www.elsevier.com/locate/ijpsycho

International Journal of Psychoph

Hostility and sex differences in the magnitude, duration, and determinants

of heart rate response to forehead cold pressor: Parasympathetic

aspects of risk

John M. Ruiz a,*, Bert N. Uchino b, Timothy W. Smith b

a Department of Psychology, Washington State University, PO Box 644820, Pullman, WA 99164-4820, USAb Department of Psychology, University of Utah, 380 South 1530 east, Room 502, Salt Lake City, UT 84112-0251, USA

Received 4 May 2005; received in revised form 25 July 2005; accepted 27 July 2005

Available online 24 August 2005

Abstract

Recent models hypothesize that hostility confers increased risk of CHD through weaker parasympathetic dampening of cardiovascular

reactivity (CVR). We tested this possibility using the forehead cold pressor task, a common maneuver which elicits the ‘‘dive reflex’’

characterized by a reflexive decrease in HR presumably through cardiac-parasympathetic stimulation. Participants were initially chosen from

the outer quartiles of a sample of 670 undergraduates screened using the hostility subscale of the Aggression Questionnaire ([Buss, A.H.,

Perry, M., 1992. The Aggression Questionnaire. Journal of Personality and Social Psychology, 63, 452-459.]). The final sample of 80

participants was evenly divided between men and women and high and low hostility. Following a 10-min baseline, participants underwent a

3-min forehead cold pressor task. The task evoked a significant HR deceleration that was mediated by PNS activation, as assessed by

respiratory sinus arrhythmia (RSA). Replicating prior research, men displayed greater decrease in HR. More important, low hostiles

maintained larger HR deceleration over time compared to high hostiles although the autonomic basis for this effect was unclear. The findings

broaden understanding of hostility and sex-related cardiovascular functioning and support the task as a method for evoking PNS-cardiac

stimulation.

D 2005 Elsevier B.V. All rights reserved.

Keywords: Hostility; Vagal tone; Respiratory sinus arrhythmia; Forehead cold pressor; Heart rate variability; Impedance cardiography

1. Introduction

Epidemiological evidence supports individual differences

in hostility and anger as risk factors for coronary heart

disease (CHD) and all-cause mortality (Barefoot et al.,

1983, 1995). These findings are based on increasingly well-

designed cross-sectional and prospective studies (Gallo and

Matthews, 2003; Rozanski et al., 1999; Suls and Bunde,

2005). For example, individual differences in hostility and

anger predict severity of carotid atherosclerosis (Julkunen et

al., 1994; Matthews et al., 1998) and incidence of MI,

cardiac death, and stroke (Everson et al., 1999; Kawachi et

al., 1996; Williams et al., 2000). In addition, a quantitative

0167-8760/$ - see front matter D 2005 Elsevier B.V. All rights reserved.

doi:10.1016/j.ijpsycho.2005.07.005

* Corresponding author. Tel.: +1 509 335 8034; fax: +1 509 335 5043.

E-mail address: ruizjx@wsu.edu (J.M. Ruiz).

review found support for a relationship between hostility

and associated behaviors and subsequent clinical manifes-

tations of CHD (Miller et al., 1996). Cardiovascular

reactivity (CVR) is one proposed mechanism linking

psychosocial risk factors and cardiovascular disease

(CVD) (Krantz and Manuck, 1984; Manuck, 1994).

Laboratory and ambulatory studies demonstrate a reliable

relationship between hostility and larger and more frequent

cardiovascular responses (Christensen and Smith, 1993;

Guyll and Contrada, 1998; Shapiro et al., 1997). Studies

have shown these physiological responses are also associ-

ated with atherosclerosis (Kamarck et al., 1997; Matthews et

al., 1993) and myocardial ischemia in the laboratory

(Blumenthal et al., 1995; Gottdiener et al., 1994; Krantz et

al., 1991) and during daily life (Bairey et al., 1990; Gabbay

et al., 1996; Legault et al., 1995).

ysiology 60 (2006) 274 – 283

J.M. Ruiz et al. / International Journal of Psychophysiology 60 (2006) 274–283 275

Recent models identify autonomic imbalance as a

potentially important mechanism linking hostility to exag-

gerated CVR (Brosschot and Thayer, 1998; Sloan et al.,

1999; Rhodes et al., 2002; Williams, 1994). Specifically,

these models hypothesize that individual differences in

negative affect including hostility and trait anger are

associated with lower parasympathetic activity or vagal

tone, resulting in less attenuation or dampening of cardiac

response. Prospective investigations have demonstrated an

association between low heart rate variability (HRV: an

index of parasympathetic influence) and recurrent coronary

events and cardiovascular and all cause mortality (Bigger et

al., 1993a,b; Kleiger et al., 1987; Tsuji et al., 1996).

Investigations involving hostility and parasympathetic

control have primarily focused on acute autonomic reac-

tivity as opposed to basal differences in control capability.

For example, in a small, mixed sex sample, Sloan and

colleagues (2001) found greater decreases in respiratory

sinus arrhythmia (RSA, a non-invasive index of para-

sympathetic control of the heart) in response to traditional

mental stressors amongst high hostiles. However, the

question of whether these responses are due to differences

in situational appraisal or other psychological mechanisms

as opposed to underlying physiological differences in

parasympathetic/vagal capability remains open. Individual

differences in parasympathetic control may impair regula-

tion of cardiac responses regardless of cognitive factors,

perhaps impeding recovery following exposure to acute

stressors.

To date, only one study has investigated the relationship

between hostility and parasympathetic cardiac control in

response to reflex challenge. Reflex challenges may provide

a less ambiguous test of underlying autonomic correlates of

hostility, due to the reduced level of psychological

mediation (e.g., appraisal) compared to other laboratory

tasks. Graham and colleagues (1996) found Cook–Medley

hostility scores were inversely related to the magnitude of

change in heart period variability (HPV: R–R interbeat

interval) in response to graded trials of bilateral carotid

baroreflex stimulation, a technique for evoking carotid–

cardiac vagal influence on the heart. Similar findings among

high Type A individuals by Fukudo et al. (1992) and

Muranaka et al. (1988) suggest that constructs similar to

hostility may be associated with weaker parasympathetic

cardiac control. However, interpretation is limited by the

lack of direct assessment of parasympathetic functioning

such as RSA (for review and recommendations see Berntson

et al., 1997). In addition, these data are limited to men.

Recent findings suggest that men show less parasympathetic

withdrawal during psychological stressors (Sloan et al.,

2001; Hughes and Stoney, 2000) and larger increases in

parasympathetic outflow in response to a facial cold pressor

task (Hughes and Stoney, 2000), suggesting greater cardiac

vagal activity in men than women. Thus, hostility, sex, and

possibly their interaction may be associated with important

differences in parasympathetic cardiac control.

1.1. The forehead cold pressor as a parasympathetic task

Cold pressor tasks are widely used to examine individual

differences in pain perception and physiological response.

The tasks reliably evoke physiological responses although

the degree and character of such responses may vary with

the instructional set. For example, research suggests that

perceptions of the task mediate affective responses with

some influence on the degree of physiological response

(Baker and Kirsch, 1991; Peckerman et al., 1991; Saab et

al., 1993). In addition, the pattern of physiological response

varies by cold pressor methodology (Durel et al., 1993).

Three methods are commonly employed, foot or leg

immersion in ice water, hand immersion, and application

of cold stimulation to the forehead. Foot and hand

immersion are commonly associated with increased periph-

eral resistance (e.g., blood pressure) and increased heart rate

(Peckerman et al., 1994; Saab et al., 1993). In contrast the

forehead cold pressor is an effective method for eliciting a

simulated ‘‘dive reflex’’, characterized by a reduction in

heart rate in response to cold temperature to the forehead

region (Heath and Downey, 1990; Khurana et al., 1980;

Peckerman et al., 1994; Reyners et al., 2000; Wildenthal et

al., 1975). Blood pressure responses specifically during

forehead cold pressor are mixed (Heath and Downey, 1990;

Peckerman et al., 1991; Saab et al., 1993).

Research has demonstrated the reproducibility of cardiac

responses to the forehead cold pressor (Durel et al., 1993;

Ryan et al., 1976). The assumed anatomical pathway

involves stimulation of trigeminal afferents in the face via

cold, producing stimulation to central brainstem connections

to parasympathetic (vagal nerve) efferents that slow the

heart (Peckerman et al., 1994; White and McRitchie, 1973).

Although more evidence on the autonomic determinants of

this task is needed, Hughes and Stoney (2000) reported

concurrent HR deceleration and increased RSA in response

to forehead cold stimulation. The forehead cold pressor has

been used to investigate between group differences in

cardiac response in a number of samples including Blacks

and Whites, individual differences in pain perception

(Peckerman et al., 1994; Saab et al., 1993), and depressive

symptoms (Hughes and Stoney, 2000). However, no studies

have used the task to examine potential hostility differences

in cardiovascular functioning.

1.2. Current experiment

The aims of the current experiment were to examine

hostility, sex, and hostility by sex differences in HR

response to the forehead cold pressor task. Participants

were told that they were part of a study of temperature

effects on cardiovascular functioning. Following a baseline

period a standard ice bag was held across the forehead and

nose for 3-min. Physiological measures were taken con-

tinuously during both the baseline and task period in order

to analyze change. Participants completed ratings of mood

J.M. Ruiz et al. / International Journal of Psychophysiology 60 (2006) 274–283276

following both the baseline and task. Impedance cardiog-

raphy was used to examine HR and its underlying

autonomic determinants while blood pressure was assessed

each minute. It was hypothesized that the task would evoke

HR deceleration and increased RSA. Low hostiles were

expected to display larger HR deceleration and a greater

increase in RSA compared to high hostile participants in

response to the task. In addition, we sought to replicate

previous findings suggesting men display greater decreases

in HR and larger increases in RSA compared to women in

response to cold stimulation.

2. Methods

2.1. Participants

Participants were chosen from the outer quartiles scores

<13, >21) of a sample of 670 undergraduates screened

using the hostility subscale of the Aggression Question-

naire (AQ; Buss and Perry, 1992). The AQ was chosen

because of its psychometric superiority as a measure of

hostility compared to other measures such as the Buss–

Durkee Hostility Inventory (BDHI; Buss and Durkee,

1957) and the Cook Medley Hostility Scale (Cook and

Medley, 1954). Despite a lack of research examining the

AQ as a predictor of CHD, individual differences in AQ-

assessed hostility are associated with expected differences

in magnitude and duration of cardiovascular reactivity

(Smith and Gallo, 1999; Smith et al., 2004). The AQ

Hostility subscale measures hostile cognitions such as

mistrust (‘‘I am suspicious of overly friendly strangers’’) or

perceived slights (‘‘Other people always seem to get the

breaks’’). Respondents reported the extent to which items

are characteristic of them on a 5-point scale ranging from 1

(extremely uncharacteristic) to 5 (extremely characteristic).

The Hostility subscale has a reported internal consistency

of .77 and test–retest reliability of .70 (Buss and Perry,

1992), and is demonstrated to have strong associations

with interpersonal antagonism (Gallo and Smith, 1998;

Ruiz et al., 2001) and other measures of hostility (e.g.,

Cook and Medley, 1954) associated with cardiovascular

morbidity and mortality.

Trait self-report instruments, even psychometrically

sound instruments like the Aggression Questionnaire, are

not perfect assessment tools (test–retest correlations <1.0).

In order to reduce potential mischaracterization error, we

chose to reassess hostility at the conclusion of the lab

session. Only participants scoring in the expected half of a

median split distribution, derived from the original sample

pool of 670 participants, were retained for analysis. Six

participants (7%) did not meet these criteria and were

excluded from the final sample. In order to maintain equal

cell size, replacement participants were chosen based on sex

and initial hostility screening criteria. Following the task,

each replacement participant was again screened for

hostility. All 6 replacement participants met the median

split criteria.

The final sample of 80 participants was evenly divided

between men and women and high and low hostility. All

were healthy undergraduates from the University of Utah.

The mean age of participants was 21.16 years (SD=3.17),

and the mean years of education was 13.63 (SD=1.96). Of

the participants 88% identified themselves as Caucasian

with the remainder self-identifying as Asian American (9%),

Hispanic (1%), and other (3%).

2.2. Procedure

2.2.1. Baseline period

Sessions were conducted in a single-occupant chamber

with adjoining space for monitoring equipment. Except for

brief interactions with the experimenter, participants were

alone. On arrival, they listened to an audiotape introducing

the experiment as examining ‘‘cardiovascular responses to

temperature.’’ They were told that their responses would be

measured during a baseline period and while holding a

standard ice bag over their forehead and eyes. To limit

anxious anticipation during baseline, we avoided further

specific description of the task or instructions. Following

initial informed consent, four mylar band sensors were

placed on the participant and connected to an impedance

cardiograph. Participants were asked handedness prior the

attachment of a blood pressure cuff. The cuff was then

placed on the upper potion of the nondominant arm to

ensure that it would not interfere with the participants’

ability to complete questionnaires during the study. The 10-

min baseline involved a minimally demanding task (i.e.,

‘‘vanilla baseline’’; Jennings et al., 1992), in which

participants were asked to examine and rate pairs of pictures

at 1-min intervals.

2.2.2. Cold procedure

Following baseline, the audiotaped instructions intro-

duced the forehead cold pressor task. A standard latex ice

bag was placed across the bridge of the nose, covering the

forehead and eyes for 180-s (Durel et al., 1993; Saab et al.,

1993). The bag contained a mixture of 4.5 cups crushed ice

and 0.5 cups water. During the task data collection was

automated, allowing the experimenter to hold the bag to

reduce movement on the part of the participant and to

monitor the participant’s comfort level and maintain

consistency in the application.

2.3. Affect measurement

Some studies have shown the cold pressor to evoke

changes in affect although no studies have done so with

specific focus on hostility (Peckerman et al., 1991, 1994).

In order to account for any potential role of affect change

in cardiovascular response participants completed an affect

measure following the baseline and cold pressor. The

J.M. Ruiz et al. / International Journal of Psychophysiology 60 (2006) 274–283 277

questionnaire consisted of twelve 4-point Likert items

reflecting anger and anxiety (see Smith et al., 2004). Ten

of the 12 items were drawn from the State–Trait Person-

ality Inventory (STPI: Spielberger, Unpublished Manual).

Items were chosen based on obvious content-validity.

Anxiety was assessed with six items (four negatively

valenced: worried, tense, nervous, anxious; two positively

valenced, reverse scored: calm, relaxed) drawn from the

state anxiety scale of the STPI. Cronbach’s alpha

coefficients for the six-item anxiety scale were 0.83 for

baseline and 0.82 for the task. The anger scale was

comprised of four negatively valenced items (annoyed,

angry, irritated, aggravated) taken from the STPI anger

subscale. Due to the lack of positively worded items

(inversely associated with anger) in the STPI we added

two additional items (friendly, kindhearted) to this scale.

Cronbach’s alpha coefficients for the six-item anger scale

were 0.71 for baseline and 0.87 for the task. Total item

correlations were not adversely affected by the inclusion of

these two positively valenced items. Prior research

demonstrated this measure to correspond to expected

differences in hostility and cardiovascular reactivity (Smith

et al., 2004).

2.4. Physiological measures

A Minnesota Impedance Cardiograph Model 304B

(Surcom, Inc., Minneapolis, MN) assessed electrocardio-

gram (ECG), basal thoracic impedance (Z0), and the first

derivative of the impedance signal (dZ / dt). Four mylar

bands were placed in the tetrapolar configuration (Sherwood

et al., 1990). A 4 mA AC current at 100 kHz was passed

through the two outer bands, and Z0 and dZ / dt were

recorded from the two inner bands. The ECG, Z0, and dZ /

dt signals were digitized at 500 Hz. Data were analyzed

using ANS Suite software (Uchino et al., 1995). We

ensemble averaged these data within 1-min epochs and

verified or edited waveforms prior to analyses. Stroke

volume (SV) was estimated using the Kubicek equation

(see Sherwood et al., 1990), and CO in 1/min was

calculated by multiplying heart rate (HR) by the product

of (SV/1000). Total peripheral resistance (TPR) was

measured in resistance units (dynes-s�cm�5) on the basis

of mean arterial pressure (MAP) and CO (i.e., TPR=

MAP/CO X 80). Preejection period (PEP) was calculated

as the time interval, in milliseconds, between the Q-point

of the ECG and the B-point of the dZ / dt signal. PEP

reflects sympathetic control of the heart (see Cacioppo et

al., 1994).

RSA provides an index of parasympathetic control of the

heart. It was calculated on the basis of the digitized interbeat

intervals (IBI) and checked and edited for artifacts using the

detection algorithm of Berntson et al. (1990). A heart period

time series was created from the IBI series using a

‘‘weighted’’ beat algorithm (Berntson et al., 1995). We

detected sharp transitions in the heart period time series

(e.g., because of arrhythmia) using the Berntson et al.

(1995) algorithm and removed them by smoothing. A linear

(first order) polynomial was fit to, and subtracted from, the

heart period time series (Litvack et al., 1995). Subtraction of

this first-order polynomial (linear detrending) acted as a

high pass filter, removing very large ultralow frequency

trends (including the DC component) from the input signal.

After linear detrending, the heart period time series was

band-pass filtered from 0.12 to 0.40 Hz using an interpo-

lated finite impulse response filter (Neuvo et al., 1984). The

power spectrum of the heart period time series was

calculated using a fast Fourier transform and scaled to

ms2/Hz. RSA was calculated as a natural log of the area

under the heart period power spectrum within the corner

frequencies of the band-pass filter (see Litvack et al., 1995).

Average RSA was calculated for each minute. A Dinamap

Model 8100 monitor (Critikon Corporation, Tampa, FL)

was used to measure systolic blood pressure (SBP), diastolic

blood pressure (DBP), and MAP. It uses the oscillometric

method to estimate blood pressure. Blood pressure was

measured once per minute.

3. Results

3.1. Affective responses and baseline equivalence of groups

Self-reported anger and anxiety were measured at base-

line and immediately following the task. No baseline

differences in affect were found in 2 (hostility groups)�2

(sex) ANOVAs. The low self-reported affect values follow-

ing the baseline suggest that participants were in a relatively

relaxed state prior to the cold pressor task. Changes in affect

were calculated to determine potential differences in task

impact between groups (see Table 1). A marginal effect for

hostility was found for self-reported anger, F(1,74)=3.88,

p =.053, g2= .050, where high hostiles reported a larger

increase in anger relative to low hostiles. High hostiles also

reported a larger increase in anxiety, F(1,74)=4.71, p <.05,

g2= .060. Finally, a significant effect was found for sex

where women reported a larger increase in anxiety than men

following the task, F(1,74)=7.58, p <.01, g2= .093.Baseline values for key physiological indices are

presented in Table 2. A 2 (high vs. low hostility)�2 (men

vs. women) ANOVA was used to test between group

differences. A significant sex effect was found for two

measures: SBP and respiration rate (RR). Compared to

women, men displayed significantly higher SBP,

F(1,76)=32.60, p <.001, and lower RR at baseline. Differ-

ences between high and low hostiles were found only for

CO where high hostiles displayed larger baseline CO,

F(1,68)=4.20, p <.05. Interactions of hostility by sex were

also found for CO, F(1,68)=7.57, p < .01, and TPR,

F(1,68)=5.36, p <05. Specifically, high hostile men dis-

played larger CO compared to low hostile men at baseline,

t(36)=3.36, p <.01. High and low hostile women did not

Table 1

Baseline values and change from baseline to task in self-reported anger and anxiety

Low hostiles High hostiles Total sample

Men Women All low Men Women All high Men Women

Baseline

Anger 8.9 (3.8) 9.2 (1.7) 9.1 (2.9) 9.2 (2.2) 10.6 (2.6) 9.9 (2.5) 9.1 (3.0) 9.9 (2.5)

Anxiety 8.3 (3.8) 7.9 (2.6) 8.1 (3.2) 8.1 (3.2) 10.2 (2.9) 9.1 (2.6) 8.2 (2.9) 9.0 (2.9)

Change to task

Anger 1.80 (.92) 3.99 (.89) 2.90 (.64) 4.46 (.89) 4.89 (.91) 4.68 (.63) 3.13 (.64) 4.40 (.63)

Anxiety 1.10 (.84) 4.61 (.83) 2.85 (.59) 4.13 (.82) 5.22 (.85) 4.67 (.58) 2.62 (.59) 4.91 (.58)

J.M. Ruiz et al. / International Journal of Psychophysiology 60 (2006) 274–283278

differ, t(32)=0.51, p =n.s. High hostile men also displayed

lower TPR compared to low hostile men, t(36)=2.68,

p <.05, whereas high and low hostile women did not differ,

t(32)=0.51, p =n.s.

3.2. Primary analyses

Consistent with prior recommendations (Llabre et al.,

1991), change scores (i.e., task minus baseline) were

computed for each minute of the task period. Because

baseline levels can affect degree of change (Benjamin,

1967), baseline values were included as a covariate in mixed

analyses of covariance (ANCOVAs). During the task period

we computed three-way mixed ANCOVAs (i.e., High vs.

Low Hostility�Sex�3 min) for each cardiovascular

measure. To follow-up significant effects involving the

trials factor, mean comparisons were calculated using

pooled error terms (Bernhardson, 1975). Impedance-derived

HR was considered the primary outcome. SBP and DBP

reactivity were also examined, and CO and TPR were

examined as determinants of blood pressure responses. PEP

and RSA were examined as determinants of HR responses.

Table 2

Means and standard deviations for baseline physiological measures

Measure Low hostiles H

Men Women Total M

SBP (mm/Hg) 120.30

(9.35)

106.50

(10.18)

113.40

(11.91)

1

(9

DBP (mm/Hg) 67.28

(4.79)

64.32

(8.09)

65.80

(6.73)

6

(5

TPR (dyne-s*cm�5) 1207.47

(343.16)

981.117

(283.29)

1100.25

(332.36)

9

(3

CO (l/min) 5.97

(1.31)

6.78

(1.59)

6.35

(1.48)

7

(2

HR (bpm) 70.66

(10.70)

70.39

(9.23)

70.53

(9.89)

6

(7

PEP (ms) 125.82

(17.95)

125.01

(9.12)

125.44

(14.27)

1

(1

RSA (natural log) 6.65

(.96)

6.74

(.69)

6.69

(.83)

6

(1

RR 15.1

(1.5)

16.8

(2.0)

15.9

(2.0)

1

(1

SBP = systolic blood pressure; DBP = diastolic blood pressure; TPR = total per

minute; PEP = preejection period; RSA = respiratory sinus arrhythmia; RR = res

As discussed above, the effects of cold stimulation were

expected to produce differential HR deceleration responses

accompanied by increases in RSA. No BP, TPR, or PEP

effects were expected.

3.3. Effects of cold on dive-reflex response

As expected, application of the cold pressor resulted in a

significant reduction in HR compared to baseline (69.48 vs.

64.49 bpm), F(1,71)=104.15, p <.001, g2= .595. Consis-

tent with expectations, a significant hostility by time

interaction was found for change in HR during the 3-min

task, F(2,140)=4.37, p <.02, g2= .059 (see Fig. 1). Low and

high hostile participants had similar initial HR decelerations

(see Table 3). Planned-comparisons were performed to

compare differences in HR both within each hostility group

as well as between groups at each minute. Planned

comparisons showed that for low hostiles, despite a

significant loss of HR deceleration between minutes 2 and

3, t(140)=1.97, p <.05, the overall deceleration across the

task from minute 1 to 3 was stable, t(140)= .30, p =ns). In

contrast, heart rate deceleration waned over the three minute

igh hostiles Total sample

en Women Total Men Women

18.50

.92)

108.18

(8.21)

113.34

(10.40)

119.40

(9.56)

107.34

(9.17)

6.98

.36)

66.02

(5.58)

66.50

(5.43)

67.13

(5.02)

65.17

(6.92)

25.31

01.95)

1029.34

(262.93)

974.27

(284.90)

1073.82

(350.35)

1003.81

(270.86)

.88

.15)

6.50

(1.62)

7.23

(2.02)

6.87

(1.98)

6.65

(1.59)

6.29

.98)

70.55

(7.78)

68.48

(8.07)

68.47

(9.57)

70.48

(8.35)

21.25

5.80)

117.63

(17.93)

119.55

(16.68)

123.65

(16.90)

121.54

(14.25)

.72

.09)

7.21

(1.09)

6.97

(1.16)

6.68

(1.07)

6.99

(.95)

5.1

.4)

15.9

(2.0)

15.5

(1.7)

15.1

(1.5)

16.3

(2.0)

ipheral resistance; CO = cardiac output; HR = heart rate; bpm = beats per

piration rate.

-7

-6

-5

-4

-3

-2

-1

01 2 3

Time (min)

Ch

ang

e in

HR

(b

pm

)

Low Hostile

High Hostile

p <.05

p <.05p <.05

p <.05

Fig. 1. Change in heart rate over time for high and low hostiles.

J.M. Ruiz et al. / International Journal of Psychophysiology 60 (2006) 274–283 279

task for high hostiles (minutes 1 to 3, t(140)=4.73, p< .001)

with a significant loss of deceleration between minutes 2

and 3, t(140)=3.10, p <.01. Comparison between groups

revealed that high hostiles displayed significantly less HR

deceleration during the 3rd minute compared to low

hostiles, t(70)=2.21, p <.05.

In addition to the hostility by time effect, an expected

significant sex main effect was also found, F(1,70)=11.30,

p <.001, g2= .139. As depicted in Fig. 2A, men displayed a

greater reduction in HR in response to the cold stimulation

as compared to women.

3.4. Analysis of HR determinants

Autonomic responses to cold stimulation (see Table 3)

were characterized by a significant increase in parasympa-

thetic (RSA; F(1,71)=44.57, p <.001, g2= .386) as well as

Table 3

Change in HR and determinants of HR during each minute of cold task

Measure Low hostiles High hostiles

Men Women All low Men

HR (bpm)

Min 1 �6.33 (1.01) �4.54 (1.07) �5.44 (.74) �7.53Min 2 �7.85 (1.08) �4.63 (1.14) �6.25 (.79) �6.43Min 3 �7.85 (1.08) �3.63 (1.11) �5.14 (.76) �4.66Total �6.95 (.94) �4.27 (.99) �4.36 (.65) �6.21

RSA (natural log)

Min 1 .74 (.19) .44 (.20) .59 (.14) .61

Min 2 1.01 (.17) .33 (.18) .67 (.13) .59

Min 3 .69 (.17) .11 (.18) .40 (.12) .49

Total .81 (.16) .29 (.17) .55 (.11) .57

PEP (ms)

Min 1 �5.32 (1.97) �6.79 (2.01) �6.06 (1.42) �5.34Min 2 �5.10 (2.67) � .35 (2.73) �2.72 (1.92) �2.80Min 3 �2.55 (1.48) �6.14 (1.51) �4.34 (1.06) �5.86Total �4.32 (1.64) �4.43 (1.67) �4.37 (1.18) �4.69

an unexpected increase in sympathetic activity (PEP;

F(1,68)=24.22, p <.001, g2= .263). A marginal main effect

for sex in the expected direction, was found on RSA,

F(1,70)=3.69, p <.06, g2= .050. Men displayed greater

increase in RSA in response to the cold task as compared

to women (Fig. 2B). However, no effects of hostility on

RSA were found, suggesting that the hostility differences in

HR were not mediated by differences in parasympathetic

functioning.

An unexpected three-way interaction of Time�Hosti-

Hostility�Sex was found for PEP, F(2,132) =4.37,

p <.02, g2= .062. This effect was driven by fluctuations

in low hostile women who displayed a significant loss of

PEP shortening from minute 1 to minute 2 (see Table 3),

t(132)=2.70, p <.01 and a significant increase in PEP

shortening from minute 2 to minute 3, t(132)= .30,

p <.05.

3.5. Mediational analyses

Mediational analyses were conducted in a manner

consistent with Baron and Kenny’s (1986) approach to

examining mediation. To test the hypothesis that the

forehead cold pressor is a task for evoking parasympathetic

stimulation to the heart, autonomic responses (RSA, PEP)

were examined as potential mediators of the aforementioned

task effect on HR. Raw baseline and task HR were entered

into a two-way ANCOVA with raw task PEP and RSA

entered together as covariates. Both task RSA, F(1,

64)= .12.86, p <.001, g2= .167, and PEP, F(1, 64)= .5.87,

p <.02, g2= .084, emerged as significant predictors and

explained the time effect on HR, F(1, 64)= .04, p =n.s.,

g2= .001. Second, we examined autonomic mediation

effects of HR in the context of change from baseline.

A Three-way mixed ANCOVAs (i.e., High vs. Low

Hostility�Sex�Three Trials) covarying mean task change

All

Women All high Men Women

(1.03) �3.58 (.99) �5.56 (.71) �6.93 (.72) �4.06 (.73)

(1.10) �2.85 (1.06) �4.64 (.76) �7.14 (.77) �3.75 (.78)

(1.06) �1.12 (1.02) �2.89 (.73) �5.66 (.74) �2.37 (.75)

(.95) �2.52 (.91) �5.61 (.68) �6.58 (.66) �3.40 (.67)

(.19) .58 (.19) .59 (.13) .67 (.13) .51 (.14)

(.17) .54 (.17) .56 (.12) .80 (.12) .44 (.13)

(.17) .31 (.17) .40 (.12) .59 (.12) .21 (.12)

(.16) .47 (.16) .52 (.11) .69 (.11) .38 (.11)

(2.01) �2.26 (2.16) �3.80 (1.48) �5.33 (1.40) �4.52 (1.47)

(2.73) �5.01 (2.93) �3.91 (2.01) �3.95 (1.90) �2.68 (1.99)

(1.51) �4.02 (1.62) �4.94 (1.11) �4.21 (1.05) �5.08 (1.10)

(1.67) �3.76 (1.79) �4.21 (1.23) �4.50 (1.17) �4.09 (1.22)

-7

-6

-5

-4

-3

-2

-1

0

Cha

nge

in H

R (

bpm

)

Men

Women

A

0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

Cha

nge

in R

SA (

natu

ral l

og)

MenWomen

B

Fig. 2. Heart rate and RSA responses for men vs. women.

Table 4

Change in BP and determinants of BP during task

J.M. Ruiz et al. / International Journal of Psychophysiology 60 (2006) 274–283280

in RSA and PEP, but not baseline, was used.1 Task change

in RSA, F(1,64)=22.24, p <.001, g2= .258, but not change

in PEP, F(1, 64)= .03, p =n.s ., emerged as a significant

predictor and mediated the time effect on change in HR

during the task, F(1,64)=2.90, p =n.s., g2= .043. Interest-ingly, inclusion of PEP and RSA as covariates did not

explain either the sex main effect, F(1,64)=4.15, p<.05,

g2= .061, nor the Time�Hostility interaction, F(2,128)=

4.23, p <.03, g2= .062. These results suggest that despite

evidence of coactivation, parasympathetic influences were

the dominant contributor to the HR deceleration effects

during the forehead cold stimulation. However, the effects

on RSA and PEP did not explain a significant portion of the

observed effect of sex and hostility.2

Finally, changes in affect (anger, anxiety) were examined

as potential mediators of the Time�Hostility and Sex

effects on task HR response. Three-way mixed ANCOVAs

(i.e., High vs. Low Hostility�Sex�Three Trials) covarying

baseline values along with the hypothesized mediators were

used. Affect and autonomic determinants were examined

separately. Change in anger and anxiety were entered

together as potential covariates. Anger emerged as a

significant independent predictor for HR, F(1,68)=5.77,

p <.05, g2= .078, lower anger predictive of greater HR

decrease during cold stimulation. However, both the sex

1 Inclusion of baseline HR did not significantly alter the observed effects.2 Because of the effects of respiration on the measurement of RSA

(Berntson et al., 1997) we examined differences in respiration rate (RR).

RR data was assessed with an EPM system (Mindlothian, VA) strain gauge.

A main effect for hostility was found for RR during the task, F(1,70)=4.86,

p <.05, g2= .065. High hostiles displayed a larger increase in RR during

cold stimulation compared to low hostiles (1.02 breaths/min vs. � .11breaths/min). Next we included change in task RR as a covariate in a three-

way ANCOVA of RSA. However, the inclusion of RR as a covariate did

not alter any of the previously observed effects on RSA. Finally, we

examined the effect of change in RR during the task on the previously

observed hostility and gender HR effects. Change in task RR was included

along with change in task RSA and PEP as potential covariates in repeated

measures ANCOVA of task HR. Higher RR emerged as a significant

independent predictor of lower HR, F(1,61)=4.36, p <.05, g2= .067, but

did not mediate the Time�Hostility nor the gender effect.

main effect (F(1,68)=9.45, p < .01, g2= .122) and the

Hostility�Time interaction, (F(2,136) = 4.39, p < .02,

g2= .061) remained significant.

3.6. Blood pressure effects

All main effects for SBP and DBP were non-significant

suggesting the forehead cold pressor was a predominantly

cardiac autonomic task (Table 4). These nonsignificant

findings are also important in that PEP changes can be

confounded by blood pressure differences and thus compli-

cate the interpretation of it as a noninvasive index of SNS

influences on the heart (Sherwood et al., 1990). The lack of

task effects for blood pressure argues for a simultaneous

sympathetic effect underlying HR changes to the cold

pressor task.

With respect to blood pressure determinants, a Hostility�Sex interaction was found for TPR, F(1,68)=4.37, p <.05,

g2= .060. Specifically, high hostile men displayed an increase

in TPR whereas TPR decreased among low hostile men,

t(68)=2.15, p <.05 (Table 4). In addition, a significant

Hostility�Sex interaction was found for CO, F(1,65)=

Low hostile High hostile Total

SBP (mmHg)

Men � .56 (1.43) 1.68 (1.39) .56 (1.04)

Women 1.97 (1.43) .93 (1.39) 1.45 (1.04)

Total .71 (.94) 1.30 (.94)

DBP (mmHg)

Men �1.14 (1.07) .75 (1.09) � .19 (.77)

Women .52 (1.07) � .42 (1.06) .05 (.77)

Total � .31 (.75) .17 (.76)

TPR (dyne-s*cm� 5)

Men �115.89 (51.28) 48.03 (49.77) �33.93 (34.63)

Women 19.10 (49.06) �59.98 (51.77) �20.44 (35.70)

Total �48.40 (34.92) �5.98 (35.97)

CO (l/min)

Men .65 (.17) .01 (.17) .33 (.11)

Women .44 (.16) .52 (.17) .48 (.12)

Total .55 (.12) .23 (.12)

J.M. Ruiz et al. / International Journal of Psychophysiology 60 (2006) 274–283 281

4.46, p < .05, g2= .064. Specifically, high hostile men

displayed less increase in CO compared to all other

Sex�Hostility cells, ts(65)>2.00, p <.05.

4. Discussion

The current experiment supports the hypothesis that the

forehead cold pressor evokes parasympathetic cardiac

activation. Interestingly, these data suggest the task is better

characterized as evoking autonomic coactivation, although

the cardiac deceleration was accounted for by parasympa-

thetic activation. Replicating prior research, men showed a

stronger cardiac deceleration to cold stimulation, marked by

larger decreases in HR and increases in RSA, compared to

women. More important, the dive reflex responses clearly

differed between high and low hostile individuals in

response to cold stimulation. As expected, high hostile

individuals displayed a weaker dive-reflex response char-

acterized by a loss of HR deceleration over time relative to

low hostile participants.

It is important to note that two critical emotional

mediators of autonomic activity, state anger and anxiety,

were examined as potential explanations for the task effects

on HR and RSA. However, these emotional states did not

mediate the effects nor were there any noticeable differences

in HR or RSA that would suggest that ratings of anger or

anxiety influenced physiological response. Hence, these

findings suggest that the observed HR responses to the task

reflect a reflexive physiological response pattern, irrespec-

tive of negative emotional states, driven by autonomic

efferents to the heart.

This experiment contributes to the literature in three

important ways. First, this is the first experiment to

demonstrate the autonomic determinants of the forehead

cold pressor response by indexing the autonomic systems

(PEP, RSA) themselves rather than assuming their activity

through HR responses. Second, these results broaden

understanding of constitutional cardiac differences between

high and low hostile individuals. Specifically, this experi-

ment demonstrated hostility differences in duration of the

reflex cardiac response to the task. This effect could have

important implications for understanding the determinants

of hostility differences in cardiovascular reactivity and

associated health vulnerabilities. Third, this experiment

replicated previous findings by Hughes and Stoney (2000)

of larger parasympathetic response to the forehead cold

pressor in men relative to women.

4.1. Qualifications and limitations

The most obvious limitation of the current experiment

was not finding a physiological basis for the hostility by

time interaction on HR. Clearly the deceleration of HR

suggests parasympathetic involvement. However, the lack

of corresponding main effect of hostility on RSA or time

interaction suggests either that other factors obscured the

effect, a problem in measurement, or that the effect was a

result of some factor not assessed (see Berntson et al.,

1991). For example, because respiration rate contributes to

vagal outflow to the heart (see Berntson et al., 1997) it was

possible that hostility differences in respiration may have

masked any parasympathetic effect on HR. Again, despite

evidence that high hostile participants breathed at a faster

rate during the task (which would lead to decreases in

estimates of RSA), respiration rate also failed to explain the

findings. A related possibility is that differences in

respiratory tidal volume that was not assessed here may

have influenced the results. Several studies have demon-

strated that RSA magnitude is positively correlated with

tidal volume (Laude et al., 1993; Grossman et al., 1991;

Kobayashi, 1998) and that such changes may impact the

spectral-frequency range in which RSA is measured (Hirsch

and Bishop, 1981).

With respect to measurement, RSA and PEP are

estimates, and thus, imperfect indices of autonomic activity.

For example, the employed high frequency spectral range

(.12 to .40 Hz), although widely accepted (Berntson et al.,

1997), is geared toward the modal frequency range of

parasympathetic functioning and therefore not inclusive of

all possible ranges of functioning. Hence, it is plausible that

gradients in hostility-related parasympathetic functioning

produced the observed HR differences but that this para-

sympathetic activity occurred in frequency ranges outside

the modal bandwidth. In addition, error in the estimation

process can be increased for more complex associations

(e.g., combined error as a function of estimating RSA as a

function of task and hostility). Thus, power to detect more

complex interactive processes such as the Hostility�Time

interaction for RSA may have been weakened.

Finally, this task was limited to producing efferent

parasympathetic activation and therefore does not address

the possibility of hostility differences in afferent or higher

order pathways that may precede such autonomic activation.

In addition, relative weakness in the vagal system may

reflect problems of conduction or non-autonomic, humoral

factors (Berntson et al., 1997; Hainsworth, 1995). Future

research should address these issues accordingly.

4.2. Conclusions

In spite of these limitations, the HR deceleration effects

extend descriptions of hostility and sex-related cardiovas-

cular functioning to include differences in underlying

physiological mechanisms, although the lack of more direct

evidence of mediation by RSA precludes firm conclusions

about the parasympathetic basis of these differences. None-

theless, the evidence regarding autonomic mediation of HR

response to the forehead cold pressor contributes to the

literature using this task and supports the procedure as an

effective method for examining the parasympathetic-cardiac

pathway.

J.M. Ruiz et al. / International Journal of Psychophysiology 60 (2006) 274–283282

Acknowledgements

We would like to thank two anonymous reviewers for

their comments on an earlier draft of this manuscript. This

project was sponsored by a Student Research Award from

the Division of Health Psychology (38) of the American

Psychological Association.

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