Journal of Human Hypertension (1998) 12, 855–860
 1998 Stockton Press. All rights reserved 0950-9240/98 $12.00
http://www.stockton-press.co.uk/jhh
ORIGINAL ARTICLE
Postexercise decrease in arterial blood
pressure, total peripheral resistance and
in circulatory responses to brief hyperoxia
in subjects with mild essential
hypertension
E Izdebska1, I Cybulska2, M Sawicki2, J Izdebski3 and A Trzebski1
1
Department of Physiology, Medical University of Warsaw; 2National Institute of Cardiology, 3National
Centre of Sports Medicine, Warsaw, Poland
The objective of our study was: (1) to compare the
influence of moderate exercise on circulatory afterresponse in mildly hypertensive (n = 8) and normotensive male subjects (n = 9); (2) to examine the circulatory
response to 3-min hyperoxic inactivation of arterial
chemoreceptors at rest and during postexercise period
in both groups. Hypertensive men (HTS) with a systolic
blood pressure (SBP) 148 ⴞ 5 mm Hg, diastolic blood
pressure (DBP) 92.4 ⴞ 4 mm Hg; and normotensive men
(NTS), with a SBP 126 ⴞ 3 mm Hg, DBP 75.6 ⴞ 1.3
mm Hg, were submitted to 20-min of moderate exercise
on a cycloergometer (up to the level of 55% of each subject’s resting heart rate reserve). Finger arterial BP was
recorded continuously with Finapres, impedance reography was used for recording stroke volume, cardiac
output and arm blood flow. In HTS a significant
decrease in SBP by 14.5 ⴞ 3.4 mm Hg, DBP by 8.9 ⴞ 1.9
mm Hg, total peripheral resistance (TPR) by 0.45 ⴞ 0.05
TPR u. (33.7 ⴞ 2.7%), and in arm vascular resistance
(AVR) by 11.0 ⴞ 2.7 PRU u. (35.6 ⴞ 7%), was observed
over a 60-min postexercise period.
NTS exhibited insignificant changes in SBP, DBP,
AVR except a significant decrease in TPR limited only to
20-min postexercise period. Hyperoxia decreased SBP,
DBP and TPR in HTS. This effect was significantly attenuated during the postexercise period. Long-lasting antihypertensive effect of a single dynamic exercise in HTS
suggests that moderate exercise may be applied as an
effective physiological procedure to reduce elevated
arterial BP in mild hypertension. We suggest also that
the attenuation of the sympathoexcitatory arterial
chemoreceptor reflex may contribute to a postexercise
decrease in arterial BP and in TPR in mildly hypertensive subjects.
Keywords: exercise; blood pressure; vascular resistance; arterial chemoreceptor reflex; hyperoxia
Introduction
Regular, dynamic, aerobic physical activity is associated with a reduced risk of hypertension1,2 A
significant inverse relationship between regular
physical activity and blood pressure (BP) has been
reported,3 although some data did not confirm
favourable effects of exercise in essential hypertension.4,5
In recent years, there has been considerable interest in circulatory after-effects of single physical
exercise.6–16 Many studies demonstrated that arterial
BP in hypertensive patients is decreased for hours
after single dynamic exercise.6–8,11,14–16 These studies were done mostly in middle-aged subjects with
essential hypertension.6–8,16,17
There are inconsistencies with regard to the sysCorrespondence: Dr Ewa Izdebska, Department of Physiology,
Medical University of Warsaw, Krakowskie Przedmieście 26/28
str,. 00–927 Warsaw, Poland
Received 24 January 1998; revised 14 July 1998; accepted 13
August 1998
temic and regional haemodynamic changes responsible for the postexercise fall in BP. Metabolic vasodilatation,
thermoregulatory
vasodilatation,10
11,13
decrease in sympathetic activity,
and resetting of
the baro- and cardiopulmonary reflex sensitivity12,14,15 have been proposed as possible mechanisms of postexercise hypotension.
One of the possibilities, not yet explored, may be
an attenuation of the sensitivity of the sympathoexcitatory arterial chemoreceptor reflex (ACR). An augmented responsiveness of ACR in primary hypertension has been shown by Trzebski et al18–21 TafilKlawe et al20, and Izdebska et al22 and is manifested
by a slight, yet significant, transient fall in arterial
BP and total peripheral vascular resistance (TPR) in
young mildly hypertensive subjects exposed to brief
hyperoxia, a condition which inactivates the neurogenic sympathoexcitatory reflex drive from the peripheral arterial chemoreceptors and reduces sympathetic nerve activity at rest.23
No systematic study has been done on the haemodynamic effects of inactivation of the arterial
chemoreceptors in hypertensive human subjects
Postexercise hypotension, hyperoxia, essential hypertension
E Izdebska et al
856
during postexercise period. The problem appears
interesting, as regular physical exercise has been frequently recommended for the prevention and
attenuation of arterial hypertension.
Therefore the aim of our study was:
(1) To test the influence of moderate exercise on the
cardiovascular system in young mildly hypertensive subjects and in a matched normotensive group.
(2) To examine the circulatory response to the hyperoxic inactivation of arterial chemoreceptors at
rest and during postexercise period.
Subjects and methods
This study was approved by the National Institute
of Cardiology ethics’ committee on human research.
Each subject gave written consent to participate in
the study.
Measurements were performed on eight untreated
mildly essential hypertensive (HTS, aged 26 ± 4
years) and nine healthy normotensive male subjects
(NTS, aged 25 ± 3 years). All subjects were found to
be free from pulmonary, renal and heart diseases.
Characteristics of both groups are presented in
Table 1.
Finger arterial BP was measured continuously
with Finapres (Ohmeda). A tetrapolar impedance
reography (Warsaw Technical University) was used
to compute continuously stroke volume, cardiac
output (CO) and arm muscular blood flow (ABF).
The first derivative of the impedance change
(associated with ventricular contraction) was used
to calculate stroke volume, using the Kubicek equation.24–26 TPR was calculated in TPR units by dividing mean arterial BP by cardiac output. Arm regional
vascular resistance (AVR) was calculated per 100 ml
tissue/min in PRU units. Heart rate (HR) was measured from the ECG recordings. All data were
synchronously sampled on five channels and collected continuously on-line with a sampling frequency of 200 Hz and 12-bite resolution. The data
were analysed with use of the specialised macro language adapted to the experimental program.
Exercise of an increasing intensity was performed
on a bicycle ergometer Monark 818E, up to the level
Table 1 Resting characteristics of the study population
Variable
Hypertensive
Normotensive
Age (yr)
Weight (kg)
Height (cm)
Resting SBP (mm Hg)
Resting DBP (mm Hg)
HR (beats/min)
CO (l/min)
CI (l/min/m2)
TPR (TPR u.)
AVR (PRU u.)
26 ± 4
92.2 ± 4
180.4 ± 1.7
148 ± 5
92.4 ± 4
73.5 ± 3
5.12 ± 0.75
2.4224 ± 0.8
1.429 ± 0.24
33 ± 1.9
25 ± 3 NS
87 ± 3.5 NS
183.4 ± 2 NS
126 ± 3**
75.6 ± 1.3**
73.6 ± 3.7 NS
6.3 ± 0.57 NS
3.078 ± 0.3 NS
0.868 ± 0.07*
10 ± 2.63**
CI = cardiac index, TPR u. = total peripheral vascular resistance
units, PRU u. = peripheral regional vascular resistance units,
other abbreviations—see text.
*P ⬍ 0.05, **P ⬍ 0.01.
of about 55% of each subject’s resting heart rate
reserve, which corresponded to the external power
output of 116 ± 4 and 119 ± 4 Watts for HTS and
NTS, respectively.
A short-lasting inactivation of the arterial chemoreceptors was produced by a brief breathing from a
mixture of 60–70% oxygen in air from a 200 litre
Douglas bag for a 3-min period. The measurements
were performed: during the 60-min rest period
(control), during the 20-min dynamic exercise, and
during the 60 to 90-min recovery. In the same subjects periods of brief hyperoxia were applied 10 min
before and 50 min after the cessation of exercise,
when the BP was stable.
All measurements were performed in the standardised condition. Each subject was in the sitting
position on the cycloergometer over all experimental periods, with both hands fixed in the horizontal plane at the level of the tricuspid valve. Such
conditions enabled us to maintain stable and reproducible measurements.
For the statistical analysis, repeated measurements ANOVA and Dunnett’s test were used for estimation of the differences between control pre-exercise value and postexercise values of systolic BP
(SBP), diastolic BP (DBP), CO, TPR in the same
group of NTS and HTS independently. One-way
analysis of variance was used to compare mean postexercise values of HTS and NTS groups. Student’s
t-test was used for the estimation of statistical significance of differences between control values of
both groups and each mean of respective before and
after hyperoxia means (unpaired and paired t-test,
respectively). Correlations were calculated by linear
regression. Values were considered significant if
they achieved a P value ⭐0.05. Results were
expressed as mean ± standard error of mean (s.e.m.).
Results
Effects of exercise
In HTS the exercise caused a significant rise in SBP
from 148 ± 5 mm Hg to 198.5 ± 15 mm Hg, in HR
from 73.5 ± 3 to 132.6 ± 2.5 beats/min, in CO from
5.12 ± 0.75 to 13.8 ± 1.45 l/min. TPR decreased significantly from 1.429 ± 0.24 to 0.648 ± 0.1 TPR u.,
DBP changed insignificantly from 92.4 ± 4 to 100.2
± 8.3 mm Hg.
In NTS the same level of exercise caused a significant increase: in SBP from 126 ± 3 to 201 ± 9.2
mm Hg, in DBP from 75.6 ± 1.3 to 99.7 ± 2.9 mm Hg,
in HR from 73.6 ± 3.7 to 137.3 ± 1.3 beats/min, CO
from 6.3 ± 0.57 to 15.1 ± 1.7 1/min and a significant
decrease in TPR from 0.868 ± 0.07 to 0.465 ± 0.05
TPR u.
The exercise induced similar increases in heart
rate in both groups. The external power outputs during exercise were not significantly different in HTS
and NTS subjects (see methods).
The mean systolic and diastolic pressure during
exercise did not differ between HTS and NTS. The
absolute and percentage increase in the systolic and
diastolic BP in NTS (an increase in SBP by 82.8 ± 8
mm Hg; by 65.58 ± 6.3% of control resting value,
Postexercise hypotension, hyperoxia, essential hypertension
E Izdebska et al
and in DBP by 23 ± 3 mm Hg; 20.2 ± 3%) were
greater than those in HTS (an increase in SBP by
48.2 ± 12 mm Hg; 32.3 ± 7.5% of the control value,
and in DBP by 9.46 ± 4.7 mm Hg; 9.9 ± 4.65%,
P ⬍ 0.05).
During physical exercise TPR decrease in HTS
was significantly greater than in NTS (by 0.845 ±
0.19 and 0.426 ± 0.04, respectively, P ⬍ 0.05).
Arterial BP, cardiac output, total peripheral
resistance and arm vascular resistance in the
postexercise period
SBP and DBP in HTS were significantly lower at
15 min of the postexercise period compared to the
pre-exercise control: by 13.6 ± 3.6 mm Hg and 8.7 ±
2.3 mm Hg, P ⬍ 0.05, respectively. After 60 min
since the end of exercise these values have been still
reduced by 16.5 ± 3.6 mm Hg and 8.9 ± 1.9 mmHg,
respectively, P ⬍ 0.01 (Figure 1).
In contrast, in NTS only nonsignificant decrease
in SBP and DBP were observed by 2 ± 2.8 and 3.4 ±
2.5 mm Hg, respectively during postexercise period
(Figure 1).
CO in HTS was significantly higher during the
postexercise recovery period compared to the preexercise control values (Figure 1), and remained
augmented still 60 min after the end of exercise by
13 ± 3.5%, P = 0.01. In contrast, in NTS, CO was
higher by 13.7 ± 4.8%, P ⬍ 0.01 only over a 20-min
postexercise period.
TPR in HTS was significantly lower over the
whole 60-min postexercise period and even afterwards. At the end of a 1 h postexercise rest TPR was
still lower by 27.8 ± 4.8%, P ⬍ 0.01 (Figure 1). In
NTS TPR was significantly reduced only over the
20 min postexercise period compared to the control
values by 18.4 ± 2.7%, P ⬍ 0.01.
HR was significantly higher in the postexercise
period in both groups. Over the last 10 min of a 1 h
postexercise period it was higher by 7 ± 1.8
beats/min in the HTS, and by 5 ± 0.7 beats/min in
the NTS. The difference was not significant.
In HTS AVR in the postexercise period was
reduced by 35.6 ± 7%, P ⬍ 0.05. In NTS AVR was
reduced over a 25-min postexercise period by 13 ±
4.6%, abating thereafter (Figure 2).
The absolute values of SBP, DBP and TPR during
the postexercise period did not significantly differ
between both groups, despite significantly higher
respective values in the hypertensive group in the
control rest period.
In HTS a significant positive correlation was
observed between the resting DBP values and postexercise TPR values, r = 0.9937, P ⬍ 0.001.
Figure 1 (A) Time course of postexercise mean values of the systolic blood pressure (SBP), diastolic blood pressure (DBP) in hypertensive subjects (HTS), and normotensive subjects (NTS). (B) Time course of postexercise mean values of the cardiac output (CO) in
hypertensive subjects and normotensive subjects. (C) Time course of postexercise mean values of the total peripheral resistance (TPR)
in hypertensive subjects and normotensive subjects. Measurements were taken in pre-exercise control period (time 0), and in every
10 min of postexercise period. Asterisks denote significant difference between mean control pre-exercise values and means calculated
for each 10-min period during postexercise period. 0 time = mean value for pre-exercise control period; ! = P ⭐ 0.05, !! = P ⭐ 0.01;
significantly different from HTS; *P ⭐ 0.05, **P ⭐ 0.01, significantly different from control, pre-exercise value, (time 0).
857
Postexercise hypotension, hyperoxia, essential hypertension
E Izdebska et al
858
Figure 2 Mean data for postexercise AVR, during the period starting 25 min after the exercise. Other descriptions as in Figure 1.
nificant increase in CO by 12.8 ± 3.6%, P ⬍ 0.05, and
a decrease in AVR by 11.5 ± 1.6%, P ⬍ 0.01. HR
decreased by 2.6 ± 0.8 beats/min, P ⬍ 0.05.
In contrast, in NTS a small yet significant increase
in DBP by 1.76 ± 0.64 mm Hg, P ⬍ 0.05, in TPR by
8.9 ± 2.9%, P ⬍ 0.01, and a nonsignificant increase
in SBP by 1.15 ± 1.56, were observed (Figures 3 and
4). CO decreased by 5.3 ± 2.1%, P ⬍ 0.05, AVR
increased slightly by 5 ± 3%, P ⬎ 0.05, HR decreased
by 5.7 ± 1 beats/min, P ⬍ 0.01.
Hyperoxia applied during the postexercise period
did not significantly change haemodynamic parameters in either group (Figures 3 and 4), except for
some decrease in HR in HTS by 3.7 ± 0.38 beats/min,
P ⬍ 0.01, and in NTS by 5.3 ± 1.4 beats/min, P =
0.01. However the difference between both groups
in HR reduction induced by hyperoxia was nonsignificant.
A significant positive correlation between the
resting DBP and the decrease in TPR during hyperoxic inactivation of the arterial chemoreceptor
reflex was found in HTS subjects: r = 0.9639,
P ⬍ 0.01.
Discussion
Figure 3 SBP and DBP response to short time lasting inactivation
of arterial chemoreceptors by brief hyperoxia. CON = control rest
period, OX = hyperoxia, CONR = control for recovery period.
Other descriptions as in Figure 1.
Effects of hyperoxia
In HTS a short time breathing with oxygen during
the control pre-exercise period caused a slight yet
significant decrease in DBP by 4.6 ± 0.86 mm Hg,
P ⬍ 0.01; in SBP by 9 ± 1.8 mm Hg, P ⬍ 0.01 (Figure
3), in TPR by 18.6 ± 1.6%, P ⬍ 0.05 (Figure 4), a sig-
Figure 4 TPR response to short time lasting inactivation of
arterial chemoreceptors by brief hyperoxia. Other abbreviations
as in Figure 3. Other descriptions as in Figure 1.
The major finding of our study is a prolonged
reduction of the systolic and diastolic BPs during
the postexercise period following a 20-min moderate
exercise
period.
Attenuated
haemodynamic
response to hyperoxia applied 50 min after the end
of exercise in the HTS suggests a long-term
decreased drive from the arterial chemoreceptors in
the postexercise period.
Haemodynamic response to exercise itself in
hypertensive patients observed in our study is not
dissimilar to other reports.6,8,17,22,27,28
The reduction in BP in the postexercise period
was parallel to the increase in CO and decrease in
the total peripheral and arm regional vascular resistance. NTS did not demonstrate significant aftereffects of exercise. Decrease in SBP and DBP was
nonsignificant and increase in CO, decreases in TPR
and AVR were of shorter duration in NTS than in
the HTS group.
Arterial BP, CO and AVR were measured continuously, non-invasively, in standardised conditions
(see methods). No increase in BP before the start of
exercise was observed. Therefore, the changes in BP
do not appear to be related to a pre-exercise cardiovascular anticipatory reaction. We applied the exercise of moderate intensity because such level of
exercise is easily tolerated and is recommended in
most training and recreational programmes.29,30
Our results are in agreement with those of Cleroux
J et al.6 However our subjects were of younger age,
the exercise period was shorter, and we observed
more pronounced postexercise decrease in TPR in
HTS as compared to the NTS.
The haemodynamic pattern during the postexercise period may depend on the age, on the haemodynamic state of the population studied, and on the
protocol used. In elderly hypertensive subjects, an
increase in TPR, a decrease in cardiac output, no
decrease in DBP, and an unchanged heart rate after
Postexercise hypotension, hyperoxia, essential hypertension
E Izdebska et al
three 15-min bouts of treadmill exercise at 50% VO2
max, were reported.17 No change in DBP was
observed in borderline hypertensive men during
postexercise period.11
In other studies arterial BP was measured at selected time points by a traditional arm cuff method. In
contrast we applied a continuously non-invasive BP
recording beat by beat along with CO, HR and AVR.
Measurements performed only at selected time
points may over- or underestimate fluctuating cardiovascular variables.
Physiological mechanisms which account for
postexercise hypotension are still unclear.9,30
Recently, it has been proposed that inhibition of
sympathetic nerve activity and vasodilatation is
responsible for the decrease in arterial BP and in
total peripheral resistance during the postexercise
period.11,13 An activation of the central opioid
endorphin systems by exercise has been suggested
to be involved in the postexercise vasodilatation.
Such activation decreases sympathetic vasoconstrictor activity.31 Naloxon, an opioid antagonist,
blocked or attenuated the postexercise hypotension.31,32 A decrease in transmission of the sympathetic activity into blood vessels has also been
observed after dynamic exercise.13 A reduced vascular alpha-adrenergic responsiveness after acute exercise has been reported in Dahl-salt sensitive rats.33
The sympathoexcitatory peripheral arterial
chemoreceptor reflex is hyperactive in mild arterial
hypertension.18–22,34–36 Our study indicates an
attenuation of circulatory BP and TPR response to
brief hyperoxia during postexercise period in hypertensive subjects. This result suggests that augmented
sympathoexcitatory tonic drive induced by overactive chemoreceptor reflex in hypertensive subjects
is reduced in the postexercise period. Such a postexercise attenuation of chemoreceptor sympathoexcitatory drive may contribute to reduced sympathetic
nerve activity observed after dynamic exercise.11,13
Unknown is the mechanism of chemoreceptor
inhibition in a postexercise period. Inhibitory
influences on the afferent activity of arterial chemoreflex may appear after exercise. Possible candidates
are: nitric oxide (NO), and/or endogenous opioids,
an inhibitory substance to the glomic chemosensory
cells, as it was shown by Trzebski et al,37 and Pokorski et al,38 respectively. Total body NO synthesis is
increased during and after physical activity.39 Exercise increases the plasma beta-endorphin level.31
Another possibility may be some inhibition in the
central chemoreceptor pathways as a result of antagonistic interaction between arterial baro- and
chemoreceptor reflexes.40 Increased carotid baroreflex gain during postexercise period has been
observed.12,14,15
Healthy subjects breathing high oxygen exhibit
reduced heart rate and cardiac output parallel with
augmented TPR.41 Increased afterload may explain
such a response. In contrast, in hypertensive subjects as shown in our previous and present study,
cardiac output is augmented during hyperoxia
despite a slightly reduced heart rate. This is a novel
observation. The mechanism is presumably due to
reduced afterload as in hypertensive patients a brief
hyperoxia reduces arterial BP whereas in healthy
subjects hyperoxia leads to transient increase in TPR
and in arterial BP.
To summarise:
(1) In mildly hypertensive subjects moderate exercise induces a decrease in arterial BP and total
peripheral resistance and arm vascular resistance.
(2) In matched normotensive subjects similar moderate exercise produces only insignificant
decrease in arterial BP and total peripheral
resistance.
(3) During postexercise recovery period arterial BP
and total peripheral resistance values in the
hypertensive subjects are reduced to the values
which do not differ from the values in the normotensive group.
(4) A fall in arterial BP and total peripheral resistance produced by short-lasting hyperoxic inactivation of peripheral arterial chemoreceptors in
hypertensive subjects is attenuated during postexercise recovery.
Conclusions
(1) An attenuation of the chemoreceptor reflex drive
following moderate exercise may contribute to the
mechanisms of the reduction of BP and total peripheral resistance during the postexercise period in
mildly hypertensive subjects.
(2) The present results suggest that moderate exercise may be applied as an effective physiological
procedure to reduce elevated arterial BP in mildly
hypertensive subjects.
Acknowledgements
This project was supported by a research grant from
the Medical University of Warsaw and KBN Grant
No. 4505A 059 09.
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