JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY 2004, 55, 4, 713–724
www.jpp.krakow.pl
IZDEBSKA E. , CYBULSKA I. , IZDEBSKI J. , MAKOWIECKA-CIEŒLA M. , TRZEBSKI A.
1
2
3
2
1
EFFECTS OF MODERATE PHYSICAL TRAINING
ON BLOOD PRESSURE VARIABILITY AND HEMODYNAMIC PATTERN
IN MILDLY HYPERTENSIVE SUBJECTS.
Department of Experimental and Clinical Physiology, The Medical University of Warsaw ,
1
National Institute of Cardiology , National Centre of Sports Medicine ,Warsaw, Poland
2
3
The objective of our study was to compare the cardiovascular effects of moderate
exercise training in heathy young (NTS, n=18, 22.9±0.44 years) and in hypertensive
human subjects (HTS, n=30, 23±1.1). The VO2max did not significantly differ between
groups. HTS of systolic blood pressure (SBP) 148±3.6 mmHg and diastolic blood
pressure(DBP) 88±2.2mmHg, and NTS of SBP: 128.8 ± 4 mmHg and DBP: 72 ± 2.9
mmHg were submitted to moderate dynamic exercise training, at about 50% VO2max
3 times per week for one hour, over 3 months. VO2max was measured by Astrand's test.
Arterial blood pressure was measured with Finapres technique, the stroke volume,
cardiac
output
and
arm
blood
flow
were
assessed
by
impedance
reography.
Variability of SBP and pulse interval values (PI) were estimated by computing the
variance
and
power
spectra
according
to
FFT
algorithm.
After
training
period
significant improvements in VO2max were observed in NTS- by 1.92 ±0.76 and in HTS
by 3±0.68 ml/kg/min). In HTS significantly decreased: SBP by 19 ±2.9 mmHg, in
DBP by 10.7±2 mmHg total peripheral resistance (TPR) by 0.28 ±0.05 TPR units.
The pretraining value of low frequency component power spectra SBP (LFSBP) was
significantly greater in HTS, compared to NTS. PI variance was lower in HTS,
compared to NTS. After physical training, in HTS PI variance increased suggesting
a
decrease
in
frequency
modulated
sympathetic
activity
and
increase
in
vagal
modulation of heart rate in mild hypertension. A major finding of the study is the
significant decrease of resting low frequency component SBP power spectrum after
training in HTS. The value of LFSBP in trained hypertensive subjects normalized to
the
resting
level
of
LFSBP
in
NTS.
Our
findings
suggest
that
antihypertensive
hemodynamic effects of moderate dynamic physical training are associated with
readjustment of the autonomic cardiovascular control system.
Key
W o r d s : hypertension,
hemodynamics
blood
pressure,
spectral
analysis,
physical
training,
714
INTRODUCTION
Hypertension is a main risk factor for coronary heart disease, heart infarction
and cerebral stroke. Blood pressure reduction diminishes incidence of death from
cardiovascular
diseases
(1).
There
is
general
agreement
that
essential
hypertension is accompanied by an increased sympathetic cardiovascular activity
(2-6), reduced parasympathetic modulations of the heart rate, and decreased heart
rate variability(7-9).
Recent studies have shown that regular aerobic exercise lowers blood pressure
in patients with essential hypertension (10-15,17-22) and attenuates the effects of
cardiovascular
risk
factors
(15,16).
The
mechanisms
responsible
for
blood
pressure reduction induced by exercise training in hypertensive subjects are still
poorly understood (13,17,18). Reduced cardiac output (19,20) versus reduced
total vascular resistance (18) were reported. Important contribution is apparently
due
to
reduction
in
cardiovascular
sympathetic
activity
observed
in
hyper-
tensives after physical training (14,21,22).
Noninvasive
classical
methods
of
quantification
of
the
cardiovascular
variability, the variance and spectral analysis of systolic blood pressure and heart
beat intervals provide an insight into autonomic control of the circulation in
hypertensive subjects (23-27). The LF component of systolic blood pressure
power
spectrum
sympathetic
(LFSBP)
activity
is
considered
addressed
to
as
a
resistant
marker
arteries
of
oscillations
(9,23-27).
of
the
Magnitude
of
LFSSBP appears related to likelihood of secondary disadvantageous cardiovascular
complications
in
essential
hypertension
i.e.
cardiovascular
remodelling
and
cardiac hypertrophy (27).
Iellamo
(28)
found
in
healthy
people
submitted
to
submaximal
exercise
training an augmented vagal cardiac modulation and a tendency to decrease
sympathetic vasomotor control, suggested from decrease in the LF component of
systolic
blood
pressure
spectral
power.
Reduction
of
arterial
blood
pressure
accompanied by lower LF component of systolic blood pressure was observed
after isometric (handgrip) training in older hypertensive subjects (29). There are
no
reports
on
the
effect
of
physical
dynamic
training
on
blood
pressure
oscillations power spectra in young hypertensive subjects. The pourpose of our
study
was
training
in
to
evaluate
mildly
the
mechanism
hypertensive
of
young
the
hypotensive
men
by
effect
analysing
of
physical
cardiovascular
variability. We compared the systolic and diastolic blood pressure (SBP and DBP
respectively), pulse interval (PI), total peripheral vascular resistance (TPR), arm
regional vascular resistance (AVR) and some indices of SBP and PI variability:
the variance of SBP and PI and LF component of the SBP power spectrum before
and after the 3-month period of dynamic physical moderate training.
Controlled
physical
training
was
performed
subjects and age matched healthy subjects.
by
young
mild
hypertensive
715
SUBJECTS AND METHODS.
Subjects
The study was approved by Ethic's Committee On Human Research of the Medical University
of Warsaw. Each subject gave consent to participate in the study. Measurements were performed on
30 untreated mildly hypertensive (HTS) and 18 healthy normotensive male subjects (NTS). The
normotensive subjects were mostly medical students. All participants were strongly motivated and
express
a
desire
to
increase
their
physical
fitness.
Hypertensive
patients
were
interested
in
decreasing the blood pressure by physical training rather than by pharmacological treatment. All
subjects
were
clinically
examined
and
free
from
pulmonary,
renal
and
heart
diseases.
Characteristics of both groups are shown in Table 1.
Pharmacological treatment was discontinued for at least two weeks before the start of the study.
Astrand's submaximal test was used to determine physical fitness by maximal oxygen consumption.
Training
All subjects were instructed on the procedure and obtained detailed explanation how to perform
by themselves individual training.
During
laboratory
measurements
on
cycloergometer
the
subjects
observed
the
changing
workload level and the response of heart rate (HR) to work load. The training consisted in dynamic
aerobic
exercise
at
a
40-50%
of
each
subject
VO2max
.The
values
of
HR
calculated
for
each
individual for 40 - 50% VO2max were established on the cycloergometer in the laboratory and known
to each subject. The subjects performed an exercise 3 times per week for about 1 hour according to
favoured kind of activity (running, cycling, tennis, swimming, volley ball, brisk walking). They
controlled heart rate by themselves to maintain the level of estimated heart rate at 40-50% VO2max.
Procedures
The procedures were always carried out in the same order. Body weight and height were
checked and arterial blood pressure was measured by mercury sphygmomanometer. During testing
electrocardiogram leads (ECG) for heart rate, chest wall electrodes for cardiac output measurements
by impedance cardiography, arm electrods for measurement arm blood flow by impedance method
were attached. The Finapres cuff was put on a finger for continous blood pressure measurement.
Finger arterial blood pressure was recorded by Finapres (Ohmeda, model 2300) at the level of
tricuspid valve, to avoid hydrostatic influences. The method has been validated for power spectral
analysis of arterial pressure variability (30). Stroke volume, cardiac output (CO) and arm muscular
blood flow were recorded with tetrapolar impedance reography (Warsaw Technical University), and
heart rate interval from one lead ECG, telemetry (Fukuda Denshi). All data were synchronously
sampled and recorded continously with sampling freqency 200 Hz and 12-bite resolution for
subsequent off-line analysis. Stroke volume and CO was calculated from the first derivative of the
Table 1. Baseline characteristics of the study groups
Normotensives
Hypertensives
n = 18
n = 30
Age (years)
22.9 ± 0.44
23.0 ± 1.1
p > 0.05
Weight (kg)
79.8 ± 1.95
84.6 ± 2.0
p > 0.05
Height (cm)
180 ± 1.66
181.7 ± 1.7
p > 0.05
BMI
24.7 ± 0.5
26.3 ± 0.8
p > 0.05
716
impedance change, using the Kubicek equation (31). TPR was calculated in TPR units by dividing
mean arterial blood pressure by cardiac output. Arm regional vascular resistance was calculated per
100 ml tissue/min in PRU units. Resting measurements were performed in comfortable sitting
position.
Measurement and assessment of systolic blood pressure variability
The variance of SBP and pulse interval variance were calculated from about 30 sec periods. Pulse
intervals were calculated in miliseconds (ms) from Finapres data by inversion of heart rate values.
The respiratory rate was assessed by impedance method. The spectral analysis was performed
with the program written for the pourpose of this study on segments of 512 consequtive points. By
visual inspection stationary series, free of ectopic beats and artefacts were selected for off-line
analysis. Hanning's window and fast Fourier transform (FFT) computation were used. The low
frequency component of the power spectrum included the power from 0.04 to 0.15 Hz, and the high
frequency component the power spectrum (HFSBP) respectively from 0.15 Hz to 0.25 Hz. The power
of each band was calculated as integral of power spectral density under the curve in the frequency
range. LFSBP and HFSBP were computed in absolute units in mmHg and in normalized units expressed
2
as a percentage of the total power.
Exercise
After completing data collection in the control preexercise period subject rested about 10 min.
Subsequently1 hour exercise of increasing intensity was performed on electric bicycle ergometer
Monark 829E, up to the level of about 40-50% of each subject's VO2max. All parameters were
continously registered during exercise. After exercise the subjects had a break for at least 1 hour.
Thereafter they were submitted to the same sets of measurements as before exercise.
Statistical
methods:
Data
were
assessed
for
normal
distribution
by
the
computation
of
standardized skeweness and standardized kurtosis. Comparisons between NTS and HTS were made
by unpaired t-test or Mann-Whitney test. Within groups differences were evaluated by paired t-test
or Wilcoxon signed rank test for nonnormally distributed data. Values were expressed as mean ±
SE. Linear regression analysis was used to calculate correlations. Statistical significance was
assumed at p < 0.05.
RESULTS
Weight
decreased
and
maximal
oxygen
uptake
increased
in
hypertensive
patients and in healthy control subjects after 3-month dynamic exercise training
(Table 2). At rest the hypertensives as compared to normotensives demonstrated
significantly higher systolic, diastolic blood pressure and TPR, (Table 3). Pulse
interval variance was significantly lower and LFSBP significantly higher in HTS,
comparing to NTS (Table 4).
The hypertensive subjects showed significant decrease in SBP and DBP after
training
period.
In
NTS
decrease
in
SBP
and
DBP
was
insignificant.
No
significant change in cardiac output was observed in either group. TPR decreased
significantly in both groups. AVR decreased slightly yet not significantly. Resting
pulse interval and PI variance increased significantly after training in both groups
(Table 4).
717
Table 2. Effect of exercise training on VO2max, weight and respiratory rate in NTS and HTS
VO2max (ml/kg/min)
Control
After training
Difference:
NTS
HTS
36.34 ± 1.9
35.14 ± 1.63
38.26 ± 1.9
38.33 ± 1.49
-1.92 ± 0.76
95%CI
-3.19 ± 0.68
-3.55 to -0.29
p< 0.01
-4.68 to -1.70
p <0.01
Weight (kg)
Control
79.80 ± 1.95
84.60 ± 2.1
After training
78.80 ± 1.92
83.87 ± 2.0
Difference
1.40 ± 0.30
95%CI
0.78 to 2.04
0.95 ± 2.0
p = 0.01
0.85 to 2.0
p = 0.01
Respiratory
Rate( breath/min)
Control
12.3 ± 0.43
12.60 ± 0.38
After training
12.0 ± 0.54
12.30 ± 0.32
Difference
0.18 ± 0.19
95%CI
0.29 ± 0.21
0.24 to -0.59
p>0.05
-0.14 to 0.72
p>0.05
Control - the values from pre-training period , 95% CI - 95% confidence interval
Table
3.
Effects
of
exercise
training
on
hemodynamic
pattern
in
normotensive(NTS)
and
hypertensive (HTS) subjects.
NTS
HTS
Control:
128.8 ± 4.7
148.0 ± 3.6 *
After training:
120.0 ± 2.6
128.3 ± 1.86
SBP [mmHg]
Difference:
95% CI
DBP [mmHg]Control:
After training:
Difference:
95% CI
8.86 ± 5.0
18.5 to 34.4
19.0 ± 2.9
NS
72 ± 2.9
13.2 to 24.96
68 ± 1.48
76.5 ± 1.4
4.35 ± 2.83
10.75 ± 2.0
-1.53 to 10.23
p<0.001
87.3 ± 2.16 *
NS
6.65 to 14.85
p<0.01
TPR [TPR u.]
1.1 ± 0.09
1.35 ± 0.1 *
After training:
Control:
0.95 ± 0.07
1.06 ± 0.07
Difference:
0.13 ± 0.05
95% CI
0.13 to 0.32
0.28 ± 0.05
p< 0.05
0.17 to 0.39
p < 0.01
AVR [PRU u.]
Control:
16.1 ± 1.30
15.8 ± 2.0
After training:
15.7 ± 0.87
13.1 ± 1.31
Difference:
0.44 ± 2.60
95% CI
-5.1 to 5.97
2.7 ± 1.33
p= 0.07
4.65 to 8.78
p = 0.056
CO [l/min]
Control:
5.07 ± 0.26
After training:
5.39 ± 0.30
5.39 ± 0.37
5.53 ± 0.30
Difference:
-0.32 ± 0.22
-0.15 ± 0.27
95% CI
-0.78 to 0.16
NS
-0.67 to -0.372
NS
p - significance level in respect to changes within the group, * - p < 0.05 in respect to differences
between groups. 95% CI - 95% confidence interval. Abbreviations - see text
718
Table 4. Effects of exercise training on systolic blood pressure oscillations and PI variance in
normotensive (NTS) and hypertensive subjects (HTS)
PI [ msec ]
Control:
After training:
Difference:
NTS
HTS
801 ± 19.5
798 ± 17.4
929 ± 24.3
890 ± 20.4
-128 ± 20.3
95% CI
-169 to -86.1
-92 ± 19
p< 0.001
-131 to -52.4
p< 0.001
PIvar [msec ]
2
Control:
5235 ± 504
After training:
7890 ± 653
6185 ± 947
-3352 ± 699
-2410 ± 678
Difference:
95% CI
-4502 to -1604
3473 ± 475 #
p< 0.001
-4448 to -1305
p <0.001
LF SBP [mmHg ]
2
Control:
14.9 ± 1.8
23.7 ± 2.9 *
After training:
16.8 ± 1.2
15.9 ± 2.1
Difference:
-1.9 ± 2.4
95% CI
-6.8 to 3.0
7.9 ± 2.2
NS
3.4 to 12.3
p < 0.01
LF SBP [ % of TP]
Control:
27.1 ± 2.2
35.8 ± 1.9 #
After training:
30.6 ± 1.7
30.6 ± 2.0
Difference:
-3.5 ± 2.7
95% CI
-8.9 to 1.9
7.9 ± 2.2
NS
3.4 to 12.3
p = 0.028
HF SBP [mmHg ]
2
Control:
4.91 ± 0.58
5.27 ± 0.72
After training:
3.56 ± 0.37
3.80 ± 0.40
Difference:
1.36 ± 2.4
95% CI
-0.16 to 2.87
1.50 ± 0.67
p=0.05
0.12 to 2.87
p = 0.06
HF SBP [ % of TP]
Control:
10.7 ± 1.9
9.30 ± 7.3
After training:
7.36 ± 1.1
9.10 ± 6.0
Difference:
3.34 ± 1.6
95% CI
-0.01 to 6.69
0.19 ± 1.3
NS
-2.53 to 2.9
NS
var. SBP [mmHg ]
2
Control:
63 ± 6.3
65.9 ± 7.3
After training:
59.4 ± 7.4
53.5 ± 6.1
Difference:
3.74 ±7.8
95% CI
-10.09 to 17.3
12.3 ± 5.7
NS
0.65 to 24.0
p = 0.039
p - significance level in respect to changes within the group, * - p < 0.05, # p< 0.01 in respect to
differences between groups. PIvar - PI variance, other descriptions - see text and Table 2
SBP
variance
decreased
significantly
only
in
HTS
subjects
(Table
4).
In
control period LFSBP was higher in HTS compared to NTS at rest (Table 4, Fig.1)
After physical training LFSBP decreased significantly in hypertensive patients to
the value not different from that in normotensive subjects (Table 4, Fig 1).
In HTS a correlation between LFSBP and SBP was positive: r =0.38, p < 0.001,
whereas in NTS a negative: r = - 0.5 p < 0.001 (Fig.2).
719
LF SBP (mmHg2)
30
#
25
NTSt
HTSc
NS
20
15
10
5
0
NTSc
*
HTSt
Fig.1 The effect of physical training on low-frequency component of systolic blood pressure power
spectrum (LFSBP) in normotensives (NTS) and hypertensive subjects (HTS). NTSc, HTSc- the pretraining values of LFSBP for NTS and HTS respectively, NTSt, HTSt - the post-training values of
LFSBP. # - p < 0.01 NTSc vs HTSc,
* - p < 0.01 HTSc vs HTSt.
HYPERTENSIVE SUBJECTS
Log LF SBP
5
r = 0.389
p < 0.001
4
3
2
1
0
120
140
160
180
200
220
SBP mmHg
NORMOTENSIVE SUBJECTS
Log LF SBP
5
r = - 0.523 p< 0.001
4
3
2
1
0
96
116
136
156
176
SBP mmHg
Fig.2 Relationship between the LFSBP
and SBP in hypertensive and normotensive subjects.
720
DISCUSSION
Increased
training
LFSBP
period
are
and
reduced
consistent
PI
variance
with
the
in
hypertensive
hypothesis
that
subjects
in
dysregulation
pre-
of
the
autonomic nervous system plays a role in the pathogenesis of hypertension (3,9).
Magnitude
of
cardiovascular
LF SBP
appears
complications
symptomatic
in
hypertension
of
increased
(28).
The
probability
positive
of
correlation
between LFSBP and SBP in hypertensive subjects may indicate the impairment in
blood
pressure
autonomic
control
in
hypertensives
(Fig.2).
The
negative
correlation between LFSBP and SBP in normotensive subjects suggests a normal
negative feedback between blood pressure and sympathetic modulation of SBP
exerted by baroreceptor reflex (Fig.2).
The
present
study
supports
the
view
that
exercise
trainig
improves
the
impaired pattern of cardiovascular autonomic regulation in hypertensive subjects
(11,12). Decrease in the blood pressure, the systolic blood pressure variability and
in
total
peripheral
vascular
resistance,
as
well
as
increase
in
pulse
interval
duration and pulse interval variability found in the present study represent a
beneficial effects of regular physical exercise on blood pressure regulation in
hypertension.(11-14). The main difference in the response to 3-month training
between
normotensives
and
hypertensives
found
in
the
present
study
is
a
significantly greater decrease in blood pressure and in LFSBP in HTS as compared
to NTS (Tables 3 and 4, Fig.1).
Our study showed for the first time that the decrease in arterial blood pressure
and in TPR in hypertensive subjects submitted to dynamic physical exercise
(Table 3) is associated with a significant decrease in LF component of SBP power
spectrum (Table. 4, Fig.1).
LFSBP correlates with the overall sympathetic activity addressed to vascular
system (24,26). The LFSBP corresponds to Mayer waves or SBP fluctuations with
10-sec periodicity and is related to changing sympathetic tone (23,24). LFSBP is
augmented
posture
during
(24,25),
manuevers
and
is
that
increase
diminished
after
sympathetic
α-adrenergic
activity,
receptors
i.e.
upright
blockade
or
ganglionic blocker trimetaphan (32). Pagani et al. (24) reported that oscillations
in
muscle
sympathetic
nerve
activity
recorded
by
microneurography
were
mirrored by oscillations of SBP. Sympathetic activation was associated with an
increase of LF component of both SBP and muscle sympathetic nerve activity.
Augmented value of LFSBP in resting hypertensive subjects, (Table 4) was
reported also in other studies (25,27). They are consistent with increase in tonic
sympathetic activity found in large mild hypertensive population by use of direct
microneurographic method applied to single sympathetic nerve units (2,4).
Decrease
provides
in
LFSBP
noninvasive
in
HTS
insight
after
into
training
the
is
of
mechanism
special
of
the
interest,
because
reduction
in
it
blood
pressure and TPR produced by regular physical activity in hypertensive subjects.
We sugest that training-induced decrease in LFSBP in HTS depends on reduction of
721
sympathetic nerve activity addressed to resistance arteries. This effect apparently
contributes to decrease in blood pressure and in TPR in HTS. Our suggestion is
in line with other observations made with the use of invasive methods (14).
Decrease in LFSBP in hypertensive patients after physical training is consistent also
with reported decrease in norepinephrine plasma level after physical training in
HTS (14,19,21,22). Reduction in sympathetic drive that follows training appears
more pronounced in patients with essential hypertension than in normotensive
individuals
(18).
Reports
on
the
effects
of
physical
training
on
resting
sympathetic vasoconstrictor nerve output to peripheral vascular bed in healthy
people are not consistent (33). In healthy humans training studies report no
change (34), increase (35) or decrease (36) in resting muscle sympathetic nerve
activity.
Mechanisms
training
in
of
reduced
hypertensive
cardiovascular
response
chemoreceptors
sympathetic
subjects
to
observed
brief
during
are
still
activity
produced
unknown
inactivation
postexercise
by
(6).
by
physical
Attenuation
hyperoxia
hypotension
of
of
arterial
suggests
that
chemoreceptor sympathoexcitatory reflex is reduced following physical exercise
(37). It is to be checked if regular physical training induces sustained attenuation
of the resting chemoreceptor pressor reflex in hypertensive subjects. Augmented
chemoreceptor
reflex
drive
appears
to
contribute
to
mechanisms
of
arterial
hypertension (37-42). Also a facilitation of baroreceptor reflex can be taken under
consideration, as an increased baroreflex sensitivity was reported after physical
exercise in hypertensive subjects (11,12,37).
In hypertensives as compared to healthy men cardiovagal tone is decreased as
suggested by diminished pulse interval variance, a finding consistent with other
reports (7-8). Exercise training tended to reverse and normalize the hypertensionrelated deficits in parasympathetic tone, as PI variance significantly increased
(Table 4).
Although in hypertensive subjects pulse interval variance was lower than in
normotensives the pulse interval duration did not differ significantly.
Physical
training
results
in
increase
in
pulse
interval
duration
and
pulse
interval variance - both in NTS and HTS (Table 4). No significant difference in
the respective responses to physical training between two groups were observed.
We choose a moderate training level, as in recent study (28) only such training
induced augmented parasympathetic cardiovascular modulation, in parallel with
it a tendency to decrease power of LF component of SBP in healthy people. In
contrast, high intensity training (above 75% of VO2max) elicited an increase in
LFSBP
and
shifted
the
neural
autonomic
cardiovascular
profile
from
vagal
to
sympathetic predominance (28), an effect potentially dangerous to hypertensive
patients by increasing probability of the adverse circulatory consequences (3).
Augmentation
in
parasympathetic
activity
with
concomitant
decreasing
sympathetic activity is desirable in hypertensive patients and coronary artery
diseased
patients
(5).
Moreover,
longitudinal
epidemiological
studies
have
shown, that low to moderate physical exercise is most effective in reducing
722
increased blood pressure in hypertensive patients than training at a vigorous
intensity (10, 13,15).
It has been documented in longitudinal studies that lowering blood pressure,
even small, reduces incidence of and mortality from cardiovascular diseases
(1,10, 15). Decreased pulse interval and heart rate interval variability correlates
strongly with future cardiovascular events (5, 8). An increase in systolic blood
pressure variability is known predictor of cardiovascular risk in patients with
blood
pressure
hypertension
elevations
are
of
(44,45).
prognostic
Noninvasive
value
for
the
cardiovascular
cardiovascular
indices
events
in
and
progression to end organ damage (3, 5,9,27,44,45). Recently, it has been shown
significant relation between short term and long term blood pressure 24-hour
variability indexes (45).
Decrease in blood pressure, total peripheral resistance and increase in pulse
interval and PI variance in HTS subjects observed in our study after physical
training are not dissimilar to other reports (11,12,14). A novel finding of possible
clinical
value
is
a
pronounced
reduction
of
LFSBP,
a
noninvasive
marker
of
sympathetic activity after physical training applied in mild hypertensive patients.
In summary we conclude that antihypertensive effects of moderate dynamic
exercise training in mild hypertensive subjects are associated with readjustment
of the autonomic cardiovascular control system which possibly contributes to
beneficial effects of regular physical exercise in hypertension.
Acknowledgements: This study was supported by KBN Grant No 4P0 5D 60 18
REFERENCES
1.
Whelton PK, He J. Blood pressure reduction. In: Hennekens CH, Buring JE, Manson JE, Ridker
PM, eds. Clinical Trials in Cardiovascular Disease. Philadelphia: WB Saunders; 1999.
2.
Greenwood
JP,
Stoker
JB,
Mary
DASG:
Single-unit
sympathetic
discharge:
quantitative
assessment in human hypertensive disease. Circulation 1999;100:1305-1310.
3.
Mancia G, Grassi G, Giannattasio C, Seravalle G: Sympathetic activation in the pathogenesis
of hypertension and progression of organ damage. Hypertension 1999;34:724 -728.
4.
Smith PA, Graham LE, Mackintosh AF, Stoker JB, Mary DASG. Relationship between central
sympathetic activity and stages of human hypertension. AJH 2004;17: 217-222.
5.
Brook
RD,
Julius
S.
Autonomic
imbalance,
hypertension
and
cardiovascular
risk.
AJH
2000;13:112S-122S.
6.
Esler
M.
Mancia
Sympathetic
G,
eds.
activity
Handbook
of
in
experimental
Hypertension.
and
human
Amsterdam,
hypertension.
In:
Netherlands:
Elsevier
Zanchetti
A,
Science
Publishing Co, Inc; 1997;17:117-169.
7.
Guzzetti S, Piccaluga E, Casati R, Cerutti S, Lombardi F, Pagani M, Malliani A. Sympathetic
predominance in essential hypertension: a study employing spectral analysis of heart rate
variability. J Hypertens. 1988; 6:711-717.
8.
Singh JP, Larson MG, Tsuji H, Evans JC, O'Donnell CJ, Levy D. Reduced heart rate variability
and new-onset hypertension. Insights into pathogenesis of hypertension: The Framingham
Heart Study. Hypertension 1998;32:293-297.
723
9.
Pagani M, Lucini D. Autonomic dysregulation in essential hypertension: insight from heart rate
and arterial pressure variability. Auton Neurosci 2001;90:76-82.
10. Fagard RH. The role of exercise in blood pressure control: supportive evidence. J Hypertens
1995;13:1223-1227.
11. Somers VK, Conway J, Johnston J, Sleight P. Effects of endurance training on baroreflex
sensitivity and blood pressure in borderline hypertension. Lancet 1991;337:1363-1368
12. Pagani M, Somers V, Furlan R, Dell'Orto S, Conway J,Baselli G, Cerutti S, Sleight P, and
Malliani A. Changes in autonomic regulation induced by physical training in mild hypertension. Hypertension 1988; 12: 600-610
13. American College of Sports Medicine Position Stand: Physical activity, physical fitness, and
hypertension. Med Sci Sports Exerc 1993; 25: R1-R10 .
14. Nelson L, Jennings G, Esler M, Korner PI. Effect of changing level of physical activity on blood
pressure and hemodynamics in hypertension. Lancet 1986;30:473-476
15. Hagberg
JM,
Park
J-J,
Brown
MD.
The
role
of
exercise
training
in
the
treatment
of
hypertension. An update. Sports Med. 2000;30: 193-206.
16. Sheperd RJ, Balady GJ. Exercise as cardiovascular therapy. Circulation 1999;99:963-972.
17. Arakawa K. Antihypertensive mechanism of exercise. J. Hypertens. 1993;11:223-229.
18. O'Sullivan SE, Bell C. The effects of exercise and training on human cardiovascular reflex
control. J Auton. Nerv. Syst 2000;81:16-24
19. Kinoshita A, Urata H, Tanabe Y, Ikeda M, Tanaka H, Shindo M. What types of hypertensives
respond better to mld exercise therapy? J Hypertens 1988;6(suppl l4): S631-S633.
20. Hagberg JM, Montain SJ, Martin WH. Effect of exercise training in 60-70- year-old persons
with essential hypertension. Am J Cardiol 1989;64: 348-353.
21. Urata, H, Tanabe Y, Kiyonaga A, Ikeda M, Tanaka H, Shindo M. Antihypertensive and volume
depleting effects of mild exercise on essential hypertension. Hypertension 1987; 9: 245-252.
22. Duncan JJ, Farr JE, Upton SJ, Hagan RD, Oglesby ME, Blair SN. The effect of aerobic exercise
on plasma catecholamine and blood pressure in patients with mild essential hypertension. JAMA
1985, 254: 2609-2613.
23. Malliani A, Pagani M, Lombardi F, Cerutti S. Cardiovascular neural regulation explored in the
frequency domain. Circulation 1991; 84:482-492
24. Pagani M, Montano N, Porta A, Malliani A, Abboud FM, Birkett C, Somers VK. Relationship
between spectral components of cardiovascular variabilities and direct measures of muscle
sympathetic nerve activity in humans. Circulation 1997; 95:1441-1448.
25. Lucini
D,
Mela
GS,
Malliani
A,
Pagani
M.
Impairment
in
cardiac
autonomic
regulation
preceding arterial hypertension in humans: insights from spectral analysis of beat-by-beat
cardiovascular variability. Circulation 2002; 106:2673-2679.
26. Pagani
M,
Rimoldi
O,
and
Malliani
A.
Low-frequency
components
of
cardiovascular
variabilities as markers of sympathetic modulation. Trends Pharmacol Sci 1992; 13: 50-54.
27. Siche JP, Tremel F, Comparat V, de Gaudemaris R, Mallion JM. Examination of variability in
arterial blood pressure at rest using spectral analysis in hypertensive patients. J Hypertens. 1995
Jan;13:147-53
28. Iellamo F, Legramante JM, Pigozzi F, Spataro A, Norbiato G, Lucini D, Pagani M. Conversion
from vagal to sympathetic predominance with strenous training in high- performance world
class athletes. Circulation 2002;105:2719-2724.
29. Taylor AC, McCartney N, Kamath MV, Wiley RL. Isometric training lowers resting blood
pressure and modulates autonomic control. Med. Sci Sports Exer 2003;35:251-256.
30. Omboni S, Parati G, Frattola A, Mutti E, Di Rienzo M, Castiglioni P , Mancia G. Spectral and
seqence analysis of finger blood pressure variability. Comparison with analysis of intraarterial
recordings. Hypertension 1993;22:26-33.
724
31. Kubicek WG, Paterson RP, Witsoe DA. Impedance cardiography as a noninvasive method of
monitoring cardiac function and other parameters of the cardiovascular system. Ann NY Acad
Sci 1970 (b); 170:724-732.
32. Diedrich A, Jordan J, Tank J, Shannon JR, Robertson R, Luft FC, Robertson D, Biaggioni I. The
sympathetic nervous system in hypertension: asssessment by blood pressure variability and
ganglionic blockade. J Hypertens 2003;21:1677-1686.
33. Narkiewicz K, Somers VK. Endurance training in mild hypertension - effects on ambulatory
blood pressure and neural circulatory control. Blood Press Monit 1997;2:229-235.
34. Ray C. Sympathetic adaptations to one legged training. J Appl Physiol 1999; 86(5): 1538- 1587.
35. Ng, A. V., R. Callister, D. G. Johnson, and D. R. Seals. Endurance exercise training is associated
with
elevated
basal
sympathetic
nerve
activity
in
healthy
older
humans.
J
Appl.
Physiol.
1994;77: 1366-1374.
36. Grassi, G., G. Seravalle, D. A. Calhoun, and G. Mancia. Physical training and baroreceptor
control of sympathetic nerve activity in humans. Hypertension 23: 294-301, 1994.
37. Izdebska E, Cybulska I, Sawicki M, Izdebski J, Trzebski A. Postexercise decrease in arterial
blood pressure, total peripheral resistance and in circulatory responses to brief hyperoxia in
subjects with mild essential hypertension. J Hum Hypertens. 1998 Dec; 12: 855-860.
38. Trzebski
A.
Arterial
chemoreceptor
reflex
and
hypertension.
Hypertension.
1992
Jun;19
the
arterial
(6 Pt 1):562-566.
39. Trzebski
A,
Tafil
M,
Zoltowski
M,
Przybylski
J.
Increased
sensitivity
of
chemoreceptor drive in young men with mild hypertension. Cardiovasc Res.1982;16:163- 172.
40. Izdebska E, Izdebski J, Trzebski A. Hemodynamic responses to brief hyperoxia in healthy and
in mild hypertensive human subjects in rest and during dynamic exercise. J Physiol Pharmacol
1996; 47: 243-256.
41. Tafil-Klawe M, Trzebski A, Klawe J, Palko T. Augmented chemoreceptor reflex tonic drive in
early
human
hypertension
and
in
normotensive
subjects
with
family
background
of
Rutkowski
B,
hypertension. Acta Physiol Pol. 1985;36:51-8.
42. Hering
D,
Zdrojewski
Z,
Kara
T,
Król
E,
Somers
VK,
Wy¿ykowski
B,
Narkiewicz K. Tonic chemoreflex activation contributes to the elevated muscle sympathetic
nerve activity in patients with chronic renal failure. J Hypertens 2004;22 (Suppl.2):S80 P1.212
43. Izdebska E, Cybulska I, Izdebski J, Makowiecka-Cieœla M, Szczypaczewska M, Borówka E,
Trzebski
A.
Effects
of
moderate
exercise
on
postexercise
baroreflex
sensitivity
in
mild
hypertension. J Hypertens 2003; 21(suppl4): S256.
44. Parati G, Ulian L, Santucciu C, Omboni S, Mancia G. Blood pressure variability, cardiovascular risk and antihypertensive treatment. J Hypertens Suppl. 1995 Dec;13:S27-34.
45. Ragot S, Herpin D, Siche JP, Poncelet P, Mallion JM. Relationship between short-term and long
term blood pressure variabilities in essential hypertensives. J Human Hypertens 2001;15:41-48.
Received:
August 5, 2004
Accepted:
November 16, 2004
Author's address: Dr Ewa Izdebska, Department of Experimental and Clinical Physiology, The
Medical University of Warsaw, 00-927 Warsaw, Poland.