Journal of Behavioral Medicine Vol 13, No. 2, 1990

Gender Differences in Cardiovascular Reactivity Stephanie V. Stone, 1 Theodore M. Dembroski, 14 Paul T. Costa, Jr., 2 and James M. MacDougalP /

Accepted for publication: August 3, 1989

Pronounced cardiovascular reactivity to stress is a behavioral mechanism that may underlie the pathophysiology o f coronary heart disease (CHD). Based on the greater incidence o f C H D among males than among females, the purpose o f the current investigation was to test the hypothesis that in young adults (ages 17-29), males (n = 47) show more cardiovascular reactivity than females (n = 61) to two stressors, a video game and cigarette smoking. Five o f the six comparisons did not support the hypothesis: females were higher on heart rate and diastolic blood pressure reactivity to both stressors; males were higher on systolic blood pressure reactivity to the video game only. The results suggest that females may be particularly physiologically reactive to cigarette smoking. KEY WORDS: coronary heart disease; gender; reactivity.

INTRODUCTION P r o n o u n c e d increases in cardiovascular reactivity are hypothesized to be one o f the p r i n c i p a l b e h a v i o r a l m e c h a n i s m s u n d e r l y i n g the p a t h o p h y s i o l ogy o f c o r o n a r y h e a r t disease ( C H D ) . A l t h o u g h it is well e s t a b l i s h e d t h a t s u s t a i n e d e l e v a t i o n in b l o o d p r e s s u r e is a s s o c i a t e d with i n c r e a s e d risk for Conduct of this research was supported by a research grant from the National Heart, Lung, and Blood Institute (HL-36027). 1Department of Psychology, University of Maryland Baltimore County, 5401 Wilkens Avenue, Catonsville, Maryland 21228. 2Gerontology Research Center, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20014. 3Department of Psychology, Eckerd College, St. Petersburg, Florida 33733. 4To whom correspondence should be addressed. 137

138

Stone, Dembroski, Costa, and MacDougall

CHD (Kannel et aL, Gordon, 1975; Pooling Project Research Group, 1978), the intent of current research in this area is to explore whether there is additional, independent coronary risk conferred by cardiovascular reactivity to environmental stimuli (Krantz and Manuck, 1984). Several fields of research implicate cardiovascular reactivity in the development of CHD. Pathophysiological studies show that experimentally induced damage to the arterial endothelium results in a buildup of atherosclerotic plaque that is histologically similar to the naturally occurring plaques characteristic of coronary artery disease (CAD) (Ross, 1981; Schwartz et aL, 1981, 1984). The proposed forces which promote this atheromatous buildup are both mechanical (hemodynamic turbulence) and chemical (catecholamines and the lipids they mobilize) (Herd, 1984). According to this "wear-and-tear" hypothesis, damage to the arterial intima consists of (1) platelet aggression, (2) smooth muscle cell proliferation, (3) connective tissue formation, (4) lipid deposition, and utimately, (5) the formation of fibrous plaques characteristic of coronary artery disease (Clarkson et aL, 1986). Several animal studies have also examined the association between cardiovascular reactivity and CHD. Kaplan et aL (1982) demonstrated in cynomolgus monkeys fed an atherogenic diet that the psychosocial stress of frequent changes in group membership was associated with severity of atherosclerosis. A subsequent study by the same group showed that this association obtained even in normocholesterolemic monkeys, indicating that the association between psychosocial stress and degree of atherosclerosis was not mediated by serum lipid concentration (Kaplan et aL, 1983). Behaviorally, the two groups did not differ on overall rates of aggression and submission, but unstable monkeys engaged in a higher proportion of severe forms of aggression (p < .05) and severe forms of submission (p < .05) and also engaged in less affiliative behavior (17 < .05). Insofar as extremes of aggression and submission are marked by differences in cardiovascular reactivity, the endothelial wear-and-tear hypothesis may explain some of the group difference in CAD severity. Studies using human subjects are another source of evidence concerning the relationship between cardiovascular reactivity and CHD. Two studies provide support for a prospective relationship between cardiovascular reactivity and CHD in humans. One study showed that in adult men (N = 279) screened for hypertension, diastolic reactivity to the cold pressor test was a better single prospective predictor of CHD than smoking, serum cholesterol, or systolic blood pressure (Keys et al., 1971). Subjects whose diastolic blood pressure rose more than 20 mm Hg to cold stress were 2.4 times more likely to die from CHD or myocardial infarction during the next 20 years than subjects whose diastolic reactivity was less than 20 mm Hg. In

Gender Differences in Cardiovascular Reactivity

139

another smaller-scale study, eight male medical students who experienced acute myocardial infarction (four fatal) within a follow-up period of 25 years had the lowest resting systolic blood pressure and the highest systolic reactivity to cold pressor compared to four other groups (suicides, mental illness, hypertension, tumor) (Thomas and Greenstreet, 1973). Evidence from concurrent CHD case-control studies is suggestive but inconsistent; Krantz and Manuck (1984) attribute these inconclusive results to studies that do not distinguish among different coronary endpoints and do not screen patients for history of hypertension and medication. They state that the most consistent result is elevated cardiovascular reactivity in patients with overt symptoms of CAD, angina or myocardial infarction, or hypertension. The concurrent association of CAD and exaggerated cardiovascular reactivity has also been observed in cynomolgus monkeys; animals that showed the highest heart rate reactivity to imminent capture were subsequently found at necropsy to have more atherosclerosis than low-heart rate reactors (Manuck et al., 1983). From their exhaustive review of the literature, Krantz and Manuck (1984) conclude that although the evidence to date does not support the conclusion that exaggerated cardiovascular reactivity is a proven risk factor for CHD, the evidence is promising and justifies continued research. To the extent that exaggerated cardiovascular reactivity underlies CHD, it is reasonable to ask whether there are gender differences in cardiovacular reactivity that might help explain the higher incidence of CHD in males (Kannel and Feinleib, 1972). There is a general consensus among studies that use catecholamine response to test gender differences that males are more adrenergically reactive than women (Forsman and Lindblad, 1983; van Doornen and Boomsma, 1985). Frankenhauser (1983), for example, reported a notable gender difference in adrenal hormone reactivity; specifically, women secrete a lesser amount of catecholamines, particularly adrenaline, than males in response to stressors. Frankhauser concluded that females have a more "economic" way of coping with achievement demands and that their health "costs" of adapting may therefore be lower. In studies that use cardiovascular parameters, however, results are far less consistent. In a sample of 58 college students, Jorgenson and Houston (1981) found no significant gender differences in cardiovascular reactivity to five stressors, the Stroop task (a color-word conflict task), a mental arithmetic task, digits backwards, shock avoidance anticipation, and a shock avoidance task. Similarly, Manuck et al. (1978) found no gender differences in systolic reactivity to a concept formation task administered under time constraints and monetary incentive. In a third study, van Doornen (1986) found no gender differences on systolic or heart rate reactivity in a sample

140

Stone, Dembroski, Costa, and MaeDougall

of 52 male and female university students to a real-life stressor. In a fourth study, Frankenhauser et al. (1976) reported that their failure to find a gender effect for heart rate over baseline, venipuncture, and Stroop test was consistent with previous studies conducted in their laboratory. In a recent fifth study on the cardiovascular effects of various combinations of nicotine, caffeine, video playing, and mental arithmetic, MacDougall et al., (1988) reported a significant gender-by-phase interaction for diastolic blood pressure and heart rate. The stressors used in these studies are notably diverse and vary considerably in the degree of challenge they provide subjects. For more comparable results to obtain in studies of cardiovascular reactivity, task content should be standardized, with special attention to the appropriateness of the task and the degree of challenge inherent in experimental instructions, both of which affect subjects' cardiovascular reactivity (Dembroski et aL, 1979; Krantz and Manuck, 1984). Of the studies that do report a gender effect for cardiovascular reactivity, systolic blood pressure is generally the salient dimension. Forsman and Lindblad (1983), for example, found that males were significantly higher than females on systolic blood pressure reactivity to a variant of the Stroop test (19 < .01). The authors stated that their results replicated those of von Eiff (1970; see also von Eiff and Piekarski, 1977). More recently, Stoney et aL (1987) performed a meta-analysis of studies published from 1965 through 1986 which provided data to test for a gender effect on heart rate (12 studies) and blood pressure (8 studies). Results showed no significant gender effects for diastolic blood pressure, nonsignificantly greater heart rate reactivity in females (17 < .07), and significantly greater systolic reactivity in males (p < .028). Gender differences in cardiovascular reactivity were also suggested by comparing the results of two studies on stress and smoking in males (MacDougall et aL, 1983) and females (Dembroski et al., 1985). MacDougall and his colleagues (1983) investigated cardiovascular reactivity (systolic, diastolic, and heart rate reactivity, and rate-pressure product index) in young males in a smoke/sham smoke by stress/no stress 2 x 2 factorial design. Participants in the smoke condition smoked an 80-mm filter-tipped cigarette containing 1.0 mg tar to within 1.0 cm of the filter; inhalations were paced at 18-sec intervals and lasted approximately 3.5 min. Sham smokers followed an identical procedure except that their cigarette was unlit. Stress was operationally defined as playing a video game (Atari "Breakout") under challenging verbal instructions: the game was described as a measure of their "eye-hand coordination and psychomotor skill"; participants were urged to do their very best and try to improve their score. The no-stress condition entailed sitting quietly with instructions to "completely relax and take it easy." Thus, after an initial lO-min baseline phase, participants played the

Gender Differences in Cardiovascular Reactivity

141

video game or relaxed for 2 min. After this test game, the following experimental sequences was repeated three times: smoking or sham smoking for 3.5 min and then playing the video game or relaxing for 2 min. Results showed a main effect for the smoke condition on all four cardiovascular parameters and a main effect for stress on all but diastolic reactivity. Three parameters, systolic and heart rate reactivity and rate pressure product index, all showed a similar pattern: reactivity to sham smoke/no stress was virtually zero; the amount of reactivity to smoking only was comparable to the amount of reactivity to stress only; and the amount of reactivity to the combination of smoking and stress significantly exceeded that of the other three conditions. Diastolic reactivity followed a similar pattern, but group differences were less dramatic. The authors concluded that the combination of relatively mild stress with cigarette smoking is capable of producing at least twice the amount of cardiovascular reactivity seen in either stress or smoking alone. In order to extend these results, Dembroski et aL (1985) conducted a similar study using females. This design was different from that used by MacDougall et al. (1983) in three respects: earlier findings suggested that males take the challenge of the video game more seriously than females (MacDougall et aL, 1981), so a monetary incentive was added (a penny per game point); because other biomedical research generally uses one to two cigarettes and because of the discomfort reported by some males in the previous study, the number of cigarettes smoked before the video game was reduced from three to one; to determine the length of time that nicotine can potentiate cardiovascular reactivity to stress, the stress/no-stress period was extended to 12 min. In addition, the Type A Structured Interview was administered to examine the excitatory effects of ingesting nicotine on speech stylistics. Dembroski et al. (1985) found that systolic, diastolic, and heart rate reactivity followed a similar pattern in females as MacDougall et aL (1983) had shown in males. In the MacDougall et al. (1983) study, the combination of smoking and stress had an additive effect on systolic and heart rate reactivity for males; in the Dembroski et al. (1985) study, the combination of smoking and stress had a larger than additive effect on systolic and heart rate reactivity for females. Taken together, the results of MacDougal et aL (1983) and Dembroski et al. (1985) suggest that males experience significantly more systolic reactivity than females to the video game alone but that, when smoking is combined with video playing, females "catch up" in systolic reactivity, rendering the gender difference in systolic reactivity nonsignificant. The authors suggested that males exhibited more cardiovascular reactivity to the video game than females because they were more competitively involved with the challenge of the video game and that the magnitude of this challenge effect may have resulted in a ceiling effect in males' reactivity to the subsequent combination of smoking and video stress.

142

Stone, Dembroski, Costa, and MacDougall

Given that these data were derived from two studies with differences in methodology, the current study was conducted to compare males and females directly within the same design. To make the current results maximally comparable to the two previous studies, the two stressors, video game and smoking, were retained. Another reason for retaining the video game comes from mounting evidence that it has shown a high test-retest reliability for periods as long as 20 months (Turner, 1990). In order to elucidate the independent effects of the two stressors, they were administered separately, not in combination: video game first, then a recovery period, then smoking. In addition, to control for between-group differences, the current study used a repeated-measures design that allowed each participant to act as his own control. Our literature review suggested that the most reliable gender difference in cardiovascular reactivity was that males showed greater systolic reactivity than females. We therefore hypothesized in the current study that males would exhibit greater systolic reactivity than females. We further reasoned that if the higher incidence of C H D in males is attributable to the arterial wear and tear conferred by exaggerated cardiovascular reactivity, then males should also demonstrate greater diastolic and heart rate reactivity than females.

METHOD

Subjects. The subjects were 108 healthy normotensive male (n = 47) and female (n = 61) college students whose ages ranged from 17 to 29 years (mean age, 20.6 years). All subjects were smokers who had smoked an average of 0.87 packs per day for at least 1 year. Some subjects were recruited from psychology classes; others were approached on campus by an experimenter and asked to participate in a study on stress and smoking. All subjects were paid a minimum of 5 dollars for participating; in addition, they were paid 1 penny per point (up to 5 dollars) scored during a second video game period. Thus, all subjects earned at least 5 dollars; those proficient at the video game could earn up to 10 dollars. Procedure. The data used in the current study were derived from a larger study on cardiovascular reactivity to multiple stressors. In the larger study, subjects were divided into two conditions, a smoke condition and a sham-smoke condition, and were subjected to a course of stressors (see Table I). For each of the stressor and recovery periods, readings of systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) were taken 15 sec after the beginning of the period and every 50 sec thereafter.

Gender Differences in Cardiovascular Reactivity

143

Table I. Design of the Stress and Smoking Study: Analyses Reported Use Baseline, Video Game

1, Recovery, Smoke 1, and Sham-Smoke Data Period Baseline Video game 1

Duration No. of HR/BP (min) measures 3 4 2 3

Recovery Mood self-report 1

2 1

3 None

Smoke 1

3

4

Video game 2

3

4

Mood self-report 2

1

None

Smoke 2

3

4

Structured Interview (lst half)

2

3

Mood self-report 3

1

None

Sham smoke

3

4

Structured Interview (2nd half)

2

3

Mood Self-report 4

1

None

Activity Sit quietly alone Play video game with moderate challenge Sit quietly alone Complete checklist of moods during video game 1 Smoke condition smokes 1st cigarette (lit); sham condition sham smokes 1st cigarette (unlit) Play video game with monetary incentive Complete checklist of moods during video game 2 Smoke condition smokes 2nd cigarette (lit); sham condition sham smokes 2nd cigarette (unlit) Administered 1st half of moderately challenging Type A Structured Interview Complete checklist of moods during 1st half of Structured Interview Smoke condition sham smokes 3rd cigarette (unlit); sham condition smokes 3rd cigarette (lit) Administered 2nd half of moderately challenging Type A Structured interview Complete checklist of moods during 2nd half of Structured Interview

W h e n subjects r e p o r t e d to the l a b o r a t o r y , they c o m p l e t e d q u e s t i o n naires for 1 hr, d u r i n g which time they did n o t smoke. Subjects were t h e n escorted to the test r o o m , seated in f r o n t o f a television m o n i t o r , i n s t r u c t e d how to play the video game, a n d fitted with a m i c r o p h o n e - t r i g g e r e d sphygm o m a n o m e t e r c u f f o n the n o n p r e f e r r e d a r m . C u f f a n d m i c r o p h o n e leads were r o u t e d to a n a d j a c e n t r o o m where a n a u t o m a t e d b l o o d pressure m o n i tor was located (Vita Stat M o d e l 900D). The accuracy o f the a u t o m a t e d m o n i t o r was determined (_+ 5 m m Hg) by mercury c o l u m n testing at the beginning of the experiment. A f t e r e x p l a i n i n g the video g a m e a n d fitting the cuff, the e x p e r i m e n t e r left the r o o m a n d i n s t r u c t i o n s were given b y m e a n s o f a p r e r e c o r d e d a u d i o

144

Stone, Dembroski, Costa, and MacDougall

tape. For the baseline period that followed, the tape instructed the subjects to "sit back and take it e a s y . . . " for 3 min while four readings were taken to obtain subjects' baseline levels of SBP, DBP, and HR. Then, all subjects played the Atari video game, "Breakout," for 2 min while three readings were taken; subjects were told that the game was a measure of their "eyehand coordination and psychomotor skill." After playing the game, subjects were instructed to stop and "relax for the next couple of minutes"; subjects recovered for 2 min, yielding three readings. After the recovery period, the experimenter reentered the room and gave subjects a self-report mood questionnaire to complete. Then the experimenter paced subjects while they smoked a cigarette: subjects in the smoke condition actually smoked a lit cigarette for 3 min, yielding four readings; subjects in the sham condition sham smoked an unlit cigarette under identical conditions for 3 min yielding four readings. During each smoke period, all subjects smoked or sham smoked one 80-mm, filter-tipped cigarette of the same brand (Marlboro), containing 1.0 mg nicotine and 16.0 mg tar, while the experimenter paced subjects' inhalations at 20-sec intervals. After the smoke period, the experimenter left the room and subjects were instructed by the tape to play the video game again, earning 1 penny per point up to 5 dollars; subjects played the video game for 3 min, yielding four readings. Then the experimenter reentered the room and gave subjects a second self-report mood questionnaire to complete. Subjects in the smoke condition then smoked a second cigarette for 3 min, yielding four readings; subjects in the sham condition sham smoked their second unlit cigarette under identical conditions for 3 min and four readings. Then all subjects were administered the first half of the Structured Interview, which lasted about 6 min; three readings were taken during the first 2 min. Afterward, they filled out a third mood questionnaire. Next subjects in the smoke condition sham smoked their first unlit cigarette; thus, over the course of the experiment, these subjects actually smoked two lit cigarettes and then sham smoked a third unlit cigarette. During the same period, subjects in the sham condition smoked their first lit cigarette; over the course of the experiment, these subjects sham smoked their first two cigarettes and then smoked a third lit cigarette. All subjects either smoked or sham smoked for 3 min and four readings. Then all subjects were administered the second half of the Structured Interview, which also lasted about 6 min, during which time three readings were taken during the first 2 min. Finally, all subjects completed a fourth mood questionnaire. The analysis conducted for the current study used part of the data from the larger study. Gender differences in cardiovascular reactivity to the combination of smoking and video stress had been suggested by the results of MacDougall et aL (1983) and Dembroski et al. (1985). Our purpose was

Gender Differences in Cardiovascular Reactivity

145

to analyze gender differences in cardiovascular reactivity to smoking and video stress when they were administered independently. The analysis compared two groups (males vs females) over four time periods (baseline, video game 1, recovery, and smoke 1/sham smoke). The first three time periods, baseline, video game 1, and recovery, were consecutive for all subjects. Smoking data were obtained when subjects first smoked; although this time period was not the same for all subjects, smoking always followed baseline, video game, and recovery. To ensure that the smoking data were not affected by the order of stressor presentation, we conducted t test comparing SBP, DBP, and HR during the smoking period for subjects in the smoke and sham conditions. The results of these analyses were uniformly nonsignificant. Data Analysis. There is general agreement among researchers that cardiovascular reactivity is the change from a baseline value in response to some discrete environment stimulus (Matthews et al., 1986). For this reason, baseline-corrected delta scores were used in univariate analyses despite their well-known statistical limitations (Bereiter, 1963; Cronbach and Furby, 1970). To obtain optimally stable estimates of the effect of the manipulations, the multiple blood pressure and heart rate readings taken during each of the four periods were averaged to obtain a single estimate. Then, in analyses that required delta scores, the average manipulation score was corrected for the average baseline value. We conducted analyses of covariance (controlling for body mass index, BMI) on change scores, i.e., delta scores, which provided very specific information about gender differences on individual data points. Males and females were first compared on absolute levels of SBP, DBP, and HR at baseline; next, males and females were compared on their reactivity to video challenge and smoking using delta scores. Delta scores were derived by subtracting baseline level from absolute level obtained during each manipulation. In addition to performing univariate analyses of covariance on delta scores, we also performed repeated-measures multivariate analyses of covariance (repeated-measures MANCOVAs) using absolute levels of SBP, DBP, and HR and covarying BMI. Researchers increasingly advocate using the multivariate repeated-measures procedure for psychophysiological data that usually violate the restrictive sphericity assumption underlying the univariate repeated measures procedure (Keppel, 1982; Jennings, 1987). There are also advantages to using the multivariate repeated-measures procedure instead of univariate analyses of variance. First, the analysis does not require the use of unreliable change scores. It is not affected by the use of absolute blood pressure as the repeated measure, because the relevant effect, the gender-by-time interaction, attends to the parallelism of the male

146

Stone, Dembroski, Costa, and MacDougall

and female performance curves over time, not their mean levels. The null hypothesis for the gender-by-time interaction term asserts that males' and females' mean time curves are parallel (Bock, 1963). Thus, a significant gender-by-time effect directly addresses the research question of whether there are gender differences in reactivity over time independent of any gender differences that may exist at baseline. Second, repeated-measures MANCOVA captures all o f the design information in a temporally accurate manner, in contrast with the selective information used, and therefore yielded, by multiple ANCOVAs. Third, reactivity studies that perform multiple ANCOVAs for different groups on several stressors and three or more parameters produce a confusing array of results. In comparison, the repeatedmeasures MANCOVA procedure produces a few results that provide a context within which specific information provided by ANCOVAs becomes considerably more interpretable. Fourth, conducting several multivariate tests instead of many univariate tests reduces the probability o f Type I error. A total of 3 repeated-measures MANCOVAs (one for each o f the three parameters, SBP, DBP, HR) and 12 ANCOVAs was performed (three parameters by four periods). Repeated-measures MANCOVAs were performed using absolute level of blood pressure and heart rate. ANCOVAs on gender differences on baseline levels also used absolute values for all three parameters. Subsequent ANCOVAs on reactivity to video game and smoking used delta pressures (absolute level minus baseline). Following Stoney et al. (1987), body mass index (BMI) was used as a covariate in every analysis to control for the confounding effect body mass may have on cardiovascular parameters. BMI was calculated by taking weight in kilograms and dividing by height in meters squared. Since controlling for body mass index did not systematically affect results, unadjusted means are reported.

RESULTS

Three repeated-measures MANCOVAs (see Table II) were performed comparing males (n = 47) and females (n = 61) on SBP, DBP, and H R over, baseline, first video game, recovery, and first nicotine ingestion (hereafter, baseline, video game, recovery, and nicotine). Body mass index was entered as the covariate. For consistency, results are reported for SBP first (Fig. 1), DBP second (Fig. 2), and H R third (Fig. 3). The average resting SBP = 110.34 (males = 117.04; females = 105.17), the average DBP = 64.31 (males = 63.63; females = 64.84), and the average HR = 70.12 (males = 66.61; females = 72.82) (see Table liD. Between-groups results showed that males' (n = 47) and females' (n = 61) absolute levels of blood pressure and heart rate pooled over the four

Gender Differences in Cardiovascular Reactivity

147

Table H. Results of Repeated-Measures MANCOVAs= Showing Magnitude of Gender-by-Time Main Effects and Trends for Cardiovascular Measures Cardiovascular measure

Effect

Effect sizeb

Systolic blood pressure

Gender Gender • Time Linear Trend Cubic Trend Quadratic Trend Time

.28*** .08* .001 .07** .01 .80***

Diastolic blood pressure

Gender Gender • Time Linear Trend Cubic Trend Quadratic Trend Time

.05* .07* .03 .02 .01 .72***

Heart rate

Gender Gender • Time Linear Trend Cubic Trend Quadratic Trend Time

.14"** .09* .06 .01 .03 .74***

=Analyses controlled for body mass index (BMI). bMultivariate effect size is comparable to univariate partial eta-square. *p < .05. **p < .01. ***p < .001.

130 ~ ~176176

a. m

120

9,.

~ ~176176176176176176

".,

................................. Men

~%"O..o..~

ooo

.-I

O I-o') >-

i./"~..~

~

Women

110

1~ BASE

I GAME

I RECV

I NICO

PERIODS

Fig. 1. Absolute systolic blood pressure over four periods.

148

Stone, Dembroski, Costa, and MacDougail

Women

o. m

. . . . . . . . . ~176176176 " " ' ~" ' ' ..~176 . . "'-,.~ .~176 .~ "".o.o. .~ ~

70

_c2 .-I

Men

0

50 BASE

I GAME

I RECV

J NICO

PERIODS Fig. 2. Absolute diastolic blood pressure over four periods 9

data points differed significantly on all parameters (SBP, p < .001; DBP, p < .002; HR, p < .001). Males were consistently higher on SBP, and females were consistently higher on DBP and HR; partial eta-squares showed that this gender difference accounted for 27.9~ of the variance in SBP, for 4.9070 of the variance in DBP, and for 13.80/0 of the variance in HR. The within-subject analysis showed that the repeated measure, time, was significant in all three MANCOVAs (p < .001); multivariate effect size was .80 for systolic, .72 for diastolic, and .74 for heart rate. These multivariate effect size estimates are comparable to univariate partial etagO

...,. Women

.o. o.OO~ .oO m

80

m I--

.~176176176176176176176176176176176176176176176 ~176o.~176176176176176176176176176176 " ' " ~176176176 , - M e n ./

-I-

70

s 60

BASE

I

I

I

GAME

RECV

NICO

PERIODS Fig. 3. Absolute heart rate over four periods.

149

Gender Differences in Cardiovascular Reactivity Table m . Results of ANCOVAs a Showing Magnitude of Gender Differences for Three Cardiovascular Measures Over Four Time Periods Cardiovascular measure

Period

Male means (n = 47)

Female means (n = 61)

Effect size

Systolic

Baseline b Video game c Recovery Nicotine

117.04 11.71 2.30 7.47

105.17 8.24 0.50 7.49

.30*** .09** .05 .002

Diastolic

Baseline Video game Recovery Nicotine

63.63 4.79 - 0.55 7.57

64.84 7.24 1.94 9.90

.03 .07** .09** .04*

Heart rate

Baseline Video game Recovery Nicotine

66.61 5.32 - 0.62 9.58

72.82 8.22 0.52 14.97

.08** .04* .04 .09**

*Raw means are reported; effect size, r 2, corrected for body mass index (BMI). bAbsolute levels reported for baseline. c Reactivity scores (absolute level minus baseline) reported for video game, recovery, and nicotine. *p < .05. **p < .01. ***p < .001.

squares; thus, in the current analysis they are partialled for the other withinsubject effect, gender by time. When the polynomial time trends were tested, all three cardiovascular parameters showed that the cubic time trend accounted for the largest portion of the time effect, attesting to the efficacy of the experimental manipulation; that is, subjects' blood pressure and heart rate rose in response to video challenge and smoking and fell in response to relaxation at baseline and recovery. The size of the cubic effect for SBP relative to that for DBP and HR indicates that SBP may be the most sensitive measure of cardiovascular reactivity. In comparison, DBP and HR have a smaller cubic component and show a substantial linear increase over the course of the experiment. A profitable issue for future research may be the relative health risk conferred by the volatility of systolic blood pressure versus the progressive rise in diastolic blood pressure and heart rate. The effect of most interest in this study, the gender-by-time interaction, was significant for SBP (t9 < .026) and HR (p < .019) and nearly significant for DBP (p < .055). The significant MANCOVA gender-by-time interactions establish that there are indeed significant gender differences in reactivity on SBP and HR in a young college sample. These significant multivariate interactions indicate that males and females change in different ways over time in response to a course of stressors. Stated another way, there is additional information about gender differences in hemodynamics

150

Stone, Dembroski, Costa, and MacDougall

over that obtained at baseline. The gender-by-time effect is roughly equal in size for SBP and HR, accounting for 8.4 and 9.1% of their variance, respectively. I f laboratory stressors are relatively weak elicitors of cardiovascular reactivity as some studies indicate (e.g., Dimsdale, 1983), in real life the size of these differences may be amplified beyond their current values. O f the three polynomial contrasts that m a k e up the gender-by-time interaction for SBP, only the quadratic contrast attained significance (p < .004), accounting for 85% o f the total gender-by-time SBP variance. A significant gender-by-quadratic time contrast indicates that the quadratic functions that describes the male and female weighted means are nonparallel; that is, the magnitude of male-female differences is different for different stressors. Inspection of the A N C O V A results corroborates this interpretation: it is the magnitude of the gender difference on SBP response to video game challenge 6o < .01, r 2 = .09) relative to the gender difference on SBP response to smoking (n.s.) that underlies the significant gender difference on the quadratic time function. None o f the polynomial contrasts for DBP attained significance. O f the H R contrasts, only the linear contrast attained significance (p < .008), accounting for 70% of the H R gender-by-time variance. Thus, males and females differ on the linear component of the repeated measure, time; specifically, the steeper slope of the line describing the transformed female means shows that for females H R increases at a faster rate than for males. This interpretation is also substantiated by inspection of A N C O V A results which showed that the magnitude o f the gender effect on heart rate increases over the course of stressors (gender effect for H R reactivity to video game, r 2 = .04; gender effect for H R reactivity to smoking, 1.2 .09). A N C O V A s were then performed using the total sample ( N = 108) for SBP, DBP, and H R (see Table III). The first set of A N C O V A s for SBP showed that males were significantly higher than females on SBP at baseline (male mean = 117.04, female mean = 105.17; p < .000, r 2 = .30). In the three additional A N C O V A s using delta values (absolute SBP minus baseline), males were significantly more reactive to the video game (male mean = 11.71, female mean = 8.24; p < .01, r 2 = .09), there was no significant gender difference in recovery, and no significant gender difference for nicotine reactivity. The second set of A N C O V A s for DBP revealed that males and females were not significantly different on DBP at baseline. In the three subsequent A N C O V A s using delta values, however, females were significantly more reactive to the video game (male mean = 4.79, female mean = 7.24; p < .01, r 2 = .07), females recovered significantly less (male mean = - .55, female mean = 1.94; p < .002, r z = .09), and females showed significantly greater reactivity to nicotine (male mean = 7.57, female mean = 9.9; p < .047, r 2 = .04). =

Gender Differences in Cardiovascular Reactivity

151

The third set of A N C O V A s for H R showed that females have significantly higher baseline H R (male mean = 66.61 female mean = 72.82; p < .008, r 2 = .08). The three A N C O V A s which followed used delta values and showed that females were significantly more reactive to the video game (male mean = 5.32, female mean = 8.22; p < .037, r 2 = .04); there was no significant gender difference in recovery, and females showed significantly greater reactivity to smoking (male mean = 9.58, female mean = 14.97; p < .005, r 2 = .09).

DISCUSSION Multivariate results showed that males and females differed in their patterns of cardiovascular reactivity over a course of stressors; univariate results elucidated the direction and magnitude of gender differences to specific stressors. Males were significantly higher on SBP and lower on H R than females at baseline. Only one of the six univariate tests supported the hypothesis that males show greater cardiovascular reactivity than females; four tests showed that females displayed greater cardiovascular reactivity, and one test resulted in nonsignificant gender differences. Specifically, females were higher on diastolic and heart rate reactivity to both video game and smoking; males were signficantly higher on systolic reactivity to the video game but not to smoking. It is notable that controlling for body mass index had no appreciable effect on these results. These results are comparable to those found in a recent study of the cardiovascular effects of combining caffeine and nicotine with mental arithmetic and a video game (MacDougall et al., 1988). Like the current study, MacDougall et al. (1988) found that females showed larger increases in DBP and H R than males across stressors; unlike the current study, however, they found nonsignificant gender differences in systolic reactivity. The current results qualify the findings of Stoney et al. (1987), who found that males showed significantly greater systolic reactivity than females. The results of the current study, that males were more systolically reactive to the video game but not to ingesting nicotine, suggests that these gender differences may to some extent be stimulus specific. Given that gender differences in cardiovascular reactivity to two different stressors are not consistent, we should consider whether the nature of the stressors themselves are responsible for the different patterns of reactivity. Many different and often redundant schemata are offered in the literature for distinguishing a m o n g the salient dimensions of stressors. Researchers variously organize stressors according to their attentional and cognitive demands [e.g., mental work or sensory intake (Lacey, 1967), sensory intake or sensory rejection (Williams, 1986)], whether they elicit active or passive coping

152

Stone, Dembroski, Costa, and MacDongaii

(Obrist et al., 1978), how much physical exertion they require (Buell et al., 1986), how psychologically stressful they are (Lazarus, 1966; Forsman and Lindblad, 1983), and how predictable and controllable they are (Seligman, 1975). Although these categories are neither exhaustive nor mutually exclusive, they provide some help in characterizing the stressors in the current study. In addition to some, presumably minimal, physical effort, the video game clearly elicits sustained engagement and mental effort (active coping), which includes elements of both sensory intake and mental work. As Krantz et al. (1986) note, it is difficult to isolate intake tasks that do not also have a mental work or challenge component. By comparison, ingesting nicotine is a predominantly physical stressor. Thus, the current results show that the nature of gender differences in cardiovascular reactivity depend not only on the cardiovascular parameter measured, but also on the kind of stressor. Specifically, males show the greatest systolic reactivity to actively coping with the video game challenge; however, in response to a stressor that is predominantly physical, ingesting nicotine, females are especially reactive, and the previous male "superiority" in systolic reactivity is rendered nonsignificant. Insofar as exaggerated systolic reactivity is associated with the progression of CHD, these data suggest that the protective effect of being female may be nullified when females smoke. Indeed, epidemiological studies show that CHD incidence in females who smoke approaches that for males (Willett et al., 1981). It is clear that the physical effort expended in performing a task has a large effect on one's cardiovascular reaction. Indeed, it has been demonstrated that there is no blood pressure variability in orthopedic patients immobilized in plaster casts over that attributable to sleep and wakefulness (Athanassiadis et al., 1969). It is the additional nonphysical demands of tasks that elicit cardiovascular reactivity that need further clarification. Further research in this area should attempt to control for the activity demands of task completion and use standardized stressors to promote the comparability of results. Comparing subject's self-reports of perceived stress with the type, pattern, and size of their cardiovascular reaction will also help to empirically determine the salient nonphysical dimensions of stressors and whether these cardiovascular determinants reside in the stressors, in their perception by subjects, or both, and if they are different for different gender and age groups. A study which attended to these issues would be better able to address, for example, whether the basis for these young men's heightened systolic reactivity to the videogame lay in their greater motoric response to the task or their greater psychological engagement with the challenge. This is not to suggest that the distinction between the physical and psychological aspects of stressors is a straightforward one. As Dembroski et al.

Gender Differences in Cardiovascular Reactivity

153

(1979) demonstrated, even response to the cold pressor test, generally regarded as a relatively pure physical stressor that elicits a reliable pattern of hemodynamic responses in healthy subjects, is affected by the degree of challenge in the experimental instructions. Given the complexity of disentangling the relative effects of pure physical effort and perception, these authors propose that researchers use physical stressors as the gold standard against which to evaluate mental stressors. The advantages are that physical stressors such as the treadmill exercise test already have well-established norms and are accepted predictors of CHD whose physiologic effects are well understood. The current results would be considerably strengthened if they were based on a greater number of diverse stressors. Future studies should administer several physical stressors (e.g., nicotine, caffeine, and cold pressor) and several psychological stressors (e.g., video game, mental arithmetic, and difficult conceptual tasks), using additional neuroendrocrine and metabolic outcomes, to establish whether gender differences to qualitatively different stressors is reproducible over a wide range of stressors and endpoints. Studies that analyze the independent effects of different kinds of stressors on physiological reactivity will help clarify the results of studies that address their conjoint effects, e.g., nicotine and video game combined. Future studies should also quantify the additional reactivity attributable to varying degrees of challenge in experimental instructions for the same task and determine whether there are significant gender differences in these challenge-induced increases in reactivity. Another important issue raised by the current inquiry is the need for a clear operational definition of cardiovascular reactivity. Despite the consensus reached by experts (Matthews et al., 1986) that reactivity be defined as a change from a baseline value, for practical purposes this definition is too all-inclusive to have prognostic value in a system which is by nature reactive. Reactivity, or change from baseline, describes how the normal cardiovascular system interacts with the environment (Clark et al., 1987). Indeed, blood pressure varies from normotensive to hypertensive in the same person over the course of a normal day (Pickering, 1987). Just as researchers require a taxonomy of stressors, they need normative standards for cardiovascular reactivity which will establish what constitutes normal versus exaggerated values. It may even be, for example, that change from baseline is not the best way to conceptualize how blood pressure confers vascular damage. A second, and widely accepted, mechanism is sustained absolute elevations (i.e., reactivity plus baseline) across all activities; a third, and lesser researched mechanism, is a high rate of pressure change (dP/dt), which results in greater pulsatile flow and potentially more damage to the arterial intima (Pickering, 1987; Texon, 1982). The increas-

154

Stone, Dembroski, Costa, and MacDougail

ing use o f a m b u l a t o r y b l o o d pressure m o n i t o r s promises to p r o v i d e some o f the d a t a necessary to develop better measures o f c a r d i o v a s c u l a r reactivity a n d to establish their age a n d gender n o r m s . I n general, the results f r o m the c u r r e n t study show that gender differences in cardiovascular reactivity are d e t e r m i n e d in part b y the n a t u r e o f the stressor a n d in part by the cardiovascular p a r a m e t e r measured. W e need a better u n d e r s t a n d i n g o f the a r o u s a l properties o f different stressors a n d o f different measures o f cardiovascular reactivity to clarify this association and, in turn, investigate the relationship between exaggerated cardiovascular reactivity a n d c o r o n a r y o u t c o m e . I n the last analysis, o n l y well-controlled prospective studies can d e t e r m i n e the risk factor status o f physiologic reactivity to challenge, b u t it is clear that m a n y issues c o n c e r n i n g the n a ture o f reactivity m u s t be resolved before such t i m e - c o n s u m i n g a n d expensive incidence studies are l a u n c h e d .

REFERENCES Athanassiadis, D., Draper, G. J., Honour, A. J., and Cranston, W. I. (1969). Variability of automatic blood pressure measurementsover 24-hour periods. Clin. Sci. 36" 147. Bereiter, C. (1963). Some persisting dilemmas in the measurement of change. In Harris, C. W. (ed.), Problems in Measuring Change, Universityof WisconsinPress, Madison, pp. 3-20. Bock, R. D. (1963). Multivariate analysis of variance of repeated measurements. In Harris, C. W. (ed.), Problems in Measuring Change, Universityof WisconsinPress, Madison, pp. 85-103. Buell, J. C., Alpert, B. S., and McCory, W. W. (1986). Physical stressors as elicitors of cardiovascular reactivity. In Matthews, K. A., Weiss, S. M., Detre, T., Dembroski, T. M., Falkner, B., Manuck, S. B., and Williams, R. B. (eds.), Handbook of Stress, Reactivity, Cardiovascular Disease, John Wiley, New York, pp. 127-144. Clark, L. A., Denby, L., Pregibon, D., Harshfield, G. A., Picketing T. G., Blank, S., and Laragh, J. H. (1987). A quantitative analysis of the effects of activity and time of day on the diurnal variationsof blood pressure. J. Chron. Dis. 40: 671-681. Clarkson, T. B., Manuck, S. B., and Kaplan, J. R. (1986). Potential role of cardiovascular reactivity in atherogenesis. In Matthews, K. A., Weiss, S. M., Detre, T., Dembroski, T. M., Falkner, B., Manuck, S. B., and Williams,R. B. (eds.), Handbook of Stress, Reactivity, Cardiovascular Disease, John Wiley, New York, pp. 35-47. Cronbach, L. J., and Furby, L. (1970). How we should measure "change"- or should we? Psychol. Bull. 74: 68-80. I)embroski, T. M., MacDougall, J. M., Herd, J. A., and Shields, J. L. (1979). Effects of level of challengeon pressor and heart rate responses in type A and B subjects. J. AppL Soc. Psyehol. 9: 209-228. Dembroski, T. M., MacDougall, J. M., Cardozo, S. R., Ireland, S. K., and Krug-Fite, J. (1985). Selective cardiovascular effects of stress and cigarette smoking in young women. Health PsychoL 4" 153-167. Dimsdale, J. E. (1983). Wet Holter monitoring: Techniques for studying plasma responses to stress in ambulatory subjects. In Dembroski, T. M., Schmidt, T. H., and Blumchen, G. (eds.), Biobehavioral Bases of Coronary Heart Disease, Karger, New York, pp. 175-183. Forsman, L., and Lindblad, L. E. (1983). Effect of mental stress on baroreceptor mediated changes in blood pressure and heart rate and on plasma catecholamines and subjective responses in healthy men and women. Psychosom. Med. 45: 435-445.

Gender Differences in Cardiovascular Reactivity

155

Frankenhauser, M. (1983). The sympathetic-adrenal and pituitary-adrenal response to challenge: Comparison between the sexes. In Dembroski, T. M., Schmidt, T. H., and Blumchen, G. (eds.), Biobehavioral Bases of Coronary Heart Disease, Karger, New York, pp. 91-103. Frankenhauser, M., Dunne, E., and Lundberg, U. (1976). Sex differences in sympathetic adrenal medullary reactions induced by different stressors. Psychopharmacology 47: 1-5. Herd, J. A. (1984). Cardiovascular disease and hypertension. In Gentry, W. D. (ed.), Handbook of Behavioral Medicine, Guilford Press, New York, pp. 222-281. Jennings, J. R. (1987). Editorial Policy on analyses of variance with repeated measures. Psychophysiology 24: 474-475. Jorgensen, R. S., and Houston, B. K. (1981). Family history of hypertension, gender, and cardiovascular reactivity and stereotypy during stress. J. Behav. Med. 4: 175-189. Kannel, W. B., and Feinleib, M. (1972). Natural history of angina pectoris in the Framingham study: Prognosis and survival. Am. J. Cardiol. 29: 154-163. Kannel, W. B., Doyle, J. T., McNamara, P. M., Quickenton, P., and Gordon, T. (1975). Precusors of sudden coronary death. Circulation 51: 606-613. Kaplan, J. R., Manuck, S. B., Clarkson, T. B., Lusso, F. M., and Taub, D. M. (1982). Social status, environment and atherosclerosis in cynomolgus monkeys. Arteriosclerosis 2: 359-368. Kaplan, J. R., Manuck, S. B., Clarkson, T. B., Lusso, F. M., Taub, D. M., and Miller, E. W. (1983). Social stress and atherosclerosis in normocholesterolemic monkeys. Science 220: 733-735. Keppel, G. (1982). Design and Analysis: A Researcher's Handbook, Prentice-Hall, Engelwood Cliffs, N.J. Keys, A., Taylor, H. L., Blackburn, H., Brozek, J., Anderson, J. T., and S0monson, E. (1971). Mortality and coronary heart disease among men studied for 23 years. Arch. Intern. Meal. 128: 201-214. Krantz, D. S., and Manuck, S. B. (1984). Acute psychophysiological reactivity and risk of cardiovascular disease: A review and methodologic critique. Psychol. Bull. 96: 435-464. Krantz, D. S., Manuck, S. B., and Wing, R. R. (1986). Psychological stressors and task variables as elicitors of reactivity. In Matthews, K. A., Weiss, S. M., Detre, T., Dembroski, T. M., Falkner, B., Manuck, S. B., and Williams, R. B. (eds.), Handbook of Stress, Reactivity, Cardiovascular Disease, John Wiley, New York, pp. 85-107. Lacey, J. I. (1967). Somatic response patterning and stress: Some revisions of activation theory. In Appley, M. H., and Trumble, R. (eds.), Psychological Stress: Issues in Research, Appleton-Century-Crofts, New York, pp. 14-44. Lazarus, R. S. (1966). Psychological Stress and the Coping Response, McGraw-Hill, New York. MacDougall, J. M., Dembroski, T. M., and Krantz, D. S. (1981). Effects of types of challenge on pressor and heart rate responses in Type A and B women. Psychophysiology 18: 1-9. MacDougall, J. M., Dembroski, T. M., Slaats, S., Herd, J. A., and Eliot, R. S. (1983). Selective cardiovascular effects of stress and cigarette smoking. J. Hum. Stress 9: 13-21. MacDougall, J. M., Musante, L., Castillo, S., and Acevedo, M. C. (1988). Smoking, caffeine, and stress: Effects on blood pressure and heart rate in male and female college students. Health PsychoL 7: 461-478. Manuck, S. B., Craft, S., and Gold, K. J. (1978). Coronary-prone behavior pattern and cardiovascular response. Psychophysiology 15:403-411. Manuck, S. B., Kaplan, J. R., and Clarkson, T. B. (1983). Behaviorally-induced heart rate reactivity and atherosclerosis in cynomolgus monkeys. Psychosom. Med. 45: 95-108. Matthews, K. A., Weiss, S. M., Detre, T., Dembroski, T. M., Falkner, B., Manuck, S. B., and Williams, R. B. (eds.). (1986). Handbook o f Stress, Reactivity, Cardiovascular Disease, John Wiley, New York, pp. 127-144. Obrist, P. A., Gaebelein, S. J., Teller, E. S., Langer, A. W., Grignolo, A., Light, K. C., and McCubbin, J. A. (1978). The relationship among heart rate carotid dp/dt and blood pressure in humans as a function of the type of stress. Psychophysiology 15: 102-115. Picketing, T. G. (1987). Strategies for the evaluation and treatment of hypertension and some impfieatious of blood pressure variability. Circulation 76 (Suppl. 1): 77-82.

156

Stone, Dembroski, Costa, and MacDougall

The Pooling Project Research Group (1978). Relationship of blood pressure, serum cholesterol, smoking habits, relative weight, and ECG abnormalities to incidence of major coronary events: Final report of the pooling project. J. Chron. Dis. 31: 201-306. Ross, R. (1981). Atherosclerosis: A problem of the biology of arterial wall cells and their interactions with blood components. Arteriosclerosis 1:293-311. Schwartz, G. E. (1984). Disregulation theory, reactivity and cardiovascular disease. In Weiss, S. W., Matthews, K. A., Detre, T., and Graeff, J. A. (eds.), Stress, Reactivity, and Cardiovascular Disease, Proceedings of the Working Conference, NIH Publication No. 84-2698, pp. 239-240. Schwartz, S., Gajdusek, C., and Sheldon, S. (1981). Vascular wall growth control: The role of the endothelium. Arteriosclerosis 1: 107-126. Seligman, M. E. (1975). Helplessness: On Depression, Development and Death, Freeman, San Francisco. Stoney, C. M., Davis, M. C., and Matthews, K. A. (1987). Sex differences in physiological responses to stress and in coronary heart disease: A causal link? Psychophysiology 24: 127-131. Texon, M. (1982). The hemodynamic basis of coronary atherosclerosis. In Santamore, W. P., and Bove, A. A. (eds.), Coronary Artery Disease, Urban & Schwarzenberg, Baltimore, pp. 129-137. Thomas, C. B., and Greenstreet, R. L. (1973). Psychobiological characteristics in youth as predictors of five disease states: Suicide, mental illness, hypertension, coronary heart disease and tumor. Hopkins Med. J. 132: 16-43. Turner, J. R. (1990). Individual differences in heart rate response during behavioral challenge. Psychophysiology (in press). van Doornen, L. J. P. (1986). Sex differences in physiological reactions to real life stress and their relationship to psychological variables. Psychophysiology 23: 657-662. van Doornen, L. J. P., and Boomsrna, D. I. (1985). Sex differences in catecholamine reactions to stress and its relevance for coronary heart disease. In Orlebeke, J. F., Mulder, G., and van Doornen, L. J. P. (eds.), Psychophysiology of Cardiovascular Control." Models, Methods, and Data, Plenum, New York, pp. 809-820. von Eiff, A. W. (1970). The role of the autonomic nervous system in the etiology and pathogenesis of essential hypertension. Jap. Circ. J. 34: 147-153. yon Eiff, A. W., and Piekarski, C. (1977). Stress reactions of normotensives and hypertensives and the influence of female sex hormones on blood pressure regulation. In de Jong, W., Provoost, A. P., and Shagiro, A. P. (eds.), Hypertension and Brain Mechanisms, Elsevier, Amsterdam, Vol. 47, pp. 289-299. Willet, W. C., Hennekens, C. H., and Bain, C. (1981). Cigarette smoking and non-fatal myocardial infarction in women. Am. J. Epidemiol. 113: 575-582. Williams, R. B. (1986). Patterns of reactivity and stress. In Matthews, K. A., Weiss, S. M., Detre, T., Dembroski, T. M., Falkner, B., Manuck, B., and Williams, R. B. (eds.), Handbook of Stress, Reactivity, Cardiovascular Disease, John Wiley, New York, pp. 109-125.

Gender differences in cardiovascular reactivity.

Pronounced cardiovascular reactivity to stress is a behavioral mechanism that may underlie the pathophysiology of coronary heart disease (CHD). Based ...
1MB Sizes 0 Downloads 0 Views