Journal of Personality and Social Psychology
1989, Vol. 57, No. 5,895-903
Copyright 1989 by the American PsychologicalAssociation, Inc.
0022-3514/89/$00.75
Type A Behavior, Personality Hardiness, and
Cardiovascular Responses to Stress
Richard J. Contrada
RutgersmThe State University of New Jersey
Type A behavior and hardiness were examined as predictors of cardiovascular responses to stress in
68 male undergraduates. Systolic and diastolic blood pressure (SBP and DBP) and heart rate were
monitored while subjects performed a difficult mirror-tracing task. Type A assessments based on
the Structured Interview, but not those based on the Jenkins Activity Survey, were associated with
significantly enhanced SBP and DBP elevations. Hardiness was associated with significantly reduced
DBP responsiveness. In addition, a significant interaction indicated that the Type B-high hardiness
group showed the least DBP reactivity. A near-significant interaction (p = .06) suggested that Type
B-high hardiness subjects also reported the least anger. Further exploration of the data indicated
that the challenge component of hardiness accounted for its relationship to DBP reactivity. These
results have implications both for the psychophysiologic study of Type A behavior and for understanding the health-promoting effects of hardiness.
Interest in the effects of personality on health and illness has
grown considerably in recent years. One factor that has drawn
attention to this topic is the extensive literature examining Type
A behavior as a contributor to coronary heart disease (CHD;
Houston & Snyder, 1988). Type A behavior consists of competitive achievement striving, hostility, impatience, and vigorous
speech and motor mannerisms. Type B refers to the relative absence of these characteristics and a more relaxed style of coping.
Initially, epidemiological work provided rather consistent evidence that individuals exhibiting Type A behavior show a
greater risk of developing C H D than their Type B counterparts
(Cooper et al., 1981 ). However, more recent studies have failed
to confirm earlier findings (Shekelle, Gale, & Norusis, 1985;
Shekelle, Hulley, et al., 1985).
Two recent meta-analyses have helped to clarify the status
of Type A behavior as a coronary risk factor. The first (BoothKewley & Friedman, 1987) included both cross-sectional and
prospective studies and suggested that Type A behavior is reliably associated with CHD. The second meta-analysis (Matthews, 1988) differed in that it focused exclusively on prospective studies, had access to more recent findings, and used
different decision rules in aggregating data across studies. Resuits indicated that Type A behavior predicts C H D (a) when
Type A is assessed using a Structured Interview (SI; Dembroski,
1978; Rosenman, 1978), but not when measured using the Jenkins Activity Survey (JAS; Jenkins, 1978; a self-administered
questionnaire) and (b) in population-based studies that exam-
ined initial C H D in subjects who were healthy at intake, but
not in studies of high-risk individuals.
As noted by Friedman and Booth-Kewley (1988), the two
meta-analyses agree in supporting the hypothesis that Type A
behavior is related to C H D but raise several issues regarding the
nature of that relationship. Most germane to the present study
are questions about the magnitude of the Type A - C H D relationship. Even in population-based studies in which Type A was
assessed by Structured Interview, results indicate only a modest
association with CHD. The Type A variable identifies as coronary prone many individuals who do not develop C H D and as
noncoronary prone many individuals who do.
Efforts to increase predictive validity have primarily taken
the approach of evaluating separately the component behaviors
reflected in global Type A assessments based on the SI. This
has led to the discovery that hostility and other anger-related
variables may constitute the "toxic" elements of Type A behavior (Dembroski & Costa, 1987). Less attention has been given
to the study of Type A behavior in conjunction with other personality factors that may contribute to coronary risk. The Matthews (1988) and Booth-Kewley and Friedman (1987) metaanalyses identified several personality constructs that appear
promising in this regard, given their relationships to C H D in
studies in which Type A was not measured.
The epidemiological literature on Type A behavior has stimulated a considerable amount of research examining mechanisms that may explain the relationship between Type A and
CHD. This work is based on the hypothesis that coronary risk is
enhanced by cardiovascular and other physiological responses
associated with psychological stress and that these responses are
more pronounced in Type A individuals. Emerging from this
research are three trends that parallel epidemiological findings:
(a) Psychophysiological research has more often yielded positive results where Type A is assessed by SI rather than by questionnaire (Contrada, Wright, & Glass, 1985); (b) reported associations account for what is, at best, only a small proportion of
I thank Lee Jussim, Suzanne Ouellette Kobasa, David Krantz, and
three anonymous reviewers for their critical comments on an earlier
version of this article. I am also grateful to Mark Patane for his assistance in conducting the second session, Jean Landeau for rating Structured Interview tapes, and Susan Hedges for coding verbalization data.
Correspondence concerning this article should be addressed to Richard J. Contrada, Department of Psychology, Tillett Hall, Rutgers University, New Brunswick, New Jersey 08903.
895
896
RICHARD J. CONTRADA
the variance (Houston, 1983); and (c) the association between
Type A and physiologic reactivity to stress is greater when this
relationship is examined separately for hostility (e.g., Dembroski, MacDougall, Shields, Petitto, & Lushene, 1978).
Further investigation of hostility and other components of
Type A may determine more precisely which aspects of the behavior pattern are most strongly associated with physiological
responses that may promote CHD. However, as in the prediction of CHD, it also might be useful to examine Type A behavior in the context of other personality characteristics, particularly those that themselves show a relationship to health. It is
reasonable to hypothesize that personality characteristics that
are conceptually distinct from Type A behavior and its components, but that also bear a relationship to physical health or
illness, may account for some of the variance in disease and in
disease-promoting physiological responses that is left unexplained by Type A.
One variable worth examining in this regard is hardiness, a
personality dimension that is believed to confer resistance
against the effects of psychological stress (Kobasa, 1979). Hardiness is a composite consisting of internal locus of control (vs.
powerlessness), commitment(vs, alienation), and challenge (vs.
threat). In a series of retrospective (Kobasa, 1979, 1982; Kobasa, Maddi, & Courington, 1981) and prospective (Kobasa,
Maddi, & Kahn, 1982) studies, results were obtained that suggest that hardiness may exert a protective effect against reported
illness.
Recent studies have raised both conceptual and methodological criticisms regarding hardiness research (e.g., Funk & Houston, 1987; Hull, Van Treuren, & Virnelli, 1987). One concern
is whether hardiness embodies a unitary construct, as originally
proposed, or a set of three independent dimensions. Another is
that hardiness appears to promote health independently of
stress, rather than operating as a buffer by reducing illness primarily among individuals experiencing high stress levels (Cohen & Edwards, 1989; Funk & Houston, 1987; Hull et al.,
1987). These issues typically have been investigated in research
oriented toward the prediction of adaptive outcomes, such as
psychological distress or reports o f physical illness.
Relatively little effort has been devoted to identifying mechanisms that may mediate the effects of hardiness on health outcomes. There is evidence to suggest that hardy individuals perceive stressful events as more positive and controllable than individuals low in hardiness (Allred & Smith, 1989; Rhodewalt
& Agustsdottir, 1984; Rhodewalt & Zone, 1989). Thus it is possible that hardiness short-circuits the stress response by influencing the processes whereby psychological threat is appraised.
However, it has yet to be demonstrated that hardy individuals
show reduced physiological responsiveness when confronted by
laboratory stressors.
It is the question of whether hardiness is related to physiological responses to stress that forms a basis for the present study.
To the degree that hardiness protects against the development
of physical disease through mechanisms associated with psychological stress, it may be predicted that individuals high in
hardiness will show less pronounced physiological responses to
a stressor than those low in hardiness. In the absence of such a
finding, pathways to disease that do not necessarily involve
stress, such as cigarette smoking, poor diet, and failure to detect
and/or act on physical symptoms, might be regarded as more
plausible explanations for data suggesting that hardiness is
health promoting. Since Type A behavior appears to be associated with enhanced physiological reactivity, it would be useful
to determine whether hardiness contributes to the prediction o f
reactivity independently of any association between hardiness
and Type A. To the extent that this is the ease, it would suggest
that research on the psychophysiology of Type A behavior might
benefit from a consideration of hardiness and, perhaps, other
personality characteristics that influence the stress response.
Accordingly, a psychophysiological experiment was conducted to assess the independent and conjoint effects of Type A
behavior and hardiness on subjective and cardiovascular responses to a frustrating psychomotor task. Previous work does
not provide a specific basis for predicting an interaction between Type A behavior and hardiness. Therefore, it was expected that Type A behavior would be positively associated with
physiological reactivity to the task, and that hardiness would
be inversely associated with reactivity, such that physiological
responses would be greatest among Type A subjects low in hardiness, and lowest among Type B subjects high in hardiness. It
also was predicted that Type A effects based on SI assessments
would be stronger than those based on the JAS.
Method
Subjects
Subjects were 68 male introductory psychology students who participated in partial fulfillment of course requirements. Subjects ranged in
age from 18 to 22 years (M = 21.1).
Measurement of Type A Behavior and Hardiness
The principal measure of Type A behavior was the student version of
the SI, administered by the author, who was trained in the technique by
Ray H. Rosenman. The interviews were tape-recorded and reviewed
independently by an auditor who had been trained by Theodore M.
Dembroski. Behavior pattern assessments were made using a 4-point
scale (A1 = 4, A2 = 3, X = 2, and B = 1). Degree of agreement between
the two raters' discrete classifications was 75%. Intercorrelation of the
4-point ratings yielded a value of.87. The 4-point ratings were averaged
to construct a continuous Type A score for use in correlational and
regression analyses. For descriptive purposes, a dichotomous measure
of Type A behavior was derived by combining discrepant ratings, with
the use of a procedure recommended by MacDougall, Dembroski, and
Mustane (1979): A1/A2 and A/X = A; B/X = B (there were no A-B
disagreements, nor did any subject receive a Type X classification from
both raters). This yielded 35 Type As and 33 Type Bs. Subjects also
completed Form T of the JAS (Krantz, Glass, & Snyder, 1974).
Hardiness was assessed through the use of five questionnaires. The
Alienation From Work and Alienation From Self scales (Maddi, Kobasa, & Hoover, 1979) were used to measure commitment. The External
Locus of Control Scale (Rotter, Seeman, & Liverant, 1962) and Powerlessness Scale (Maddi et al., 1979) were used to measure control. The
Security scale of the California Life Goals Evaluation Schedule (Hahn,
1966) was used to measure challenge. For each of these measures, high
scores reflect a relative lack of hardiness. Following procedures described by Kobasa et al. (1982), the appropriate scale scores were standardized and then summed to create measures of commitment and control. Because challenge was measured by only one scale (Security), its
scores were doubled before adding together the five standardized scores
TYPE A, HARDINESS, AND STRESS
to construct a composite hardiness measure. A median split was used
to derive a dichotomous measure of hardiness on the basis of this overall
index.
Measurement of Cardiovascular Responses
Measurements of systolic and diastolic blood pressure (SBP and
DBP) were obtained with an Arteriosonde 1216 (Roche). The compressing cuff and transducer were placed over the brachial artery of the
subject's nondominant arm. Heart rate (HR) was monitored as digital
pulsation, with the use of a photocell plethysmograph attached to the
second finger of the nondominant hand. Readings were taken during
the 30-s interval beginning immediately after the compressing blood
pressure cuff had deflated. A digital display indicated the number of
pulses for the 30-s period, which was doubled in order to express HR in
beats per minute (bpm). Physiological recording equipment was located
in an observation room adjacent to the experimental chamber, where
the subject could be monitored by means of closed-circuit television.
Experimental Task
The mirror-tracing task consisted of a 96 × 96 cm wooden platform
in which was cut a channel measuring 1 cm wide and 1 crn deep that
formed the shape of a six-pointed star. Distance from the apex of one
point of the star to its opposite measured 48 era. The sides of the channel were lined with conductive material wired to a 24-era stylus. Contact
between the stylus and the sides of the channel completed an electric
circuit powered by a 12-V direct current source. Completion of the circuit activated a buzzer. Adjoining one edge of the platform at a 90* angle
was a second 96 × 96 cm wooden panel, on which was mounted a 48 ×
48 cm mirror. Direct visual access to the star was prevented by a third,
56 × 56 cm wooden panel that rested on 4 wooden legs at a height of
24 cm above the platform. The reflection oftbe star in the mirror could
readily be observed by looking over the third panel.
Successful performance required that the subject use the stylus to
trace the star, guided only by its reflection, without touching the sides
of the channel. This is virtually impossible to do without considerable
practice, and none oftbe subjects in this study completed a single tracing in the allotted 5 rain. Factors contributing to difficulty were (a) narrowness of the channel and (b) the fact that mirror images are reversed.
The first factor makes it difficult to negotiate even the straight edges of
the star without touching the sides; the second leads to problems in
deciding which way to turn at the c o m m . Because these aspects of mirror-tracing are not immediately obvious, the task is deceptively difficult,
and can be quite frustrating.
Affective Measures
Affective responses to task performance were measured using the
State-Trait Personality Inventory (Spielberger, Jacobs, & Russell, 1983),
which contains three 10-item subscales: Anger, Anxiety, and Curiosity.
Instructions requested that the subject respond with reference to his
feelings while working on the mirror-tracing task. The Anger and Anxiety scales were used to assess subjective distress. The Curiosity scale was
included to detect positive appraisals of the task situation, such as might
he expected from Type Bs or subjects high in hardiness. It contains
items reflecting interest, desire to explore, and inquisitiveness.
Procedure
Subjects participated individually in two sessions. At the first session,
I greeted the subject and escorted him to a small office where the purpose of the study was described as an attempt to determine the effects
of personality on subjective and physiological correlates of psychomotor
897
activity. Informed consent was obtained at this point. The experimenter
then administered the SI. Following the interview, the JAS and hardiness questionnaires were completed in an order individually randomized for each subject. An appointment for the second session then was
scheduled, and the subject was thanked and dismissed.
Session 2 was conducted by a second male experimenter who was
unaware of the hypotheses under study as well as the subject's Type A
assessment and hardiness scores. The subject was escorted to a soundattenuated experimental room, where the experimenter reiterated the
purposes of the study. A baseline period ensued, during which time the
subject was asked to sit quietly and relax. Measurements of SBP, DBP,
and HR were taken at 2-min intervals, until SBP values remained relatively stable (-+5 mmHg) across two successive readings, after a minimum of 8 min had elapsed. Means for the final two readings on each
cardiovascular measure were taken as baseline values.
Following the baseline period, the experimenter reentered the experimental room, placed the mirror-tracing task on the table, and gave the
subject a single sheet of paper containing task instructions. The experimenter then left the room, after explaining that any further communication would take place over an intercom system. Instructions described
the mirror-tracing task as a measure of spatial ability and hand-eye coordination, and indicated that the subject was to attempt to complete at
least one tracing, without activating the buzzer, within a 5-min period. It
was stated that "about 50%" of the subjects participating in the project
had been able to do this, and that the main concern of the investigators
was that the subject give his best effort. These instructions were developed on the basis of research indicating that Type As are most likely to
show enhanced physiological activity in response to tasks characterized
by moderate levels of difficulty (Contrada et al., 1985).
The instructions went on to request that the subject "think aloud"
while working on the task. The subject was encouraged to verbalize
whatever thoughts and feelings he might experience, whether or not they
were related to the immediate situation. It was explained that these verbalizations would be used to determine the information processing style
used by the subject in working on the task.
When the subject was ready to proceed, the experimenter activated a
tape recorder (connected to the hidden microphone serving the intercom system from the experimental room) and then instructed the subject to begin working. Blood pressure and HR measurements were initiated 5 s later, and every 60 s thereafter, for the next 5 min. After recording the final measurements, the experimenter instructed the subject to
stop working, reentered the experimental room, and administered the
postexperimentai questionnaire. Following completion of the questionnaire, the first experimenter conducted a postexperimental interview
and debriefing.
Data Reduction and Analysis
The principal mode of statistical analysis was multiple regrcssion
analysis, since both predictors (Type A and hardiness) and dependent
measures (cardiovascular activity and affect) reflect continuous dimensions. However, in order to maintain comparability with most previous
research on Type A, which has taken an analysis of variance approach,
Verbalization instructions were included both to support the cover
story and as a means of acquiring data reflecting subjective reactions to
task performance. Verbalizations were transcribed and coded by two
raters who were unaware of subjects' Type A classifications and hardiness scores. Coding categories included swearing, laughter, performance attributions, and expression of positive or negative affect. There
were no significant effects of Type A behavior or hardiness on amount
of verbalization (ps ~ .09). Analysis of verbalization content indicated
few statistically reliable relationships with Type A, hardiness, or cardiovascular reactivity; those that were obtained appeared uninterpretable.
898
RICHARD J. CONTRADA
significant regression effects were described by reporting means for
groups formed on the basis of the dichotomous Type A and hardiness
measures described earlier. Crossing the dichotomous Type A and hardiness classificationsyielded the followingnumbers of subjects in each
category: Type A-high hardiness, 21; Type A-low hardiness, 14; Type
B-high hardiness, 13; Type B-low hardiness, 20.
As in previous research, physiologicalreactivity was measured as the
difference between baseline and task values for each cardiovascular
measure. Preliminary analysis indicated that reactivity on each of the
cardiovascular measures showed no reliable changes over the five task
readings, and that this pattern held, regardless ofSI, JAS, and hardiness
scores (ps > .20). Therefore, a single index of reactivity was computed
for each variable by averaging across the five change scores. Baseline
values from which change scores were derived were included in the regression model in order to remove variance attributable to initial values
(Wilder, 1968).
Figure1. Diastolic blood pressure (DBP) elevationsas a
function of Type A and hardiness classifications.
Results
Intercorrelations Among Type A and
Hardiness Measures
Intercorrelations between the Type A and hardiness measures are presented in Table 1. The SI and JAS showed a moderate degree of association (r =.38, p < .01). Relationships among
the hardiness components were similarly modest in magnitude
(rs ranging from .28 to .49, ps < .05). Intercorrelations between
the SI and each of the hardiness components, as well as the composite hardiness index, were low and nonsignificant (rs ranging
from - . 18 to -.06). The JAS showed a similar dissociation with
hardiness (rs from - . 18 to -.02), except for a significant relationship with control (r = - . 2 8 , p < .05), indicating that subjects scoring in the Type A direction tended to report feeling
capable of influencingthe events in their lives.
Table 1 also presents the internal consistencies of the Type A
and hardiness measures. Reliability coefficients for all measures
are acceptable, except for Challenge (Cronbach's a = .56).
Resting Cardiovascular Activity
A series of regression analyses was conducted to determine
the relationships between Type A and hardiness and cardiovascular baselines. The only significant effect was a Type A × Hardiness interaction for resting SBP values, F(I, 64) = 4.54, p <
.04. Among Type Bs, subjects high in hardiness had a lower rest-
Table 1
Internal Consistency and lntercorretations
of the Hardiness and Type A Measures
Measure
1.
2.
3.
4.
5.
6.
1
2
3
4
5
Challenge
(.56) .28* .34** .74** -.02
Commitment
(.75) .49** .76** -.14
Control
(.83) .78** -.28*
Hardiness Composite
(.86) -.18
Jenkins ActivitySurvey
(.73)
Structured Interview
6
-.06
-.18
-.11
-.15
.38**
(.87)
Note. Cronbach alpha coefficients are given in parentheses, except for
the Structured Interview,where the interrater correlation is presented.
*p<.05. **p<.01.
ing SBP than those low in hardiness (Ms = 98.4 mmHg and
105.2 mmHg, respectively); by contrast, among Type As, those
high in hardiness had a higher resting SBP than those low in
hardiness (Ms = 109.8 m m H g and 101.7 mmHg, respectively).
No other effect approached significance for any of the cardiovascular measures (ps > . 18).
Cardiovascular Reactivity
As expected, a regression analysis for SBP change scores
yielded a significant main effect for Type A, F(I, 63) = 4.97,
p < .03. Type As showed significantly greater reactivity than
Type Bs (Ms = 20.1 mmHg and 15.2 mmHg). Whereas subjects
low in hardiness tended to have higher SBP elevations than
those high in hardiness (Ms = 19.1 mmHg and 16.3 mmHg),
neither the hardiness main effect nor the Type A X Hardiness
interaction was significant (ps > .40). 2
Also consistent with predictions was a Type A main effect for
DBP change scores, F(1, 63) = 6.54, p < .02. As in the case of
SBP, Type As showed significantly greater DBP responses than
their Type B counterparts (Ms = 14.5 mmHg and 10.9 mmHg,
respectively). There was also a hardiness main effect, F( 1, 63) =
7.54, p < .01. As expected, DBP elevations were significantly
higher among subjects with low hardiness scores compared with
those high in hardiness (Ms = 14.0 mmHg and 1 l.l mmHg,
respectively). The two main effects were qualified by a Type A X
Hardiness interaction, F(1, 63) = 4.22, p < .05. The relevant
data are depicted in Figure 1. It can be seen that the interaction
reflected particularly low DBP elevations among Type B subjects with high hardiness scores, the group expected to be least
reactive.
An analysis of HR change scores yielded only a nonsignifi2 It seems unlikely that the Type A × Hardiness interaction for SBP
baseline contributed to the Type A main effect for SBP change scores.
Type A subjects had slightly higher SBP baselines than Type Bs (Ms =
106.6 mmHg and 102.5 mmHg, respectively, ns), and SBP baselines
showed a nonsignificant trend toward an inverse relationship with
change scores (p = . 16). Therefore, higher SBP baselines tended to be
associated with lowerSBP change scores, working against the obtained
Type A main effect.
899
TYPE A, HARDINESS, AND STRESS
Table 2
Three Regression Models Predicting DBP Reactivity
From Type A and Hardiness
Predictor
Beta weight
Model 1: Hardiness compositea
TypeA
Hardiness
Type A × Hardiness
.28*
.82**
-.62*
Model 2: Three hardiness componentsb
Type A
Challenge
Type A × Challenge
.31 *
.76*
-.70*
Model 3: Five hardiness scalesc
TypeA
Challenge
Type A × Challenge
.31"*
.88**
-.81"
Note. The regression models are described in the text. Only significant
terms are presented in the table. Not shown are regression results for
DBP baseline values, which were significant in each model.
a F(4, 63) = 6.09, p < .0005, corrected R 2 = .23. b F(8,
59) = 3.71, p < .002, corrected R 2 = .24. OF(12, 55) = 2.82,
p < .005, corrected R 2 = .25.
*p < .05. **p <.01.
cant trend toward a Type A effect, F ( I , 63) = 2.74, p = . 10. Type
As showed somewhat higher H R elevations than Type Bs, which
was in the expected direction (Ms = 2.3 bpm and - 1 . 7 bpm).
Neither hardiness nor the Type A × Hardiness interaction approached significance (ps > .40).
The foregoing analyses were repeated substituting JAS scores
as the Type A measure. Only a significant hardiness main effect
for DBP, duplicating the result reported earlier, approached significance (all other ps > . 10).
Effects o f Type A and Hardiness on Affective Measures
Regression analysis of State Anger scores yielded a reliable
hardiness main effect, F ( I , 63) = 4.13, p < .05, and a nearsignificant Type A X Hardiness interaction, F(I, 64) = 3.68,
p = .06. As reflected by the marginal interaction, the hardiness
main effect was carried primarily by the Anger scores of the
Type B-high hardiness group ( M = 14.0), which were lower
than those of Type B-low hardiness subjects ( M = 16.0) and the
two Type A groups (both Ms = 16.9). No other effects approached significance for any of the state affect scales (ps > . 10).
Correlations between Anger ratings and cardiovascular
change scores only approached significance in the case of DBP
(r = . 19, p = . 11). This suggests that the effects of Type A behavior and hardiness on anger were largely independent of the reactivity effects.
Hardiness Components and Cardiovascular Reactivity
In order to explore the relative contributions of the individual
components of hardiness in predicting DBP reactivity, two additional multiple regression analyses were carried out. One in-
eluded the following predictors: DBP baseline values, SI Type
A assessments, individual scores on the five scales that make up
the hardiness composite, and product terms reflecting interactions between Type A ratings and each of the hardiness scales.
The second analysis differed in that the External Locus of
Control and Powerlessness scales were combined into a single
measure of control, and the Alienation from Self and Alienation
from Work scales were combined into a single measure of commitment. The Security scale was included as a measure of challenge and, as in the first series of regressions, product terms
were constructed to reflect the interaction between Type A and
each hardiness component. Thus, the two regression analyses
allow a comparison of two levels of decomposition of the overall
hardiness variable: One resolves hardiness into measures of its
three constituent constructs, the other into five individual scale
scores.
Significant effects are presented in Table 2, which also summarizes the initial regression analysis that used the overall hardiness index. Because the number of predictors in the models
varies, each capitalizes on chance to a different degree. Therefore, the R 2 coefficients were adjusted using the shrinkage correction formula described by Olkin and Pratt (1958). Inspection of these data suggests a number of conclusions. First, after
correction for shrinkage, the three models are shown to account
for a similar, statistically significant portion of the variability in
DBP responses to the task. Second, each model contains a term
reflecting a hardiness effect that adds significantly t ° the prediction of DBP responses above and beyond the contribution of
Type A behavior. Third, the relationship between hardiness and
DBP responses largely reflects a single hardiness component,
challenge. Whether the remaining four scales are considered individually (Table 2, Model 3), combined into control and commitment scores (Table 2, Model 2), or summed together with
challenge scores to generate a single composite index o f hardiness (Table 2, Model 1), they add little to the ability of the challenge component to predict individual differences in DBP responses to the task. The only exception appeared in Model 2 in
the form of a nonsignificant trend toward a main effect for the
control component (p = .08).
Table 3 presents simple correlations between control, challenge, and overall hardiness and DBP change scores. It can be
seen that the pattern of results for challenge resembles that of
the composite hardiness index. High scores (indicating low
challenge) were associated with heightened DBP reactivity to
the task, and this relationship is evident among Type Bs but not
among Type As. Similarly, DBP reactivity tended to be greater
Table 3
Correlations Between Significant Hardiness
Predictors and DBP Reactivity
Predictor
Type A
Type B
Combined
Challenge
Control
Hardiness composite
-.06
.13
.11
.45***
.38**
.44**
.19
.21"
.22*
Note. N = 68 (33 Type B and 35 Type A).
*p<.10.
**p<.05.
***p<.01.
900
RICHARD J. CONTRADA
among subjects who reported a lack of control, and this relationship was also somewhat stronger among Type Bs than
Type As.
Discussion
The results of this study suggest the following observations
regarding the role of Type A behavior and personality hardiness
in accounting for physiological responses to stress. First, the
data are consistent with previous studies demonstrating that
Type A assessments based on the SI show a modest but reliable
association with cardiovascular reactivity. Second, individual
differences in reactivity that are left unexplained by SI Type A
assessments are significantly related to other aspects of personality encompassed by the term hardiness. Third, an exploration
of the relationship between hardiness and cardiovascular responses to stress supports the utility of examining separately
the individual characteristics that make up the hardiness composite. In particular, the stress-dampening effects of hardiness
in the present study were largely attributable to the challenge
component.
Type A Behavior and Cardiovascular Reactivity
As expected, Type A assessments based on the SI were associated with enhanced SBP and DBP responses to task performance. The HR data yielded only a nonsignificant tendency
toward greater reactivity among Type As (p = . 10). By contrast,
the JAS was unrelated to reactivity. These results are consistent
with the preponderance of previous findings demonstrating that
the SI is more strongly associated with physiological reactivity
than the JAS (Contrada et al., 1985). Moreover, as noted earlier,
these reactivity data are congruent with epidemiological findings that support the validity of SI assessments in the prediction
of CHD in population-based studies, but draw into question
the status of the JAS as a measure of coronary-prone behavior
(Matthews, 1988). In view of these observations, it would seem
incumbent on the investigator who relies on the JAS as a measure of Type A behavior to justify its use on some basis other
than its relevance to CHD.
That Type A effects were obtained for SBP also accords with
earlier studies in that positive results have been observed more
consistently for SBP than for any other cardiovascular parameter. However, the fact that a significant Type A effect was obtained for DBP but not for HR is somewhat surprising, because
HR effects have been obtained more frequently than DBP
effects in previous research. Both the absence of a significant
Type A-B effect for HR and the overall low level of H R reactivity (M = 1.0 bpm) may be consequences of a cognitive requirement of mirror-tracing (close attention to sensory inputs),
which has been associated with reduced cardiac rate (Williams,
1986). This same factor may account for the positive DBP
effects, because sensory intake also appears to produce vasoconstriction in skeletal muscles, which would tend to increase
peripheral resistance, and could raise DBP (Williams, 1986).
Whatever the explanation, mirror-tracing does seem to elicit
pronounced DBP elevations, as seen in the present study as well
as in a recent investigation by Kasprowicz, Manuck, and
Krantz (1988). This suggests that inconsistencies in findings for
DBP in Type A research might reflect qualitative variations in
the tasks used to induce reactivity in those studies.
Hardiness and Cardiovascular Reactivity
Analyses using the composite hardiness index indicated that
DBP responsiveness was significantly lower among subjects
with high hardiness scores than among those low in hardiness.
The main effects of Type A and hardiness on DBP responses
were qualified by a significant interaction indicating that the
combination of a Type B behavior classification and high hardiness scores was associated with lowest DBP reactivity. Although
an interaction was not specifically predicted, it was expected
that Type B subjects high in hardiness would show the lowest
levels of cardiovascular response.
These data provide initial support for the notion, implicit in
the hardiness construct, that the hardy individual possesses
some attribute that dampens the body's response to psychological stress. This conclusion should be viewed guardedly, because
two recent studies unexpectedly found hardiness to be associated with enhancedcardiovascular responsiveness to psychological stress (Allred & Smith, 1989; Van Treuren & Hull, 1987).
Note, however, that these unanticipated findings involved SBP
and HR, not DBP. Moreover, AUred and Smith reported a marginally significant trend toward reduced finger pulse volume in
hardy subjects during anticipation of the experimental task. Reductions in finger pulse volume, like the DBP elevations reported here, reflect the constriction of blood vessels resulting
from increased sympathetic nervous system activity. Thus, it
may tentatively be concluded that hardiness is associated with
lower levels of a physiologic response pattern that was elicited
by some feature of the mirror-tracing task used in the present
study and, perhaps, during the anticipation phase of the Allred
and Smith study.
The fact that hardiness exerted a greater modulating effect
on the stress response among Type B as compared with Type A
individuals deserves comment. Although it would be of theoretical interest if Type As were less likely than Type Bs to benefit
from the health-promoting effects of hardiness, clearly it would
be premature to conclude this on the basis of the present investigation. Indeed, in another study relevant to this issue, Kobasa,
Maddi, and Zola (1983) reported data suggesting that hardiness
may exert a greater health-protective effect among Type As,
rather than among Type Bs. However, the interaction term reflecting that effect fell short of statistical significance. In addition, Kobasa et al. (1983) measured Type A behavior using the
JAS, whereas the DBP results reported here were based on SI
assessments. It is generally recognized that the SI and the JAS
measure substantially different aspects of the Type A behavior
pattern. Behavioral classifications derived from the SI are based
mainly on manifest hostility and the use of vigorous speech and
motor mannerisms, whereas the JAS is largely a self-report
measure of a pressured drive to succeed (Matthews, Krantz,
Dembroski, & MacDougall, 1982). It remains for future research to determine how the specific Type A behaviors reflected
in SI and JAS assessments may interact with hardiness in determining health outcomes.
TYPE A, HARDINESS, AND STRESS
Hardiness Components and Cardiovascular Reactivity
Multiple regression analyses provided interesting information concerning the contribution of the individual hardiness
components to the prediction of physiological responses to
stress. Under the conditions of this study, it would appear that
challenge, as measured by the Security scale, accounted for the
overall effect of the hardiness composite in dampening DBP
reactivity among Type Bs. Challenge contributed significantly
and to an equivalent degree to the prediction of DBP change
scores in the context of regression equations in which the remaining hardiness indicators showed no significant relationship with DBP, regardless of whether those indicators were
treated independently or combined into measures of control
and commitment. In addition, summing all five scales together
to form a single hardiness index conferred no predictive power
beyond that attributable to the challenge component alone.
These results must be interpreted with caution. Even modest
associations (i.e., multicollinearity) between predictors in a
multiple regression equation introduce a degree of instability
in the results. In the present study, the challenge and control
variables were correlated both with each other and with DBP
change scores (see Tables 1 and 3). Therefore, firm conclusions
about the results for Model 2 (see Table 2), indicating an independent association between challenge and DBP, must await
cross-validation in a larger sample.
With this qualification in mind, it is worth considering the
implications of the positive results reported here for the challenge variable. At a general level, these data support the utility
of treating the hardiness components as independent constructs
in order to determine the degree to which they are differentially
associated with adaptive outcomes. This view was not reflected
in early hardiness research, in which commitment, control, and
challenge were treated as indicators of a single underlying dimension (e.g., Kobasa et al., 198 I). However, the trend in more
recent work has been to consider the components separately,
and this has generated evidence suggesting that the health-promoting effects of hardiness are obtained more reliably for some
components than for others (Hull et al., 1987). In this sense, the
results of the present study are consistent with other developments in hardiness research. It would appear that future work
in this area would benefit from efforts to generate hypotheses
concerning the conditions under which the individual hardiness
components may differentially influence health-related outcomes.
That subjects high in challenge showed lower physiological
reactivity to a frustrating task is consistent with Kobasa's
(1979) conceptualization of challenge as a tendency to construe
life changes and obstacles in a positive way. Evidently, this orientation is measured somewhat indirectly by the Security scale,
which contains items dealing with the desire for protection
against physical and economic threat (e.g., "The more able person has a greater responsibility for the welfare of the less able"
and "There are no conditions which justify endangering the
health, food, and shelter of one's family or of oneself"). Previous research does not provide a basis for expecting that challenge would fare better than commitment and control in accounting for physiological responses to stress. Indeed, the Security scale and its variants have been criticized both for their low
901
levels of internal consistency and for their failure to contribute
to the prediction of health outcomes. These findings have led
to the recommendation that researchers interested in hardiness
focus on the commitment and control components and, presumably, discard the challenge concept (Hull et al., 1987).
Results of the present study favor a somewhat different perspective. To be sure, the internal consistency of proposed micasures of the challenge component is inadequate. However, the
data reported here suggest that efforts to improve those measures might well prove rewarding: To the limited degree that the
Security scale items reflect a single underlying dimension, that
dimension is associated with physiological responses to stress.
This relationship is consistent with the construct meaning of
challenge, and provides evidence for its nomological validity
(Cronbach & Meehl, 1955). Therefore, the present study should
serve as a stimulus for reconsidering the construct definition of
challenge and for developing additional items that better fit that
definition in order to revise the scale and improve item homogeneity (Jackson, 1971 ).
Results for the challenge component also raise questions concerning the practice of using illness reports as the sole basis for
assessing the validity of the hardiness concept and for evaluating the relative importance of the hardiness components. Illness
reports are a convenient starting point for demonstrating that
a personality characteristic may have some relevance to health.
However, given the ambiguities of self-report indexes of physical
well-being, they should not be relied on too heavily as a criterion for either establishing or disconfirming linkages to disease.
Even quite serious medical disorders (e.g., cancer and hypertension) may exist asymptomatically and, therefore, go undetected by subjective measures of health. Researchers have
tended to ignore this possibility, however, focusing instead on
the hypothesis that illness reports often may have no basis in
organic dysfunction, reflecting what has been referred to as negative affectivity (Watson & Clark, 1984) or a neurotic tendency
to report high levels of unfounded somatic complaints (Costa
& McRae, 1987). Following this line of reasoning, two recent
studies reported that significant associations between hardiness
and self-reported health were eliminated when individual
differences in psychological adjustment were controlled statistically (Funk & Houston, 1987; Rhodewalt & Zone, 1989). Although these findings might be taken to indicate that the healthenhancing effects of hardiness observed in earlier studies have
been inflated, such a conclusion would apply only to self-reported illness.
It is interesting to note, moreover, that neither Rhodewalt and
Zone (1989) nor Funk and Houston (1987) examined the relationship between hardiness and health separately for each of the
hardiness components. Furthermore, Funk and Houston reported that challenge was unrelated to the two measures of psychological maladjustment that were used to evaluate the neuroticism confound. It is possible, therefore, that challenge was
associated with illness in both studies. In any case, it clearly
remains for future research, which would, preferably, involve
objective measures of disease, to confirm or refute the validity
of the hardiness components as personality characteristics that
provide resistance to stress-related disorders.
It is worth reiterating that an important adjunct to work that
examines disease end points is research concerned with mecha-
902
RICHARD J. CONTRADA
nisms that may culminate in illness, such as physiological responses to stress. Note that stress-response d a m p e n i n g represents only one process whereby hardiness may promote health.
For example, there is evidence that hardy individuals engage in
health-promoting practices, such as proper diet and personal
hygiene (Wiebe & McCallum, 1986), and may be less likely to
report physical discomfort (Van Treuren & Hull, 1987). Further
examination of factors such as physiological reactivity, healthpromoting behaviors, and reactions to symptoms may lead to a
better understanding of the relationship between hardiness and
physical well-being.
Conclusion
This study demonstrates that weak associations between
Type A behavior and physiological reactivity may, in part, reflect a failure to assess other sources of variation in reactivity.
Specifically, although individual differences in reactivity are
likely to reflect constitutional and environmental influences
(Krantz & Manuck, 1984), the present data support the hypothesis that personality hardiness contributes to this variation as
well. This finding has implications for understanding the healthpromoting effects of hardiness, because the sympathetic nervous system activity underlying heightened DBP responses
might reflect processes involved in the development of physical
disorders. Results of the present study also support the utility
of a more multivariate approach in research concerned with the
relationship between personality and health.
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Revision received March 17, 1989
Accepted May 9, 1989 •
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