Journal of Human Hypertension (2007) 21, 486–493
& 2007 Nature Publishing Group All rights reserved 0950-9240/07 $30.00
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ORIGINAL ARTICLE
Beta-blockers do not impair the
cardiovascular benefits of endurance
training in hypertensives
TH Westhoff1,4, N Franke1,4, S Schmidt1, K Vallbracht-Israng2, W Zidek1, F Dimeo3,5
and M van der Giet1,5
1
Medizinische Klinik IV – Nephrology, Charité – Campus Benjamin Franklin, Berlin, Germany; 2Department
of Cardiology, Charité – Campus Virchow Klinikum, Berlin, Germany and 3Medizinische Klinik III – Section of
Sports Medicine, Charité – Campus Benjamin Franklin, Berlin, Germany
Aerobic physical exercise is broadly recommended as
a helpful adjunct to obtain blood pressure control in
hypertension. Beta-blockade interacts with heart rate,
sympathetic tone, maximal workload and local lactate
production. In the present randomized-controlled study,
we compared the cardiovascular effects of an endurance
training programme in elderly hypertensives with or
without beta-blockers and developed a first approach to
determine a lactate-based training heart rate in presence
of beta-blockade. Fifty-two patients (23 with beta-blocker, 29 without beta-blocker) X60 years with systolic 24-h
ambulatory blood pressure (ABP) X140 mm Hg and/or
antihypertensive treatment were randomly assigned to
sedentary activity or a heart-rate controlled 12-week
treadmill exercise programme (lactate 2.0 mmol/l). In the
exercise group, the training significantly decreased
systolic and diastolic 24-h ABP, blood pressure on
exertion (100 W) and increased endothelium-dependent
vasodilation (flow-mediated vasodilation, FMD) and
physical performance both in the presence and absence
of beta-blockade (Po0.05 each). The extent of ABP
reduction did not significantly differ in the presence
or absence of beta-blockade (D systolic ABP 10.6710.5
vs 10.678.8 mm Hg, D diastolic ABP 5.778.6 vs
5.874.0 mm Hg). Mean training heart rate was significantly lower in the patients on beta-blockers (97.277.7
vs 118.377.5/min, Po0.001). Lactate-based aerobic
endurance training evokes comparable cardiovascular
benefits in the presence and absence of beta-blockade
including a marked improvement of endothelial function. In the present study, target training heart rate with
beta-blockers is about 18% lower than without.
Journal of Human Hypertension (2007) 21, 486–493.
doi:10.1038/sj.jhh.1002173; published online 1 March 2007
Keywords: exercise; blood pressure; endothelial function; beta-blocker
Introduction
Aerobic physical exercise is recommended as basic
lifestyle modification in the treatment of arterial
hypertension.1,2 Whereas cardiovascular training
can induce systolic and diastolic blood pressure
reductions of approximately 3–4 mm Hg in normotensives, this phenomenon is even more pronounced in hypertensives.3 Shear stress – as induced by
physical exercise – is a potent stimulus on endothelial cells for an increase in nitrous oxide (NO)production leading to improved endothelial function and reduced vascular resistance.4 The extent of
Correspondence: Dr TH Westhoff, Medizinische Klinik IV –
Nephrology, Charité – Campus Benjamin Franklin, Hindenburgamm 30, 12200 Berlin, Germany.
E-mail: [email protected]
Sources of financial support: None.
4
These authors contributed equally to this work.
5
These authors contributed equally to this work.
Received 24 August 2006; revised 17 December 2006; accepted 20
January 2007; published online 1 March 2007
cardiovascular benefits, however, depends strictly
on the concept of the endurance programme. Guidelines recommend modest levels of aerobic exercise
on a regular basis, such as walking, jogging or
swimming for 30–45 min, 3–4 times a week.1,5,6
Training should be performed at 40–60% of maximum O2 uptake.7 Physical exercise beyond 60% of
maximal O2 consumption does not lead to further
reductions of blood pressure and might even
increase blood pressure in hypertensives.8,9 The
intensity of exercise is generally monitored by heart
rate. Adequate training heart rate can be assessed by
determination of the anaerobic threshold using
ventilatory parameters or lactate.10,11 This procedure, however, is too time-consuming and expensive to be used in general practice. Therefore, target
heart rates are usually determined on the basis of
empirical experiences. The percentage of maximal
heart rate is the most widely accepted parameter for
the description of training intensities. The American
College of Sports Medicine and the American
Heart Association recommend training intensities
Endurance training and beta-blockade
TH Westhoff et al
between 5512 and 65–85% of maximal heart rate.13
As beta-blockers reduce heart rate both in rest and
under exertion, target heart rates might differ from
general recommendations.14 Furthermore, acute
treatment with beta-blocking drugs modifies local
muscular metabolic properties and impairs endurance exercise capacity resulting in an increase in
perceived exertion, lower VO2max and lower work
rate, whereas the influence of chronical administration of beta-blockers is discussed controversially.15 It
has been shown that non-selective beta-blockers can
increase lactate levels during exercise, for example,
through b2-associated peripheral vasoconstriction.16
Furthermore, metoprolol – as a selective b1-selective
antagonist – induces a left-shift of both lactate and
ventilatory aerobic threshold.17 In a small study of
10 young healthy men, a small dose of bisoprolol
given for 2 weeks reduced the percentage of
maximal heart rate at the aerobic and anaerobic
threshold.18 Thus, it may be speculated that cardiovascular benefits of exercise at a defined heart rate
differ in the absence and presence of beta-blockade.
The aim of the present study is to determine the
differential effects of lactate-based exercise prescription on hypertensives with or without chronic betablockade.
In the present study, we compared the cardiovascular effects of a heart-rate controlled 12-week
endurance training programme between elderly
hypertensives with or without beta-blockers and
a sedentary control group. We developed a first
approach to determine a lactate-based training heart
rate in the presence of beta-blockade.
487
Methods
Study population
Patients were recruited from the hypertension outpatient clinic of our university hospital and by press
announcement to assess cardiovascular benefits of
exercise training on treated hypertensives. Inclusion
criteria for the current study were systolic ambulatory blood pressure (ABP) X140 mm Hg and/or
current antihypertensive treatment, age X60 years.
Before the exercise programme, cardiac function
was examined by electrocardiogram (ECG) and
echocardiogram. Exclusion criteria were continuous
engagement in physical exercise training 460 min/
week in the past 12 weeks before inclusion in the
study, symptomatic peripheral arterial occlusive
disease, aortic insufficiency or stenosis 4stage I,
hypertrophic obstructive cardiomyopathy (HOCM),
congestive heart failure (4NYHA II (New York
Heart Association, grade II)), uncontrolled cardiac
arrhythmia with hemodynamic relevance, systolic
office BPX180 mm Hg, signs of acute ischemia in
exercise electrocardiography, change of antihypertensive medication in the past 6 weeks before
inclusion or during the follow-up period. Further
indication of hypertension-associated target-organ
damage was not regarded as exclusion criteria.
According to these criteria, 52 patients (26 male,
26 female) were enrolled to the study. Patients’
characteristics including concomitant diseases are
presented in Table 1. All patients were treated with
at least one antihypertensive drug. Irrespective of
presence or absence of beta-blockade, patients were
Table 1 Patients’ characteristics (age and number of antihypertensive drugs presented as mean7s.d.)
Exercise
Female
Male
Age (years)
Concomitant diseases
Diabetes mellitus
Hyperlipidemia
Smoking
Family history of
cardiovascular disease
Cardiac endorgan damage
Antihypertensive medication
Number of
antihypertensive drugs
ACE inhibitors
Angiotensin receptor
blockers
Calcium-channel blockers
Diuretics
Alpha blockers
Clonidine
Control
All (n ¼ 25)
Betablockade
(n ¼ 9)
No betablockade
(n ¼ 16)
All (n ¼ 27)
Betablockade
(n ¼ 14)
No betablockade
(n ¼ 13)
12 (48%)
13 (52%)
67.874.7
6 (67%)
3 (33%)
66.473.4
6 (38%)
10 (63%)
68.575.2
14 (52%)
13 (48%)
68.975.2
6 (43%)
8 (57%)
68.975.2
8 (62%)
5 (38%)
69.075.3
4
13
3
12
(16%)
(52%)
(12%)
(48%)
0
5
3
6
(0%)
(56%)
(33%)
(67%)
4
8
0
6
(25%)
(50%)
(0%)
(38%)
5
11
2
13
(19%)
(41%)
(7%)
(48%)
4
7
1
7
(29%)
(50%)
(7%)
(50%)
1
4
1
6
(8%)
(31%)
(7%)
(46%)
14 (56%)
3 (33%)
9 (56%)
13 (48%)
6 (43%)
7 (54%)
2.471.4
2.971.4
2.171.3
3.271.4
3.971.0
2.271.2
8 (32%)
11 (44%)
4 (44%)
4 (44%)
4 (25%)
7 (44%)
9 (33%)
12 (44%)
5 (36%)
8 (57%)
4 (31%)
4 (31%)
11
13
2
2
3
6
0
1
8
7
2
1
16
17
4
1
(44%)
(52%)
(8%)
(8%)
(33%)
(67%)
(0%)
(11%)
(50%)
(44%)
(13%)
(6%)
(59%)
(63%)
(15%)
(4%)
11
12
2
1
(79%)
(86%)
(14%)
(7%)
5
5
2
0
(38%)
(38%)
(15%)
(0%)
Abbreviation: ACE, angiotensin-converting enzyme.
Journal of Human Hypertension
Endurance training and beta-blockade
TH Westhoff et al
488
randomized to exercise or control group. Twentyfive patients were randomised to the exercise group,
27 were randomized to the control group. Nine
patients in the exercise and 14 patients in the
control group were on beta-blockers. In the exercise
group, patients were on metoprolol, bisoprolol or
atenolol. In the control group, two patients were on
carvedilol, one patient on nebivolol and the other
patients were on metoprolol, bisoprolol and atenolol
as well. There were no patients on negative chronotropic calcium-channel blockers such as verapamil
or diltiazem. Mean number of antihypertensive
drugs and pattern of antihypertensive medication
is presented in Table 1 for exercise and control
group. The pre-existing antihypertensive medication remained unchanged throughout the study.
Written informed consent was obtained from all
participants before inclusion in the study. The study
was approved by the local ethics committee at the
Charité Berlin.
progressively increased to 30, 32 and 36 min and
carried out without interruption. Training intensity
corresponded to the speed necessary to reach a
lactate concentration of 2.070.5 mmol/l in capillary
blood. Heart rate during training was controlled by
a heart-rate monitor (Polar Sport Tester, Kempele,
Finland); blood pressure was measured according
to Riva-Rocci every 5 min with the proband still
walking; lactate concentration was controlled every
fifth training day. As lactate concentration sank
below 1.8 mmol/l or increased beyond 2.2 mmol/l,
target heart rate was adapted until target levels
were reached. If exercise heart rate decreased by
more than 5/min as a result of training adaptation,
treadmill speed was increased by 0.5 km/h or
elevation was increased by 3% to maintain training
intensity. We have previously shown that this
training protocol leads to a substantial increase
of physical performance in short time.20 During
training, patients were continuously supervised by
a physician. Patients in the control group did not
participate in a structured exercise programme.
Protocol
Assessment of physical performance and 24-h ABP
monitoring were performed before and after the
observation period. Assessment of physical performance was carried out by a treadmill stress test
using a modified Bruce protocol (begin with 3 km/h,
increase of speed by 1.4 km/h after 3 min, thereafter
increase of elevation by 3% at constant speed) under
continuous ECG monitoring.19 In this protocol, each
workload corresponds to an increase of 25 W for
a patient of 75 kg weight. Lactate concentration in
capillary blood was determined at the end of each
workload and lactate thresholds were determined
according to Kindermann et al.11
Twenty-four-hour ABP monitoring was performed
using Spacelabs 90207 monitors (Spacelabs, Redmond, WA, USA). As sports affect night-time
blood pressure (BP) values only marginally and
several probands denied to wear their devices at
night because of the sleep-disturbances, only daytime (0600–2200) values are presented. There was
one measurement before and after the observation
period. Intervals between single measurements were
set to be 20 min. The follow-up BP and vascular
measurements of the training group were conducted
within 2 days after the last training session.
The training programme, consisting of walking on
a treadmill according to an interval-training pattern,
was carried out three times a week for 12 weeks. If
patients missed a training session, the programme
was prolonged until they performed 36 workouts.
The initial duration of training sessions was 30 min.
During the first week, training consisted of five
workloads of 3 min; between workloads, patients
walked with half-speed for 3 min. Exercise duration
was gradually increased to 4 5 min/day in the
second week, 3 8 min/day in the third, 3 10 min/
day in the fourth and 2 15 min/day in the fifth
week. In the sixth and further weeks, exercise was
Journal of Human Hypertension
Assessment of endothelial function by flow-mediated
dilation
Endothelial function was assessed in the brachial
artery as reported previously.21,22 By means of highresolution ultrasound, diameter changes in response
to reactive hyperaemia (flow-mediated vasodilation,
FMD) and glyceroltrinitrate (GTN), were measured,
according to standard protocols.22–25 Accuracy and
reproducibility of the method had been documented
previously.21,22 Flow-mediated vasodilation in response to reactive hyperaemia (FMD) represents
endothelium-dependent vasoreactivity, whereas
vasodilation in response to GTN indicates smooth
muscle-cell function and is independent of endothelial function.23 The brachial artery was examined by
two-dimensional ultrasound images, with a 10-MHz
linear array transducer and a standard 128XP/
10c-system (Acuson, Mountain View, CA, USA).
The transducer was positioned proximal to the
elbow to obtain a longitudinal picture of the brachial
artery. Diameters were measured by a computerised
edge-detection programme (Cardiovascular Imaging
Software, Information-Integrity, Boston, MA, USA);
the images were acquired ECG-triggered at enddiastole throughout the study.
A resting scan was recorded for 2 min. A pneumatic tourniquet, placed distal of the subject’s
elbow, was then inflated to a pressure of 300 mm
Hg for 3 min. The release immediately induces
increased blood flow in the subject’s forearm for a
few seconds, which represents the stimulus for
endothelium-dependent vasodilation. A break of
10 min with the patient continuously staying in a
supine position was required before the scan for
endothelium-independent vasodilation was started.
After a resting scan of 2 min, 400 mg GTN was
administered sublingually; the scan was completed
Endurance training and beta-blockade
TH Westhoff et al
489
5 min after application. The same experienced
person performed all of the scans. The computerassisted calculation of vessel diameters was
conducted in a blinded manner as reported
previously.21,22 FMD represents the percentage of
diameter increase caused by shear stress compared
with baseline. The nitrous oxide (NO)-independent
dilation represents the percentage of diameter
increase induced by GTN compared with baseline.
Statistical analysis
Results are presented as mean7s.d. Number of
antihypertensive drugs in each group is presented
as median and range. Comparison of systolic ABP,
diastolic ABP, BP on exertion, FMD, GTN and BMI
(body mass index) at baseline and comparison of the
baseline-adjusted change of these parameters were
performed using an analysis of variance (ANOVA).
Lactate curves of initial treadmill stress tests
(Figure 1a) were constructed using a third-order
polynomial regression. Po0.05 was regarded to be
statistically significant.
Results
Exercise and control groups were homogeneous
for age and number of antihypertensive drugs as
presented in Table 1 (P40.05 each). At the initial
examination, diastolic ABP was slightly but signifi-
Figure 1 Effect of beta-blockade on baseline treadmill stress tests. (a, b) Lactate levels (mmol/l) and average lactate curve (polynomial
third-order regression), (c, d) physical performance (W), (e, f) perceived exertion according to Borg rating scale (1–20) in dependence of
heart rate in absence or presence of beta-blockade. Data derived from baseline stress tests of training and control group.
Journal of Human Hypertension
Endurance training and beta-blockade
TH Westhoff et al
490
Table 2 Cardiovascular effects of exercise
Exercise group (n ¼ 25)
Systolic ABP (mm Hg)
Diastolic ABP (mm Hg)
Systolic BP at 100 W
(mm Hg)
Diastolic BP at 100 W
(mm Hg)
Endothelium-dependent
vasodilation (%)
Endotheliumindependent
vasodilation (%)
BMI (kg/m2)
Control (n ¼ 27)
Exercise vs control
Baseline
Follow-up
Delta
Baseline
Follow-up
Delta
Baseline
(P)
Delta
(P)
141.7713.5
80.278.4
194.3726.9
131.179.4
74.477.5
170.0723.1
10.6710.5
5.875.9
24.3726.6
137.9711.1
75.377.1
194.6726.4
138.2713.5
74.778.4
187.5723.8
0.379.3
0.675.4
7.1721.8
0.28
0.03
0.35
o0.01
o0.01
0.07
76.978.4
67.176.2
9.877.0
74.6715.6
70.4711.0
4.278.2
0.10
0.04
5.571.7
7.972.9
2.472.2
6.172.3
6.372.4
0.273.1
0.98
o0.01
13.076.7
12.876.3
0.275.0
10.175.7
9.373.9
1.275.3
0.58
0.48
27.774.4
27.574.4
0.270.7
30.174.4
30.374.6
0.370.9
0.07
0.07
Abbreviations: ABP, ambulatory blood pressure; BP, blood pressure; BMI, body mass index; NS, nonsignificant.
Delta, change of parameter in the observation period; data presented as mean7s.d.; Po0.05 was regarded significant.
Table 3 Cardiovascular effects of exercise with and without beta-blockade
Patients on beta blockers (n ¼ 9)
Systolic ABP (mm Hg)
Diastolic ABP (mm Hg)
Systolic BP at 100 W
(mm Hg)
Diastolic BP at 100 W
(mm Hg)
Endothelium-dependent
vasodilation (%)
Endotheliumindependent
vasodilation (%)
BMI (kg/m2)
Performance at 2 mmol/l
lactate (W)
Performance at 3 mmol/l
lactate (W)
Patients without beta blockers (n ¼ 16)
Beta blockade vs no
beta blockade
Baseline
Follow-up
Delta
Baseline
Follow-up
Delta
Baseline
(P)
Delta
(P)
140.4719.9
78.3711.3
195.0729.5
129.9710.3
72.775.2
153.3719.7
10.6713.5
5.778.6
41.7731.3
142.478.9
81.276.4
194.0726.9
131.879.1
75.378.5
176.7721.4
10.678.8
5.874.0
17.3721.9
0.74
0.43
0.94
1.0
0.94
0.06
80.8710.2
69.272.0
11.7710.3
75.377.4
66.377.2
9.075.4
0.18
0.44
5.871.9
8.972.3
3.172.1
5.371.6
7.373.2
1.972.2
0.53
0.20
14.077.8
13.376.4
0.675.6
12.57 6.2
12.676.4
0.174.8
0.61
0.75
25.474.9
77.1744.7
25.274.7
141.5733.2
0.270.3
64.4754.1
28.873.8
104.6729.6
28.773.9
152.6729.9
0.270.8
48.0728.3
0.07
0.08
0.99
0.34
126.9750.2
160.6736.0
47.8752.0
139.7728.4
181.3733.5
41.6722.2
0.43
0.72
Abbreviations: ABP, ambulatory blood pressure; BP, blood pressure; BMI, body mass index; NS, nonsignificant.
Delta, change of parameter in the observation period; data presented as mean7s.d., Po0.05 was regarded significant.
cantly lower in the control than in the exercise
group (75.377.1 vs 80.278.4, P ¼ 0.03; Table 2).
There was no significant difference for baseline
systolic ABP, systolic BP at 100-W activity, diastolic
BP at 100-W activity, endothelium-dependent vasodilation, endothelium-independent vasodilation
and BMI in exercise and control group (P40.05
each; Table 2). Furthermore, there were no significant differences between baseline physical performance at 2 mmol/l lactate (94.3737.6 vs 93.2748.0
W, P ¼ 0.94) and at 3 mmol/l lactate (135.3736.8 vs
125.4750.9 W, P ¼ 0.50). Within the exercise group,
the beta-blocker- and non-beta-blocker subgroups
were homogeneous for age, number of antihyperJournal of Human Hypertension
tensive drugs, ABP values, BP at exertion, endothelium-dependent and -independent vasodilation,
BMI and physical performance as well (P40.05
each, Table 3).
All patients completed the study. Comparison of
the changes of BP in exercise and control group
showed that the exercise programme resulted in
a significant decrease of systolic and diastolic ABP
of 10.6710.5 and 5.875.9 mm Hg, respectively
(Po0.01, Table 2). Systolic BP on exertion (100 W)
tended to be largely decreased by 24.3726.6 mm Hg
(P ¼ 0.07, Table 2) and diastolic BP on exertion (100
W) was significantly diminished by 9.877.0 mm Hg
(P ¼ 0.04, Table 2) compared with the changes in
Endurance training and beta-blockade
TH Westhoff et al
491
the control group. The decrease of BP cannot be
ascribed to a reduction of body weight, as BMI
was not significantly altered (Table 2). Endotheliumdependent vasodilation, however, significantly
improved from 5.571.7 to 7.972.9% (Po0.01). In
contrast to endothelium-dependent vasodilation,
endothelium-independent vasodilation as induced
by application of GTN was not significantly changed
(P40.05, Table 2).
At the initial treadmill stress test, the average
lactate curve of the beta-blocker patients of the
whole study population shows a lower slope compared with the non-beta-blocker patients. Furthermore, there is a left-shift indicating that higher
lactate values were reached at lower heart rates
(Figure 1a and b). Physical performance and perceived exertion were higher at lower heart rates as
well (Figure 1c–f). In the exercise group, the betablocker patients tended to show lower physical
performance at lactate concentrations of 2 mmol/l
(P ¼ 0.08, Table 3). Both in the beta-blocker and nonbeta-blocker patients, the exercise training evoked
significant reductions of systolic ABP, systolic BP
on exertion and diastolic BP on exertion (Po0.05
each, Table 3). FMD was significantly increased in
both groups (Po0.05, Table 3), whereas GTN was
not significantly altered (P40.05, Table 3). Diastolic
ABP was significantly reduced in the non-betablocker group (Po0.01, Table 3) and tended to be
lower in the beta-blocker group without reaching
significance (P ¼ 0.08, Table 3). The extent of BP
reduction and improvement of endothelial function did not significantly differ between beta-blocker
and non-beta-blocker patients (P40.05 each,
Table 3). Furthermore, there was no significant
impact of the different beta-blocking substances on
the decrease of systolic BP (P40.05). Physical
performance was increased both in the beta-blocker
and non-beta-blocker groups as indicated by the
right-shift of average lactate curves (Figure 2a and
b), whereas the lactate curve remained unchanged
in the control group (Figure 2c). Performance at
2 and 3 mmol/l lactate improved significantly
with and without beta-blockade (Po0.05 each,
Table 3). There was no significant difference of
improvement of performance at these levels between
beta-blocker and non-beta-blocker patients (P40.05,
Table 3).
Heart rate was measured every 5 min during a
training session. Calculated for the 12 weeks of
exercise, mean training heart rate was 97.277.7/min
in the presence of beta-blockade and vs 118.377.5/
min in the absence of beta-blockade. This difference
was highly significant (Po0.001). Mean heart rate at
rest was 68.277.5/min in the beta-blocker group
and 84.979.4/min in the non-beta-blocker group
(Po0.001). Lactate was measured every fifth training session. Mean lactate concentration did not
differ significantly in the beta-blocker and in the
non-beta-blocker group (1.970.4 vs 2.170.5 mmol/
l, P40.05).
Figure 2 Effect of exercise training on lactate curves in absence
and presence of beta-blockade. Data derived from treadmill stress
tests before and after the training programme from patients with
(a) and without (b) beta-blockers. Lactate levels are presented in
mmol/l, lactate curves are constructed by polynomial third-order
regression and (c) patients of the control group at baseline and
follow-up.
Discussion
The present work constitutes the first randomized,
controlled trial on the differential effects of a lactatebased cardiovascular exercise training on BP and
vascular function in the absence and presence of
Journal of Human Hypertension
Endurance training and beta-blockade
TH Westhoff et al
492
beta-blockade. Our data provide first insight into
lactate-based assessment of training heart rates for
hypertensives with beta-blockers.
The 12-week exercise programme led to a marked
improvement of physical performance as represented by the right shift of the lactate curve. The
American College of Sports Medicine criticised that
in most studies on endurance training, BP was not
measured by a blinded observer or an automated
device and emphasised the need for studies using
24-h ABP monitoring.26 We complied with this
recommendation and our data objectively present a
significant improvement of daytime ABP. Furthermore, the exercise programme led to a significant
decrease of blood pressure on exertion. A recent
meta-analysis, which involves 72 trials on exercise
training including 30 hypertensive study groups
describes an average decrease of resting BP and
daytime ABP of 3.0/2.4 and 3.3/3.5 mm Hg, respectively. The reduction of resting BP was more
pronounced in the hypertensive study groups
(6.9/4.9 mm Hg) than in others (1.9/1.6 mm
Hg).3 Compared with these data, our results reveal
even higher reductions of BP, indicating an efficient
training concept. As reflected by the increase of
FMD, the decrease of BP is associated with an
improvement of endothelial function. The lacking
increase of vasodilation to GTN shows that the
improvement of endothelium-dependent vasodilation was not based on an alteration of the mechanical dilatory properties of the artery. As BMI values
remained unchanged during the observation period,
the reduction of BP cannot be attributed to a loss of
body weight.
Beta-blockers are known to reduce heart rate by
10–20% both in rest and under exertion.14 The drug
lowers the sympathoadrenergic discharge to the
heart and circulation, particularly in states of
elevated sympathetic tone. In healthy subjects,
beta-blockade leads to a decrease of stroke volume,
cardiac output and maximum aerobic performance
capacity, whereas the arteriovenous oxygen difference increases.27 These effects are shared by all
types of beta-blockers.28 Our data show that chronic
beta-blockade induces a left-shift of physical performance, lactate-levels and perceived exertion in
dependence of heart rate in hypertensives. The
training-induced cardiovascular benefits, however,
are not diminished by beta-blockade. Endotheliumdependent vasodilation can be elicited by application of b2-mimetic drugs (Zitat: Wilkinson et al.29).
In the exercise group, all patients with beta-blockade were on b1-selective drugs. These drugs are
supposed to show no interaction with endotheliumdependent vasodilation. As the exercise-induced
improvement of endothelium-dependent vasodilation may be of crucial relevance for the BP
reduction, this might contribute to the explanation
of the present findings.
Systolic and diastolic ABP decrease by an almost
identical extent in beta-blocker and non-beta-blocker
Journal of Human Hypertension
patients. Endothelium-dependent vasodilation is
improved in both groups as well. The reduction
of BP on exertion even tends to be higher in
the presence of beta-blockade. The difference only
slightly fails to be significant for systolic values.
Thus, it may be summarised that beta-blockers
do not constitute a drawback for an efficient cardiovascular endurance training.
Regular physical exercise is a helpful adjunct to
control BP even in old hypertensives. Our findings
show that exercise can be recommended to patients
with beta-blockers as well. Both the reduction of BP
and the improvement of endothelial function
decrease cardiovascular risk. In order to avoid potentially harmful BP peaks or coronary events under
exertion, stress ECG is recommended before initiation of training in patients at high risk of coronary
artery disease or with high resting blood pressure.
How to determine the optimum training heart rate
in the presence of beta-blockade still remains the
question. In the present study, an average lactatelevel of about 2 mmol/l corresponded to a training
heart rate of about 97/min at a mean patients’ age of
66 years. This heart rate was 18% lower than in
the non-beta-blocker group with patients of comparable age. It has to be kept in mind that the study
population reviewed various types and doses of betablockers. Therefore, this finding has to be regarded
as a first rough estimation of target heart rate for
cardiovascular endurance training in the presence of
beta-blockade. In order to find out whether this heart
rate is the optimum training heart rate, further
studies are required, comparing beta-blocker patients
who perform exercise trainings at different target
lactate levels with identical doses of beta-blocking
agents. The following table summarises what the
present study adds to our knowledge on the effects
of endurance training in hypertensives.
Summary of the findings of the present study
What is known about endurance training of hypertensives and
beta-blockade
K Depending on the concept of the training program, aerobic
endurance training can lead to a substantial decrease of blood
pressure in hypertensives.
K Percentage of maximal heart rate is the most widely accepted
parameter for the prescription of training intensities.
K Acute treatment with beta-blocking drugs modifies local
muscular metabolic properties and impairs endurance
exercise capacity resulting in an increase in perceived
exertion, lower VO2max and lower work rate, whereas the
influence of chronical administration of beta-blockers is
discussed controversially.
What this study adds to this knowledge
Lactate-based aerobic endurance training evokes comparable
cardiovascular benefits in presence and absence of betablockade and beta-blockade does not attenuate the exerciseinduced improvement of endothelial function.
K Chronic application of beta-blockers induces a left-shift of
physical performance, lactate-levels, and perceived exertion
in dependence of heart rate.
K In the present study target training heart rate with betablockers is about 18% lower than without.
K
Endurance training and beta-blockade
TH Westhoff et al
493
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