with decreased reactivity
at one standard deviation above the mean of chronic stress
(b = .80, s.e. = .23, p b .001), but not at the mean or one standard
deviation below the mean. These results indicate that there was a
stronger link between generalized obesity and cardiovascular reactivity among those reporting concurrently high levels of chronic stress
compared to those reporting average or low chronic stress. In addition, the results for generalized obesity are similar to those for abdominal obesity. This outcome would be expected given the high
correlation between the two measures.
4. Discussion

Fig. 1. Simple slopes analysis for SBP reactivity. Simple slopes of the association between
abdominal obesity and systolic blood pressure (SBP) reactivity at 1 standard deviation
above mean chronic stress (high), mean chronic stress, and 1 standard deviation below
mean chronic stress (low).

Numerous studies have examined the association between cardiovascular reactivity, abdominal obesity, and chronic stress. However,
existing studies have only tested the individual effects of abdominal
obesity and chronic stress on cardiovascular reactivity. In this study,
we observed that abdominal obesity was not only associated with
smaller SBP and MAP change during stress tasks, but also interacted
with chronic stress to signicantly predict blunted SBP and MAP
change. Specically, individuals with concurrently high abdominal

78

K. Singh, B.-J. Shen / International Journal of Psychophysiology 90 (2013) 7379

obesity and chronic stress exhibited blunted cardiovascular reactivity,

suggesting a blunted cardiovascular response. In addition, given the
high correlation between the two measures, it was not surprising
that models testing the effects of generalized obesity (e.g., BMI)
yielded similar results to those examining abdominal obesity.
Although past research has yielded mixed results, previous studies
that have employed stringent statistical controls also demonstrated an
inverse relationship between abdominal obesity and cardiovascular reactivity (Hamer et al., 2007; Phillips, 2011). For example, Carroll et al.
(2008) demonstrated that after the inclusion of a number of statistical
covariates, previously observed positive associations between abdominal obesity and cardiovascular reactivity were no longer signicant, and
in some cases became negatively associated. In the current study, the
association between abdominal obesity and cardiovascular reactivity
was negative, regardless of the inclusion of statistical covariates. It is
plausible that this nding may be due to the strict exclusion criteria
resulting in a homogeneous sample. The majority of existing studies
did not employ strict exclusionary criteria in sample selection, and
thus, extraneous inuences may have had a stronger effect on study
outcomes. Future studies may consider screening for and excluding variables known to inuence the cardiovascular system. In addition, essential statistical controls (e.g., baseline cardiovascular responding) should
be carefully considered and included in all statistical models examining
change in cardiovascular response.
Our nding of high basal cardiovascular activity among the abdominally obese but reduced reactivity during stress is consistent with previous observations (Carroll et al., 2008; Piccirillo et al., 1996). Further
evidence of blunted reactions to stress has been demonstrated. For example, compared to normal-weight individuals, obese individuals
were found to show a signicantly smaller postprandial sympathetic
nervous system response after the ingestion of a meal, suggesting a
blunted sympathetic nervous system response (Tentolouris et al.,
2003). The results reported from these studies suggest that obese individuals, in particular, may incur difculty mounting appropriately-sized
cardiovascular responses during acute stress. Although the mechanisms
were not directly tested in this study, one promising explanation is that
the hormonal (e.g., leptin, insulin, glucocorticoids) and autonomic activity characteristic of the abdominally-obese state may contribute to
high basal cardiovascular activity, potentially producing dysregulated
beta-adrenergic receptor responsivity. The inuence of ongoing,
long-lasting chronic stress may further potentiate beta-adrenergic receptor dysregulation and further suppress cardiovascular responding
in the face of acute stress.
Given the pattern of high basal cardiovascular activity and blunted
cardiovascular reactivity during stress among obese individuals, it is
worth noting that high basal cardiovascular activity was unlikely to
inuence the degree of change during stress as baseline measures of
SBP, DBP, and MAP were not signicantly associated with their respective change values. In other words, the signicant results for
these variables were unlikely due to a ceiling effect. Interestingly,
for the cardiovascular variables that were not associated with any
measure of obesity or chronic stress (e.g., HR, PEP, RSA), the baseline
values were signicantly associated with each of their respective
change values. Thus, a possible ceiling effect due to high basal activity
limiting the degree of change following stress may help explain the
non-signicant ndings for HR, PEP, and RSA.
A number of studies have demonstrated that abdominal obesity
may be a stronger predictor of health-related risk compared to generalized obesity (Lee et al., 2008; Price et al., 2006; Wei et al., 1997). The
results from the current investigation support the notion that abdominal and generalized obesity have important inuences on cardiovascular regulatory processes. Although the large majority of literature
indicates that abdominal obesity is particularly detrimental to health,
some existing research suggests that generalized and abdominal
obesity may be similar predictors of pathophysiology (Dalton et al.,
2003; Neovius et al., 2004; Vazquez et al., 2007), particularly for

cardiovascular outcomes (Huxley et al., 2009). In addition to the measurement of abdominal obesity, future studies examining the role of
obesity on cardiovascular regulation should carefully consider the assessment of generalized obesity as an additional anthropometric
measurement.
There are a few limitations in the current study that should be
noted. They also point to directions for future research. First, although
we had a fairly comprehensive assessment of cardiovascular functioning, we did not assess endocrinal functioning before and during
stress. Therefore, we were not able to test specic mechanisms that
may have potentially contributed to the observed moderation. The assessment of hormonal functioning before and during stress may have
also allowed us to explain the tendency for obese individuals to produce a blunted vascular (e.g., SBP, DBP, MAP) rather than cardiac response (e.g., HR, PEP, RSA). In fact, previous studies have suggested
that insulin, a sympatho-activating hormone that promotes vasoconstriction, may especially predispose obese individuals to express an
exaggerated vascular response to stress (Jern et al., 1992). The possibility exists, however, that with repeated and prolonged insulin exposure, obese individuals may become resistant to its sympathoactivating effects; thus producing a blunted vascular response. The
assessment of hormonal functioning may have allowed us to test
this specic mechanism. Second, although the rate of generalized
obesity, on the basis of BMI, in this sample was quite high (56 of
the total 122 [46%] participants), it is also important to note that
only 23 of the 122 (19%) participants met criteria for abdominal obesity. Thus, future studies should aim to include as many participants
with high abdominal obesity as possible. In addition, this study focused on the cross-sectional relationships between chronic stress, abdominal obesity, and cardiovascular responses to acute laboratory
stressors. Without longitudinal data over a longer period, we were
not able to determine the directionality of inuence among these variables. Finally, we were not able to examine the inuences of chronic
stress and abdominal obesity on recovery after stress. Prolonged recovery after stress exposure has been found to inuence long-term
cardiovascular health, and may even be a more useful predictor of
long-term blood-pressure changes than reactivity (Borghi et al.,
1986). Future studies examining the interaction of chronic stress
and obesity on cardiovascular reactivity should also test the inuences of these variables during a prolonged recovery period.
4.1. Conclusions
The current investigation was the rst to examine the interaction of
abdominal obesity and chronic stress on cardiovascular reactivity. We
tested cardiovascular activity across a multitude of measures in a particularly heavy sample. Since important exclusion criteria and statistical
controls were included, the pattern of ndings were unlikely attributable to a ceiling effect due to high baseline cardiovascular activity. Instead, our results suggest a blunted cardiovascular response system
among the obese, as they more frequently expressed blunted cardiovascular responses during acute stress compared to normal-weight participants. This effect was moderated by chronic stress such that obese
participants who were under high levels of chronic stress expressed a
particularly blunted cardiovascular stress response relative to obese
participants under moderate or low levels of stress.
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