Impaired cardiovascular recovery following stress predicts
3-year increases in blood pressure
Andrew Steptoe and Michael Marmot
Objective To assess whether variation in the rate of
cardiovascular recovery following exposure to acute
psychological stress predicts changes in blood pressure
longitudinally, independently of blood pressure at baseline
and other covariates.
Design A 3-year longitudinal study.
Participants A total of 209 men and women aged 45–59
years at baseline, with no history of cardiovascular disease
Method Measurement of blood pressure, heart rate, heart
rate variability, cardiac index and total peripheral resistance
at rest, during two moderately stressful behavioural tasks
and up to 45 min post-stress. Stress reactivity was defined
as the difference in values between tasks and baseline, and
post-stress recovery as the difference between recovery
levels and baseline.
Outcome measures Resting blood pressure measured at
baseline and 3 years later. Seven individuals had been
prescribed hypertensive medication on follow-up.
Results Increases in systolic blood pressure (SBP) were
predicted by impaired post-stress recovery of SBP
(P < 0.001), diastolic blood pressure (DBP) (P < 0.001) and
total peripheral resistance (P U 0.003), independently of
baseline blood pressure, age, gender, socio-economic
status, hypertensive medication, body mass and smoking.
The adjusted odds of an increase in SBP >—5 mmHg
were 3.50 [95% confidence interval (CI) 1.19 to 10.8] for
individuals with poor compared with effective post-stress
recovery of SBP. Three-year increases in diastolic
pressure were predicted by impaired recovery of SBP
(P < 0.001) and DBP (P U 0.009) pressure and by heart rate
variability during tasks (P U 0.002), independently of
Conclusions Impaired post-stress recovery and less
consistently heightened acute stress reactivity may index
disturbances in the regulation of cardiovascular stress
responses that contribute to longitudinal changes in blood
pressure in middle-aged men and women. J Hypertens
23:529–536 Q 2005 Lippincott Williams & Wilkins.
Journal of Hypertension 2005, 23:529–536
Keywords: stress, blood pressure, recovery, cardiovascular reactivity,
International Centre for Health and Society, Department of Epidemiology and
Public Health, University College London, 1–19 Torrington Place, London WC1E
Sponsorship: This research was supported by the Medical Research Council and
the British Heart Foundation.
Correspondence and requests for reprints to Andrew Steptoe, Psychobiology
Group, Department of Epidemiology and Public Health, University College
London, 1–19 Torrington Place, London WC1E 6BT, UK.
Tel: +44 (0)20 7679 1804; fax: +44 (0)20 7916 8542;
Received 11 May 2004 Revised 17 August 2004
Accepted 4 October 2004
The assessment of acute cardiovascular responses to
mental stress tests has been used extensively for the
investigation of psychosocial factors in the development
of hypertension and coronary heart disease (CHD). A
large number of studies have measured cardiovascular
stress responses in hypertensives and normotensives,
people varying in parental history of hypertension and
in relation to factors such as social support, hostility
and background chronic stress [1–3]. One concern about
the value of this approach is whether stress responsivity
is significant clinically and predicts changes in blood
pressure and or future disease states longitudinally. A
recent review of more than 20 prospective studies indi-
heart rate stress responsivity predict future BP level and
hypertension independently of baseline BP and other
factors . Nonetheless, there are a number of incon-
sistencies in this literature, and the additional variance
accounted for by cardiovascular stress responses is often
Although the magnitude of cardiovascular responses dur-
ing stress exposure is usually measured, rate of recovery
during the post-stress period is also important. Recent
stress research has highlighted impaired recovery as a key
marker of psychobiological dysfunction . Impaired or
delayed cardiovascular recovery has been associated
cross-sectionally with a family history of hypertension
in young adults, low physical fitness and with high levels
of background stress [3,8,9]. Our group has previously
shown that post-stress recovery of BP is impaired in lower
socio-economic status individuals, and that this effect is
sustained by heightened total peripheral resistance
0263-6352 ? 2005 Lippincott Williams & Wilkins
[10,11]. In the present study, measurements of clinic BP
were carried out in healthy middle-aged men and women
who had undergone mental stress testing 3 years earlier.
The influence of cardiovascular responses to tasks and
post-stress recovery on longitudinal changes in systolic
blood pressure (SBP) and diastolic blood pressure
(DBP) was tested, after controlling for initial BP, age,
socio-economic status, smoking and body mass index
These data were collected as a follow-up to the psycho-
biology sub-study of the Whitehall II study. The White-
hall II cohort is a sample of 10 308 London-based civil
servants recruited in 1985–1988 when aged 35–55 years,
to investigate demographic, psychosocial and biological
risk factors for coronary heart disease . The psycho-
biology sub-study involved 228 volunteers (123 men, 105
women) who underwent detailed laboratory investigation
[10,11]. Participation was based on the following criteria:
white European origin, aged 45–59 years, living in the
London area, not planning to retire for at least 3 years, no
history or objective signs of coronary heart disease and
no previous diagnosis or treatment for hypertension. The
3-year follow-up data were collected during a screening
session from 209 individuals (111 men and 98 women, a
92% response rate). Of the remaining 19, one had died;
four were lost to follow-up; two did not attend screening
despite repeated requests; three had withdrawn from the
Whitehall II study and nine had moved out of London, so
were not invited to the screening session.
Laboratory mental stress session
Blood pressure and heart rate were monitored continu-
ously from the finger, using a Portapres-2 (Finapres
Medical Systems, Amsterdam, The Netherlands), a por-
table version of the Finapres device that shows good
reproducibility and accuracy in a range of settings .
Absolute BP levels obtained with the Finapres were
corrected against simultaneous brachial recordings. Car-
diac output and stroke volume were determined from
the Portapres using the aortic flow waveform method
described by Wesseling et al.  and embodied in
Modelflow 2.1 software (FMS, Amsterdam, The Nether-
lands). Stroke volume was calculated from the systolic
area, i.e. the area under the arterial pressure wave
between the onset of the blood pressure rise and the
dichrotic notch, on a beat by beat basis corrected by a
calibration factor related to aortic compliance. Total
peripheral resistance (TPR) was predicted from mean
pressure and computed aortic flow. Good agreement has
been obtained between Modelflow computations of
stroke volume and cardiac output from intra-arterial
and finger blood pressure measures and between fin-
ger-based measures and thermodilution [15,16]. Heart
rate variability was assessed as the root mean square
of successive differences in R-R intervals (RMSSD)
obtained from a three-lead electrocardiogram in 143
participants using an ambulatory cardiac impedance
device (VU-AMS, Free University, Amsterdam, The
Mental stress was induced by two behavioural tasks: a
computerized colour-word interference task and mirror
tracing. Both tasks have been extensively used in cardi-
ovascular stress research [18–20]. The colour-word task
involved the presentation of a succession of target colour
words in incongruous colours. At the bottom of the
computer screen were four names of colours displayed
in incorrect colours and the task was to press a computer
key that corresponded tothe positionat the bottom of the
screen of the name of the colour in which the target word
was printed. Mirror tracing involved the tracing of a star
with a metal stylus, which could only be seen in mirror
image. Participants were told that the average person
completed five circuits of the star in the time available
and were asked to give accuracy priority over speed on
Participants were tested in either the morning or after-
noon in a light and temperature-controlled laboratory.
They were instructed not to have drunk tea, coffee, or
caffeinated beverages, or to have smoked for at least 2 h
prior to the study and not to have consumed alcohol or
exercised on the evening before, or the day of testing.
Following instrumentation and the insertion of a venous
cannula for the periodic collection of blood samples (not
described here), the participant rested for 30 min. BP and
heart rate were recorded for the last 5 min and heart rate
variability for the last 10 min of this period (baseline
trial). Two measures using a standard arm cuff (A&D
UA779) were also obtained and these values were aver-
aged to index time 1 (T1) clinic SBP and DBP. The two
tasks were then administered in random order with a
5 min inter-task interval. Each lasted for 5 min, during
which BP and heart rate were recorded continuously.
Post-stress recovery was assessed with 5 min recordings
of BP and heart rate made 15–20 and 40–45 min after
tasks. Participants rested quietly during the recovery
period. The study was approved by the UCL/UCLH
Committee on the Ethics of Human Research.
The 3-year follow-up BP data were collected as part of a
screening session for the full Whitehall II cohort. The
interval between the stress session (T1) and follow-up
(T2) averaged 3 years, 21 days ? 110 days. Two BP read-
ings were obtained by a research nurse with the partici-
pant seated. The correlations between the two readings
were 0.89 for SBP and 0.95 for DBP, so measures were
averaged. Body weight and height were measured and
BMI calculated. Smoking and alcohol consumption were
assessed by questionnaire. Seven individuals (four men
Journal of Hypertension
2005, Vol 23 No 3
and three women) had been prescribed hypertensive
medication at T2.
TheSBP, DBP, heart rate, cardiac output, TPR and heart
rate variability during the stress session were averaged
into five trials: baseline, the two tasks and recovery
periods 1 (15–20 min post-stress) and 2 (40–45 min
post-stress). Cardiovascular responses to the two tasks
were highly correlated, with increases in SBP and DBP
responses to the tasks correlating 0.86 and 0.87, respec-
tively across participants. Consequently, we averaged
task measures to produce a mean task value for each
variable. Cardiac output was transformed into cardiac
index by correcting for body surface area.
Responses during the stress session were analysed using
repeated measures analysis of variance with gender as the
recovery 2) as the within-subject factor. The Green-
house–Geisser correction was applied whereappropriate.
Stress reactivity was defined as the difference between
the average task and baseline values and recovery, as the
difference between recovery trial 2 and baseline.
The two BP readings obtained by standard sphygmoma-
nometry after 30-min rest in the laboratory constituted
T1 BP. The two readings obtained during the screening
session 3 years later were the T2 follow-up data, and
change scores were computed by subtracting T1 from T2
values. The predictors of change in BP over the 3-year
period were analysed using multiple regression on T2
values controlling for T1 level. The other control vari-
associated with increases in BP over time independently
of stress responsivity. They included age, gender, grade
of employment, hypertensive medication (entered as a
binary dummy variable), BMI and smoking status at T2.
The influence of stress reactivity was assessed by enter-
ing task values into the regression and the impact of
recovery, by entering recovery trial 2 values. This pro-
cedure is statistically equivalent to entering reactivity
and recovery change scores. The independent effects of
reactivity and recovery are presented as unstandardized
regression coefficients (B) with 95% confidence intervals
(CI). The inclusion of alcohol consumption into the
regression models did not alter the associations with
cardiovascular stress response parameters, so alcohol
was not added as a covariate.
Predictive effects were further analysed by calculating
the proportion of participants who showed a definite
increase in SBP or DBP. Based on the distribution of
those who showed an increase ? 5 mmHg SBP and
? 3.5 mmHg DBP, though other cutpoints produced
similar results. These data were analysed by multiple
logistic regression and the odds (with 95% CI) of showing
an increase inBP above criterion fora standard difference
in the levels of predictor variables were calculated, as
detailed in the Results section. Data are presented as
means ? standard deviations.
Details of study participants are summarized in Table 1.
Men were slightly older than women on average
(P ¼ 0.045), but there were no differences in socio-
economic status defined by grade of employment. The
proportions of male and female smokers did not differ,
and there was no difference in BMI or alcohol consump-
tion. Average levels of SBP and DBP were low in both
men and women at the two time points. There was a
small decrease in SBP and DBP between T1 and T2 in
men, which was significant in the case of DBP only
(P < 0.001). Women showed an increase in SBP (P ¼
0.013) and a decrease in DBP (P ¼ 0.028). Importantly,
there was wide variation in the changes in SBP and DBP
over the 3-year period, as evidenced by the large standard
deviation for difference scores (12.0 mmHg for SBP and
8.10 mmHg for DBP).
Cardiovascular stress responses
SBP and DBP rose during stress, with increases averaging
22.8 and 13.9 mmHg, respectively (P < 0.001). Blood
pressure fell between tasks and post-task recovery trials
(P < 0.001), but nevertheless remained above baseline
levels for recovery trials 1 (15–20 min) and 2 (40–45 min,
both P < 0.001). Interestingly, neither SBP nor DBP
decreased between the two post-task recovery trials
(Fig. 1). There was no interaction between gender and
an increase in SBP ? 5 mmHg over the 3-year follow-up
period, while 18.7% increased DBP ? 3.5 mmHg.
Heart rate was higher on average in women than men
(P ¼ 0.02, Fig. 2). In addition, there was a significant
gender by trial interaction (P ¼ 0.004), since heart rate
8.17 versus 6.07 beats/min (bpm), P ¼ 0.01]. Unlike the
pattern for BP, heart rate was below baseline levels
Stress recovery and future blood pressure Steptoe 531
Men (n ¼ 111)
52.6 ? 2.6
Women (n ¼ 98)
51.8 ? 2.8Age T1 (years)
Grade of employment
Smoking T2 (%)
Body mass index T2 (kg/m2)
Alcohol consumption at least
daily T2 (%)
Systolic blood pressure T1 (mmHg)
Systolic blood pressure T2 (mmHg)
Diastolic blood pressure T1 (mmHg)
Diastolic blood pressure T2 (mmHg)
25.9 ? 3.8
25.4 ? 4.4
121.3 ? 12.4
119.5 ? 11.9
74.5 ? 8.9
70.4 ? 10.3
113.4 ? 14.2
116.7 ? 15.0
71.5 ? 9.9
69.7 ? 10.5
during post-task recovery trials 1 and 2 (both P < 0.001,
Fig. 2). The increase in heart rate during trials was
associated with a significant reduction in heart rate varia-
bility (P < 0.001), followed by an increase above baseline
levels during the recovery period (P < 0.001). There was
no interaction between gender and trial in the analysis of
heart rate variability.
Total peripheral resistance did not differ significantly at
baseline in men and women (P ¼ 0.86), but resting
cardiac index was higher in women (P ¼ 0.005). There
was a significant rise in both TPR and cardiac index
during tasks (P < 0.001, Fig. 3). The gender by trial
interaction was significant for TPR (P ¼ 0.043), but not
cardiac index. This was due to the increase in TPR
during tasks being greater in women than men (P ¼
0.04). Total peripheral resistance remained elevated
above baseline throughout the post-task recovery period
(P < 0.001), but cardiac index fell below baseline during
the two recovery trials (P < 0.001). Thus the elevation in
SBP and DBP during the recovery period was sustained
by higher vascular resistance, with low heart rate, cardiac
index and enhanced parasympathetic cardiac control.
Prediction of SBP change
SBP at T2 was positively associated with T1 resting SBP
(P < 0.001) and with BMI at T2 (P ¼ 0.034), and was
lower in smokers than non-smokers (P ¼ 0.006). It was
not related independently to gender, grade of employ-
ment,or to SBP responses to behavioural tasks.However,
the change in SBP between T1 and T2 was predicted by
SBP during recovery trial 2, independently of T1 resting
BP, age, gender, grade of employment, hypertensive
medication, BMI and smoking (B ¼ 0.33, CI 0.16–0.49,
P < 0.001). Participants whose BP failed to return to
baseline levels during post-stress recovery showed
greater SBP increases over the 3-year follow-up period.
This effect was explored further by analysing the factors
predicting an increase in SBP of ? 5 mmHg between T1
and T2, dividing SBP during recovery trial 2 into tertiles.
The proportion of individuals with a SBP increa-
se ? 5 mmHg ranged from 26.1% in the lowest recovery
trial tertile to 50.1% in those in the highest tertile
(Table 2). Compared with the lowest tertile, the odds
of an increase ? 5 mmHg were 3.59 (CI 1.19–10.8,
P ¼ 0.024) for the highest tertile of SBP during recovery,
Journal of Hypertension
2005, Vol 23 No 3
Systolic blood pressure
Diastolic blood pressure
15–20min 40–45 minBase
Mean (a) systolic blood pressure and (b) diastolic blood pressure,
during the baseline, task and post-stress recovery trials. Values for men
are shown in solid lines and women in dashed lines. Error bars are
standard error of the mean (SEM).
Heart rate variability
Mean (a) heart rate and (b) heart rate variability, during the baseline,
task and post-stress recovery trials. Values for men are shown in solid
lines and women in dashed lines. Error bars are standard error of the
mean (SEM). bpm, beats per minute; RMSSD, root mean square of
successive differences in milliseconds (ms).
independently of T1 resting SBP, age, gender, grade
of employment, hypertensive medication, BMI and
Change in SBP between T1 and T2 was also predicted
by DBP during task (P ¼ 0.003) and recovery trials
(P ¼ 0.002), independently of resting T1 DBP and other
covariates. When these two effects were entered compe-
titively into a stepwise regression, recovery DBP entered
the model first and the effect of task values was no longer
significant. The regression coefficient for the association
between DBP during recovery trial 2 and SBP at T2 was
B ¼ 0.32 (CI 0.10–0.55, P ¼ 0.005), independent of cov-
ariates. As shown in Table 2, 58.1% of participants with
DBP in the highest recovery tertile showed an increase in
SBP ? 5 mmHg, compared with 28.1% of those in the
lowest tertile. The adjusted odds of an increase in
SBP ? 5 mmHg were 4.10 (CI 1.28–13.1, P ¼ 0.018)
for participants whose DBP was in the highest tertile
during the recovery period.
Changes in SBP over the 3-year period were not asso-
ciated with heart rate, heart rate variability, or cardiac
index during the stress session. But an effect of TPR was
observed, since the increase in SBP between T1 and T2
was greater in people whose TPR was higher in recovery
trial 2 (B ¼ 0.012, CI 0.004–0.020, P ¼ 0.004), indepen-
dently of resting TPR, resting T1 SBP, gender, grade of
employment, hypertensive medication, BMI and smok-
ing. The proportion of participants with SBP increa-
ses ? 5 mmHg was 32.0% in the lowest and 52.3% in
the highest tertile of TPR during recovery (adjusted odds
2.82, CI 1.18–6.77, P ¼ 0.02). Gender did not interact
with recovery effects in any of these analyses.
Prediction of DBP change
(P < 0.001),BMI(P ¼ 0.01)andnegativelywithsmoking
(P ¼ 0.02). The change in DBP was also predicted by
SBP during the post-stress recovery period, but not by
reactions to tasks. DBP increased to a greater extent over
the 3-year period in those with greater SBP during
recovery trial 2, independently of T1 resting SBP and
DBP, age, gender, grade of employment, BMI and smok-
ing (B ¼ 0.20, CI 0.08–0.33, P < 0.001). Table 3 sum-
marizes the associations between post-task recovery BP
and increases in DBP ? 3.5 mmHg between T1 and T2.
Individuals in the highest tertile of SBP during post-task
recovery trial 2 had substantially elevated odds of an
increase in DBP ? 3.5 mmHg independently of covari-
ates (odds ratio 8.59, CI 2.08 to 35.4, P ¼ 0.003).
Changes in DBP between T1 and T2 were associated
both with DBP measured during stress tasks (P ¼ 0.013)
and recovery trial 2 (P ¼ 0.01), independently of resting
DBP at T1. In stepwise regression, DBP during recovery
entered the model first and the effect of task levels was
not independently significant (B ¼ 0.22, CI 0.06–0.38,
P ¼ 0.009). As shown in Table 3, increases in DBP ?
3.5 mmHg over 3 years were observed in 30.9% of
participants with recovery DBP in the highest tertile,
Stress recovery and future blood pressure Steptoe 533
Base Tasks15–20min 40–45min
BaseTasks 15–20min 40–45min
c . e
5 -s .
Total peripheral resistance
Mean total (a) peripheral resistance and (b) cardiac index during the
baseline, task and post-stress recovery trials. Values for men are shown
in solid lines and women in dashed lines. Error bars are standard error
of the mean (SEM).
post-task recovery effects
Prediction of 3-year increase in systolic blood pressure by
SBP ? 5 mmHg
Odds of increase in
SBP ? 5 mmHg
SBP recovery trial 2
DBP recovery trial 2
resistance recovery trial 2
1.86 (0.85 to 4.08)
3.59 (1.19 to 10.8)
0.94 (0.39 to 2.23)
4.10 (1.28 to 13.1)
0.78 (0.33 to 1.83)
2.82 (1.18 to 6.77)
?Adjusted for age, gender, grade of employment, hypertensive medication, BMI,
smokingandT1systolicblood pressure(SBP).yAdjusted forage,gender,grade of
employment, hypertensive medication, body mass index, smoking, T1 SBP and
baseline diastolic blood pressure (DBP).
employment, hypertensive medication, body mass index, smoking, T1 SBP and
baseline total peripheral resistance. CI, confidence interval.
zAdjusted for age, gender, grade of
compared with 12.8% for those in the lowest tertile
(P ¼ 0.029, see Table 3).
The change in DBP was not associated with heart rate,
TPR, or cardiac index responses during the stress session.
There was, however, a significant relationship with heart
rate variability. Lower heart rate variability during stress
tasks predicted changes in DBP from T1 to T2 indepen-
dently of T1 resting DBP, resting heart rate variability,
age, gender, grade of employment, hypertensive medica-
tion, BMI and smoking (B ¼ –0.83, CI –0.30 to –0.07,
P ¼ 0.002). Some 26.4% of participants with heart
rate variability in the lowest tertile increased DBP ?
3.5 mmHg over the 3-year period, compared with 9.6%
of individuals in the highest tertile, but the adjusted odds
were not significant (2.72, CI 0.71–10.5, P ¼ 0.15).
The main findings of this study were that increases in
SBP and DBP over a 3-year period were predicted by
impaired post-stress cardiovascular recovery. Although
some associations with cardiovascular activity during
stress tasks were observed, these were generally less
strong than the recovery effects. Increases in SBP were
predicted by high levels of SBP and DBP and TPR
during the recovery period, while increases in DBP were
predicted byhigh levels ofSBP and DBP during recovery
and by reduced heart rate variability during stress tasks.
The impact of these variables was independent of
the influence of baseline BP at T1, age, gender, socio-
economic status, hypertensive medication, smoking and
BMI. Response rates were high, so selection factors are
unlikely to have accounted for the pattern of results.
A number of previous studies have shown associations
between longitudinal changes in BP and cardiovascular
stress reactivity . The literature is not all consistent,
and it is notable that positive associations between stress
reactivity and longitudinal changes have generally been
recorded in young samples, but not in middle-aged
cohorts such as the one studied here [6,21]. Impaired
cardiovascular recovery has been related to longitudinal
changes in BP in only one previous study, but the follow-
up rate in that investigation was only 39%, so selection
factors may have been operating . It is plausible that
post-stress recovery becomes more important as people
grow older for two reasons. First, post-stress recovery
tends to be rapid and efficient in young people; indeed,
the majority of studies of recovery in young adults and
adolescents have not continued monitoring for more than
10 min after stress termination . The scope for indi-
vidual differences to have an impact is therefore limited.
Second, impairment of post-stress recovery may emerge
after prolonged and repeated exposure to moderate stress
activation over many decades. McEwan and colleagues
stability of physiological systems in the face of environ-
mental challenge. Chronic or repeated challenge over
long periods may lead to a condition of allostatic load, a
key element of which is chronic dysregulation of biolo-
gical response systems. One manifestation of this state is
failure to adapt efficiently post-stress. Several of the
studies that have failed to show strong associations
between cardiovascular stress reactivity and future BP
have not included post-stress recovery in the analysis
Predictors of increases in BP were analysed using both
linear and logistic regression techniques in this study.
Linear regression utilizes the complete range of data, but
correlation and regression coefficients are typically low
and relatively little of the variance in BP is accounted for.
It has been argued that such methods may be misleading
and underplay the clinical significance of associations
. By way of analogy, the substantial long-term mor-
tality risk associated with raised BP that was described in
the Chicago Heart Association Detection Project in
Industry corresponds to a correlation of less than 0.1
(accounting for 1% of the variance) . We therefore
computed the odds of a definite increase in BP being
associated with impaired post-stress recovery. The odds
of definite increases in SBP were three-fold for indivi-
duals in the upper compared with the lower tertile of
recovery BP and as high as 8.11 in the case of DBP.
and women with no signs of hypertension, CHD or
diabetes at baseline, although a small number had been
diagnosed and treated for hypertension by the time of
follow-up. Their relatively healthy status is reflected in
the fact that there were small decreases in DBP over the
3-year period in both men and women on average. The
associations that were observed with post-stress recovery
may therefore underestimate the significance of these
factors in more representative samples, where upward
drift in BP is more apparent .
Journal of Hypertension
2005, Vol 23 No 3
post-task recovery effects
Prediction of 3-year increase in diastolic blood pressure by
DBP ? 3.5 mmHg
Odds of increase
in DBP ? 3.5 mmHg
SBP recovery trial 2
2.77 (0.95 to 8.12)
8.59 (2.08 to 35.2)
DBP recovery trial 2
0.86 (0.29 to 2.60)
3.38 (1.14 to 10.1)
?Adjusted for age, gender, grade of employment, hypertensive medication, body
mass index, smoking, T1 diastolic blood pressure (DBP) and baseline systolic
blood pressure (SBP).yAdjusted for age, gender, grade of employment, hyper-
tensive medication, body mass index, smoking and T1 DBP. CI, confidence
The behavioural tasks utilized in this study elicited
marked acute increases in SBP and DBP. These were
sustained during task periods by a combination of raised
cardiac output and TPR (Fig. 3). But during the post-task
recovery period, heart rate and cardiac index fell below
baseline levels, while the increased TPR was sustained.
Thus the elevation in BP recorded during the recovery
period was underpinned by vascular rather than cardiac
index and prolonged changes in TPR has been recorded
during extended mental stress testing . We do not
know how long BP would take completely to return to
baseline, since monitoring stopped after 45 min. Raised
peripheral resistance in response to stress may be asso-
ciated with enhanced cardiovascular disease risk . For
example, BP stress responses are maintained to a greater
extent by vascular than cardiac adjustments in black
compared with white hypertensives , young adults
with hypertensive parents  and in lower socio-
economic status (SES) men and women . Our group
has also shown that lower SES individuals show more
factors  and in inflammatory cytokine release .
This study has a number of limitations. Data were col-
lected from middle-aged white men and women and
results may not generalize to other populations. The
sample size was not sufficient to investigate possible
interactions between post-stress recovery and socio-
economic position, but this is potentially important in
view of the greater risk of CHD in less privileged sectors
of the population. Because of equipment problems, heart
rate variability was only assessed in a proportion of parti-
to the evidence that disturbances of post-stress cardiovas-
cular regulation and the restitution of normal function are
potentially significant for cardiovascular disease.
We are grateful to Pamela J. Feldman, Sabine Kunz-
Ebrecht, Bev Murray, Natalie Owen and Gonneke Will-
emsen for their participation in data collection and data
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