Download Efficacy and position of endurance training as a non-drug

Journal of Human Hypertension (1997) 11, 651–655
 1997 Stockton Press. All rights reserved 0950-9240/97 $12.00
ORIGINAL ARTICLE
Efficacy and position of endurance
training as a non-drug therapy in the
treatment of arterial hypertension
RG Ketelhut 1, IW Franz2 and J Scholze 1
1
Medizinische Poliklinik, Ambulante Spezialmedizin, Universitätsklinikum Charité, Berlin; 2Rehaklinik
Wehrawald der BfA, Todtmoos, Germany
Regular conditioning has been well documented to exert
a beneficial effect on cardiovascular risk factors and to
improve overall cardiovascular health and to reduce the
incidence of coronary disease. There are conflicting
results concerning the effect of physical exercise on
blood pressure (BP) in hypertensive patients and its
importance in the treatment of hypertension. Therefore
10 male patients with mild arterial hypertension were
studied in order to define the BP response to long-term
aerobic training (60 min twice a week) under resting
conditions, during standardised ergometric workload,
during isometric exercise, during cold pressor testing
and during 24-h BP monitoring.
After 18 months of regular training there were significant reductions in arterial pressures at rest, during and
after standardised ergometry and during isometric and
cold pressor testing when compared with pre-training.
The heart rate also decreased significantly during exercise testing thus implying a decrease in myocardial oxygen consumption.
After long-term training, a reduction in systolic and
diastolic BP could also be shown during 24-h ambulatory BP monitoring.
These results demonstrate that long-term aerobic
training leads to a decrease in systolic and diastolic BP
at rest, during exercise and during 24-h BP monitoring
and imply a beneficial effect in the management of
hypertension that is nearly comparable to that of drug
therapy.
Keywords: arterial pressure; physical training; exercise
Introduction
Arterial hypertension is a major risk factor for cardiovascular disease.1–3 Morbidity and mortality
increases as arterial pressure rises, with no evidence
of a threshold of risk.4 Regular conditioning has
been well documented to exert a favourable influence on cardiovascular risk factors in physically
inactive subjects and has been demonstrated to
effectively reduce the incidence of non-fatal and
fatal coronary heart disease.5–13
The effective control of the major risk factors such
as high blood pressure (BP) is essential from the
standpoint of preventive medicine and public
health. It must be asked, however, whether the drug
therapy of hypertension will continue to play the
dominant role in hypertensive management given
the large financial burden that is imposed by the use
of antihypertensive drugs on a broad scale.
Exercise training has been advocated in the management of hypertension,14,15 since experimental
investigations with animals15 and longitudinal and
cross-sectional studies in humans have demonstrated a lower resting BP in athletic and trained
Correspondence: RG Ketelhut, Barkenhof 14, 14163 Berlin, Germany
Received 21 March 1997; revised and accepted 6 June 1997
populations when compared with their respective
untrained groups. It has been stated previously that
the reduction of BP by endurance training depends
on the group that is selected for study.16–21 In most
of the studies there are no data on the quality and
quantity of training and the behaviour of body
weight. However, this information is a prerequisite
for assessment if exercise can lower high BP. Hypertensive patients have a lower cardiac output and
stroke volume, a higher heart rate and a markedly
elevated peripheral resistance than normotensives at
the same level of exercise.22,23
The question of whether endurance training has a
positive effect on the high peripheral vascular resistance in hypertensives is still unknown. Previously24
we could show that during a single bout of aerobic
exercise there is a continuous decrease in systolic
and diastolic pressure in hypertensive humans during aerobic exercise under steady-state conditions.
A following transient post-exercise hypotension has
been shown to persist for as long as 1 h.
We undertook the present study to assess the
effects of regular aerobic training on BP not only at
rest but also during aerobic and isometric exercise
and during cold pressor testing and 24-h BP monitoring.
Aerobic exercise and arterial hypertension
RG Ketelhut et al
652
Subjects and methods
Ten male hypertensives (WHO stage I) (aged
43.3 ± 3.1 years) participated in the study. Consent
was obtained from each patient after they were well
briefed about the nature and purpose of this study.
All patients had mild hypertension at rest and during and after standardised ergometric testing. 25
There were none with coronary heart disease or
heart failure, and their serum creatinine concentration did not exceed 1.1 mg/dl. Careful physical
and laboratory examinations were performed to rule
out secondary hypertension and serious cardiovascular and cerebrovascular complications. All the
patients had sedentary lifestyles, as defined by the
absence of a regular exercise programme during the
preceding 10 years.
Patients were evaluated on a work-free Saturday.
Arterial pressure was measured indirectly with a
cuff and a mercury sphygmomanometer in a supine
position. Then the patients were subjected to standardised ergometric testing in a half-sitting position
on a bicycle ergometer under controlled conditions,
using techniques given in the Proposal for International Standardisation of Ergometry.26 The exercise load started at 50 watts, with an increase of 10
watts every minute to a maximum of 100 watts. During this bicycle ergometry arterial pressure readings
and heart rate were taken every 1 min. BP was measured according to the Riva-Rocci-Korotkoff cuff
method, using Korotkoff phase IV for diastolic pressure. The product of rate times pressure was calculated at 100 watts.
Furthermore, BP response to isometric exercise,
which involved holding a 2.4 kg weight in the left
hand with the arm extended horizontally for 2 min,
and response to cold pressor testing, which involved
dipping one hand into iced water (4°C) for 2 min,
was measured.
Additionally, in five patients the 24-h ambulatory
BP profiles were investigated before and after the
training period, using a portable Pressurometer III
(Delmar Avionies, USA). Measurements were made
at 7.5 min intervals. The patients were encouraged
to go about their usual daily activities and to relax
their arms during inflation and deflation. Ambulatory BP monitoring was always performed on a working day. All patients worked on daytime shifts, and
their tasks involved mainly desk work. Average BP
was calculated for the entire 24-h period.
Patients were advised not to alter their dietary
habits during the study and not to participate in
exercise programmes outside of the scheduled
classes. All the tests were then repeated under identical conditions after 18 months of regular aerobic
training.
The training programme consisted of outdoor running training twice a week for 1 h each training session. Exercise sessions started with a 5-min warmup period (stretching and walking). Subjects then
ran a distance of 1 km in the beginning and
increased distance progressively to 10 km at the end
of the study. Group training sessions were supervised by a trainer who also kept records of attendance. Patients exercised at approximately 70% of
the predicted maximal heart rate by regularly checking their pulses.
Statistical analysis was performed using the Student’s t-test for paired observations, and data were
expressed as mean ±1 s.d. A P-value ,0.05 was considered statistically significant.
Results
Because there was no control group the patients
were used as their own control with an initial
3.3 ± 1.2 months recruitment period prior to the
onset of training taken as the control period.
After this period there was a significant decrease
in arterial pressure at rest from 151 ± 11/96 ± 7
mm Hg to 139 ± 9/96 ± 6 mm Hg (P , 0.01). During
ergometric testing at 100 watts, pressure did not
change significantly from 188 ± 9/106 ± 6 to
184 ± 10/107 ± 6 mm Hg.
After 18 months of training there was a significant
reduction in resting BP from 139 ± 9/96 ± 6 mm Hg
before training to 133 ± 14/91 ± 7 mm Hg after
18 months of aerobic training (P , 0.05) (Figure 1).
During the standardised ergometric testing at a
workload of 100 watts, systolic pressure decreased
significantly from 184 ± 10 mm Hg to 170 ± 10
mm Hg (P , 0.05) and diastolic pressure decreased
from 107 ± 6 mm Hg to 96 ± 7 mm Hg (P , 0.01)
(Figure 1). Simultaneously the heart rate dropped
significantly (P , 0.01) from 116 ± 11/min to
106 ± 9/min and rate pressure product, an indication
of myocardial oxygen consumption, was significantly decreased from 21.344 before training to
18.020 after 18 months of training (P , 0.01, 15.6%).
BP in the 5th min of the recovery period after
exercise decreased from 143 ± 12/100 ± 8 mm Hg
before training to 135 ± 10/88 ± 7 mm Hg after 18
months of training (P , 0.01 for diastolic pressure).
Aerobic training produced reductions in arterial
pressure
during
isometric
exercise
from
173 ± 22/125 ± 10 mm Hg before training to
168 ± 19/113 ± 7 mm Hg after the training period
(P , 0.01) (Figure 2).
Figure 1 Systolic and diastolic pressure in hypertensive patients
at rest, during ergometric testing (100 watts) and in the 5th min
of the recovery phase before and after long-term aerobic training.
Aerobic exercise and arterial hypertension
RG Ketelhut et al
During cold pressor testing there was a decrease
from 145 ± 17/106 ± 13 mm Hg before training to
146 ± 21/99 ± 8 mm Hg after 18 months of training
(P , 0.05 for diastolic pressure (Figure 2).
In all patients with 24-h ambulatory BP-profile
available before and after long-term training, a
reduction in systolic and diastolic BP could be demonstrated
from
131 ± 7/94 ± 8
mm Hg
to
129 ± 12/83 ± 8 mm Hg after the training period.
Although the number of investigated patients was
small, there was a significant (P , 0.05) reduction in
diastolic pressure during 24-h pressure monitoring
(Figure 2).
There was no significant change in body weight
after training when compared with pre-training.
Discussion
The purpose of this study was to determine the
effect of regular training on arterial pressure. The
results demonstrated that in hypertensive subjects
regular aerobic exercise training resulted in a significant reduction of systolic and diastolic pressure,
not only at rest but also during exercise and stress
testing and during a 24-h BP profile.
It is generally known that hypertensive patients
are endangered not only by higher arterial pressures
at rest but especially by larger increases in pressure
during exercise and a delayed return to baseline levels after work.25,27–30 In the assessment of antihypertensive therapy, therefore, the response to exercise
should be analysed.25
In this regard it could be demonstrated that the
decrease in systolic pressure of 7.6% during ergometric workload (100 watts) is more intensive than
what we found using prazosin (3.2%, n = 24),
diuretics (4.3%, n = 54), gallopamil (4.4%, n = 40) or
enalapril (6.2%, n = 26) and is in the range of moderate nifedipine doses (20 mg: 7%, n = 35; 40 mg:
9.2%, n = 45), but substantially lower than betablocking agents (16.6%, n = 473) (Figure 3). The
effect of aerobic training on arterial pressure at rest
Figure 2 Systolic and diastolic pressure in hypertensive patients
during isometric and cold pressor testing and during 24-h BP
monitoring before and after long-term aerobic training.
653
Figure 3 Percentage reduction in systolic pressure during ergometric exercise (100 watts) with drug therapy and aerobic training.
in this study is consistent with the summarised
training induced changes of 48 study groups as analysed by Fagard.31
The clinical significance of these provocative findings remains to be documented. However, data
from a recent study32 allow us to calculate that the 6
mm Hg decrease in resting diastolic pressure in this
study would translate into a 38% reduction in the
odds of fatal or non-fatal stroke, and a 16%
reduction in the odds of coronary heart disease
death or non-fatal myocardial infarction.
One can argue that the decrease during ergometric
testing results from adaptation to aerobic exercise
or, moreover, from a placebo effect of an activity
such as physical training. But even though the
patients did not practise isometric exercise throughout the training period, there was a reduced increase
in arterial pressure during isometric testing as well.
Furthermore, a high reproducibility of BP
response to ergometry has been demonstrated in
some of our earlier studies and has been confirmed
by other authors as well with a very low variance
factor on a single day and for day-to-day variability.25
The observations in this study were based on a
small sample size and are weakened by the lack of
a definite control group. We used the patients as
their own control with the initial 3–4 months prior
to the onset of training taken as the control period.
After this control period arterial pressure during
ergometric testing was reproducible with no statistically significant differences, whereas arterial pressure at rest decreased significantly in the respective
period.
The underlying mechanisms responsible for the
exercise-induced reduction in BP remain unclear.
Physical aerobic training probably achieves this goal
by effecting a redistribution of systemic blood flow
and by increasing metabolic vasodilatation, which
significantly lowers the total peripheral resistance.
Furthermore, an increase in the capillary bed in the
skeletal muscle and functional changes in the arterioles are also under discussion,33 which would restitute the ability for vasodilation, probably by changing the sensitivity and/or number of a-receptors of
the vascular bed.
The bradycardia due to training allows the
assumption that other factors, eg, altering central
Aerobic exercise and arterial hypertension
RG Ketelhut et al
654
circulatory regulation, also may play an essential
role in the down-regulation of BP.
Recent evidence shows that insulin resistance and
hyperinsulinaemia may contribute to the pathogenesis of hypertension.34–37 Changes in BP may also
reflect training-induced changes in insulin-sensitivity.38 Although training induced changes in insulin-sensitivity were not measured in this study, its
positive correlation with fitness is well documented39 and longitudinal studies have shown regular exercise to be effective in increasing insulinsensitivity.40 Another possible mechanism for lowering arterial pressure may be directly related to a
diminished sympathetic nerve activity41–44 as well
as changes in the numbers of b-receptors. 45 A
reduction in sodium intake has to be discussed as
well since it is known that a moderate reduction in
sodium intake is effective in lowering arterial pressure in normotensives and hypertensives irrespective
of the baseline pressure.46 But as mentioned before,
the patients studied were advised not to alter their
dietary habits during the study, therefore it is
unlikely that their habitual sodium intake was
reduced.
It is unlikely that the BP reduction in this study
was attributable to a weight reduction, because there
was no significant change in body weight during the
training period.
In summary, the present study demonstrates that
in hypertensive patients long-term aerobic training
leads to a decrease in systolic and diastolic pressure
at rest, during exercise and during 24-h BP monitoring and implies a beneficial effect in the management of hypertension that is nearly comparable to
that of drug therapy. The advantage of physical
activity is that it has other healthy ‘side effects’ and
that the patients are motivated to change their lifestyle. The disadvantage of taking drugs daily with
its risk of side effects and costs may be avoided, and
patients feel that they can affect their wellbeing and
are not victims of disease. Therefore, regular aerobic
exercise should be recommended in the management of arterial hypertension.
20
References
21
1 MacMahon S, Peto R, Cutler J. Blood pressure, stroke,
and coronary heart disease. I. Prolonged differences in
blood pressure: prospective observational studies corrected for the regression dilution bias. Lancet 1990;
335: 765–774.
2 National High Blood Pressure Education Program
Working group report on primary hypertension. Arch
Intern Med 1993; 153: 186–208.
3 Stamler J, Stamler R, Neaton JD. Blood pressure, systolic and diastolic, and cardiovascular risks: U.S.
population data. Arch Intern Med 1993; 153: 598–615.
4 Neaton JD, Wentworth D. Serum cholesterol, blood
pressure, cigarette smoking, and death from coronary
heart disease: overall findings and differences by age
for 316.099 white men. Arch Intern Med 1992; 152:
56–64.
5 Billman GE, Schwartz PJ, Stone HL. The effects of
daily exercise on susceptibility to sudden cardiac
death. Circulation 1984; 69: 1182–1189.
6 Ekelund LG et al. Physical fitness as a predictor of cardiovascular mortality in asymptomatic North Amer-
7
8
9
10
11
12
13
14
15
16
17
18
19
22
23
24
25
ican men: the Lipid Research Clinics Mortality Followup Study. N Engl J Med 1988; 319: 1379–1384.
Garcia-Palmieri MR, Costas R, Cruz-Vidal M. Increased
physical activity: A protective factor against heart
attacks in Puerto Rico. Am J Cardiol 1982; 50: 749–753.
Kallio V, Hämäläinen H, Hakkila J, Luurila OJ.
Reduction of sudden deaths by a multifactorial intervention programme after acute myocardial infarction.
Lancet 1979; 2: 1091–1094.
Kannel WB, Sorlie P. Some health benefits of physical
activity: The Framingham Study. Arch Intern Med
1979; 139: 857–861.
Leon AS, Connett J, Jacobs DR Jr, Rauramaa R. Leisuretime physical activity levels and risk of coronary
artery disease and death: the Multiple Risk Factor
Intervention Trial. JAMA 1987; 258: 2388–2395.
Paffenbarger RS, Jr, Hale WE. Work activity and coronary heart mortality. N Eng J Med 1975; 292: 545–550.
Pekkanen J, Marti B, Nissinen A, Tuomilehto J.
Reduction of premature mortality by high physical
activity: A 20-year follow-up of middle-aged Finnish
men. Lancet 1987; 1: 1473–1477.
Powell KE, Thompson PD, Caspersen CJ, Kendrick JS.
Physical activity and the incidence of coronary heart
disease. Ann Rev Public Health 1987; 8: 253–287.
Hagberg JM. Exercise, fitness, and hypertension. In:
Bouchard C et al. (eds). Exercise, Fitness, and Health.
Human Kinetics: Champaign, IL, 1990, pp 455– 466.
Tipton CM. Exercise, training and hypertension: an
update. In: Holloszy J (ed). Exerc Sport Sci Rev. Williams and Wilkins: Baltimore, 1991, pp 447–505.
Blair SN, Goodyear NN, Gibbons LW, Cooper KH.
Physical fitness and incidence of hypertension in healthy normotensive men and women. JAMA 1984; 252:
478– 490.
Franz IW. Therapie der hypertonen Kreislaufregulationsstörungen bzw. Hypertonie durch dosiertes Training. Schweiz Z Sportmed 1978; 3: 117–121.
Franz IW, Eismann D, Mellerowicz H. Einfluβ von
Training und Gewichtsabnahme auf koronare Risikofaktoren. In: Heck H, Hollmann W, Liesen H, Rost R
(eds). Sport: Leistung und Gesundheit. Deutscher Ärzteverlag: Köln, 1983, pp 373–374.
Hanson JS, Nedde WH. Preliminary observations on
physical training for hypertensive males. Circ Res
1970; 26 (Suppl): 49–53.
Johnson W, Grover J. Hemodynamic and metabolic
effects of physical training in four patients with essential hypertension. Canad Mes Ass J 1967; 96: 842–846.
Jokl E, Ball M, Frankel L. Ergometry, exercise and
hypertension. In: Mellerovicz H, Hansen G (eds). 2. Int
Seminar für Ergometrie. Ergon: Berlin, 1967.
Lund-Johansen P. Hämodynamik bei der essentiellen
Hypertonie in Ruhe und während Ergometrie und
deren Beeinflussung durch Diuretika, b-Rezeptorenblocker und Vasodilatatoren. In: Franz IW (ed). Belastungsblutdruck bei Hochdruckkranken. Springer:
Berlin, Heidelberg, New York, 1981, pp 107–124.
Sannerstedt R. Hemodynamic response to exercise in
patients with arterial hypertension. Acta Med Scand
1966; 180 (Suppl): 458– 463.
Ketelhut R, Franz IW. Zur Wirkung einer akuten und
chronischen Ausdauerleistung auf das Blutdruckverhalten bei Hochdruckkranken. In: Franz IW, Mellerowicz H, Noack W (eds). Training und Sport zur Prävention und Rehabilitation in der technisierten Umwelt.
Springer: Berlin, Heidelberg, New York, Tokyo, 1985,
pp 704 –708.
Franz IW (ed). Ergometry in Hypertensive Patients –
Implications for Diagnosis and Treatment. Springer:
Berlin, Heidelberg, New York, Tokyo, 1986.
Aerobic exercise and arterial hypertension
RG Ketelhut et al
26 Agreement of the research committee of the ICSPE for
the international standardization. In: Mellerowicz H,
Hansen G (eds). International seminar of ergometry.
Ergon: Berlin, 1986, pp 314 –321.
27 Littler WA, Honour AJ, Pugsley DJ, Sleight P. Continuous recording of direct arterial pressure in unrestricted
patients – its role in the diagnosis and management of
high blood pressure. Clin Exp Pharmacol Physiol
1975; 2 (Suppl): 159–162.
28 Taylor SH. The circulation in hypertension. In: Burley
DM, Birdwood GB, Fryer JH, Taylor SH (eds). Hypertension – its nature and treatment. Metropolis Press:
London, 1975, pp 29–31.
29 Rowlands DB et al. Assessment of left ventricular mass
and its response to antihypertensive treatment. Lancet
1982; I: 467– 470.
30 Sokolow M, Perloff D, Cowan R. A 10-year prospective
study of the incidence of cardiovascular events in
hypertensive patients utilizing ambulatory blood
pressure measurements. In: Ninth Scientific meeting of
the International Society of Hypertension, Mexico
City, 1982 (abstract).
31 Fagard RH. The role of exercise in blood pressure control: supportive evidence. J Hypertens 1995; 13:
1223–1227.
32 Cutler JA, Psaty BM, MacMahon S, Furberg CD. Public
health issues in hypertension control: what has been
learned from clinical trials. In: Laragh JB, Brenner BM
(eds). Hypertension: Pathophysiology, diagnosis, and
management. Raven Press: New York, 1995, pp 253–
270.
33 Blomquist CG, Saltin B. Cardiovascular adaptations of
physical training. Ann Rev Physiol 1986; 45: 169–174.
34 Ferrannini E, Buzzigoli G, Bonadonna R. Insulin resistance in essential hypertension. N Eng J Med 1987; 317:
350–357.
35 Reaven GM. Role of insulin resistance in human disease. Diabetes 1988; 37: 1595–1607.
36 Modan MH et al. Hyperinsulinaemia: a link between
hypertension, obesity and glucose intolerance. J Clin
Invest 1985; 75: 809–817.
37 Kannel WB, Wilson PWF, Zhang TJ. The epidemiology
of impaired glucose tolerance and hypertension. Am
Heart J 1991; 121: 1268–1273.
38 Reaven GM. Insulin resistance and compensatory hyperinsulinaemia: role in hypertension, dyslipidaemia,
and coronary heart disease. Am Heart J 1991; 121:
1283–1288.
39 Vranic M, Wassermann D. Exercise, fitness, and diabetes. In: Bouchard C et al. (eds). Exercise, fitness, and
health: a consensus of current knowledge. Human Kinetics Books: Champaign, IL, 1988, pp 467– 495.
40 Lampman RM, Schteingart DE. Effects of exercise
training on glucose control, lipid metabolism, and
insulin sensitivity in hypertriglyceridemia and noninsulin dependent diabetes mellitus. Med Sci Sports
Exerc 1991; 23: 703–712.
41 Hartley LH, Mason JW, Hogan RP. Multiple hormonal
responses to graded exercise in relation to physical
training. J Appl Physiol 1972; 33: 607–610.
42 Lehmann M, Keul J, Huber G. Plasma catecholamines
in trained and untrained volunteers during graded
exercise. Int J Sport Med 1981; 2: 143–147.
43 Péronnet HJ et al. Plasma norepinephrine response to
exercise before and after training in humans. J Appl
Physiol 1981; 51: 812–815.
44 Winder WW, Hickson RC, Hagberg JM. Training
induced changes in hormonal and metabolic responses
to submaximal exercise. J Appl Physiol 1979; 46:
766–771.
45 Bieger W, Zittel R. Effect of physical activity on betareceptor activity. In: Knuttgen HG, Vogel JA, Poortmans J (eds). Biochemistry of exercise. Human Kinetics
Publishers: Champaign, IL, 1982, pp 715–722.
46 Cappuccio FP et al. A modest reduction in sodium
intake lowers blood pressure in an elderly population.
J Hypertens 1996; 12: 1517–1518.
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