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Journal of Human Hypertension (2005) 19, 585–587
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COMMENTARY
Exercise and hypertension
A Choudhury and GYH Lip
Haemostasis, Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital,
Birmingham, UK
Journal of Human Hypertension (2005) 19, 585–587. doi:10.1038/sj.jhh.1001851; published online 19 May 2005
It is a sign of modern times that increasing rates
of urbanisation and associated behavioural changes
have led to a higher prevalence of a sedentary
lifestyle and less exercise. For example, it is
estimated that children today spend 600 kcal/day
less on physical activity than their counterparts 50
years ago.1 Unsurprisingly, we are facing an epidemic of hypertension, obesity, metabolic syndrome
and diabetes mellitus — which, unless tackled
proactively, will result in an increase in cardiovascular diseases, especially in the young and middle
aged. Lifestyle changes — especially exercise — and
relationships to hypertension may need greater
attention, especially at a population level.
There is little doubt about the burden and adverse
prognosis of hypertension on a population basis.2,3
Hypertension is a substantial risk factor for cardiovascular disease, and efforts to attain a blood
pressure target of 140 mmHg would result in a
reduction of 28–44% in stroke and 20–35% in
ischaemic heart disease, depending upon the age.2
These efforts could potentially prevent approximately 21 400 stroke deaths and 41 400 ischaemic
heart disease deaths each year — equivalent to
approximately 42 800 strokes and 82 800 ischaemic
heart diseases saved per year in the United Kingdom
alone.2 Besides being a hallmark but modifiable
risk factor for stroke and coronary artery disease,
hypertension also leads to atrial fibrillation, congestive heart failure and renal insufficiency, as
well as being a major component of the metabolic
syndrome, that currently affects nearly a quarter of
the population in the Western societies.4 While the
precise cause of metabolic syndrome is not known,
the interaction of obesity, sedentary lifestyle, diet
and unknown genetic factors is certainly important.
Many national guidelines for the prevention and
treatment of hypertension recommend lifestyle
modifications in the form of ‘regular aerobic exCorrespondence: Professor GYH Lip, Haemostasis, Thrombosis
and Vascular Biology Unit, University Department of Medicine,
City Hospital, Dudley Road, Birmingham, UK.
E-mail: [email protected]
Published online 19 May 2005
ercise’, as well as a reduction of dietary sodium
intake, weight loss and moderation of alcohol
intake.5 However, large well-conducted randomised
trial evidence on ‘regular aerobic exercise’ in
hypertension are relatively limited — a placebocontrolled trial of exercise alone, independent of
any other lifestyle change and treatment or demographic confounders, in essential hypertension is
clearly difficult. Thus, characterisation of the pathophysiological associates of exercise and hypertension may perhaps merit more attention.
For many years, physical inactivity has been recognised as a risk factor for coronary heart disease (CHD)
and most recommendations suggest regular physical
activity as a part of the strategy in preventing/reducing
CHD.6 However, much has also been made of the
higher transient risk of sudden death during and
shortly after exercise, particularly in sedentary individuals who are not accustomed to regular strenuous
physical stress.7 Meta-analyses of randomised control
trials assessing the effectiveness of exercise training
in lowering blood pressure reveal significant heterogeneity, reflecting the varied subject demography and
exercise schedules used in different studies.8,9
The available data suggest that moderate-intensity
(40–70% VO2 max) aerobic exercise is associated
with a significant reduction of blood pressure in
hypertensive and normotensive participants and in
overweight, as well as normal-weight participants.9
Interestingly, increasing exercise intensity to above
70% VO2 max did not have any additional impact
on blood pressure reduction. The effects of moderate- and high-intensity exercise on haemostasis and
platelet function also appear to be different.10,11 For
example, moderate exercise yields an enhancement
of fibrinolysis without a concomitant increase in
markers of blood coagulation, whereas heavy exercise activates both systems simultaneously.10–12
Moreover, moderate exercise seems to suppress
platelet adhesiveness and aggregation, whereas
heavy exercise induces a transient increase in
agonist-induced platelet aggregation, as well as
increase platelet count, adhesiveness and secretary
activity.10,11 These effects seem to be more pronounced in sedentary than active healthy subjects,
Exercise and hypertension
A Choudhury and GYH Lip
586
thus potentially explaining the risk of sudden death
in susceptible sedentary individuals or in patients
with pre-existing atherosclerotic vascular disease.
However, the absolute risk of sudden death during
any particular episode of heavy exercise is low
(1 sudden death per 1.5 million episodes of exertion) and, reassuringly, habitual heavy exercise did
attenuate the relative risk of sudden death that is
associated with an episode of vigorous exercise.7
Thus, recent guidelines from the Department of
Health suggest that each individual should participate in a minimum of 30 min of moderate intensity
activity (40–70% VO2 max) at least 5 days a week.8
A frequency of three exercise sessions per week has
been considered to be the minimal frequency for
blood pressure reduction.
The beneficial effect of regular exercise in hypertension is not limited to reduction of blood pressure
only. It has also been shown to reduce left
ventricular hypertrophy,13 improve exercise capacity and quality of life.14 When combined with
dietary alterations, regular exercise causes reduction
of oxidative stress, increases nitric oxide availability
and improves the overall metabolic profile.15 There
may also be beneficial effects on the prothrombotic
state associated with hypertension,10 although some
inconsistencies in studies are apparent.
Are the benefits in hypertension uniform? Even
though it is well established that moderate exercise
lowers blood pressure in most hypertensives, about
a quarter do not respond to exercise training.16 In
particular, patients with ‘nondipping’ hypertension
(ie, hypertensive patients with o10% reduction in
average nighttime blood pressure compared to
average daytime blood pressure — thought to reflect
a greater blood pressure ‘load’) have been suggested
to be nonresponders to exercise training.17 However,
it must be emphasised that many beneficial effects
of exercise reverse back to the pre-training state after
a period of deconditioning, reflecting the importance of regular moderate exercise in order to
maintain the above benefits.
Various reasons have been suggested for the lack
of blood pressure response to exercise in hypertensives, including genetic and pathophysiological
differences. There is also evidence documenting
disturbed sleep and increased nighttime activity
among nondippers, which might explain the lack of
nocturnal drop of blood pressure in this group.18
Further interest has been created given the increasing body of evidence documenting higher cardiovascular complications among patients with
nondipping hypertension compared to those with
dipping hypertension.19–21 Thus, specific data on
an effective exercise programme for patients with
nondipping hypertension will be most welcome.
In this issue of the Journal of Human Hypertension, Park et al22 assess the relationship of time of
day for exercise on blood pressure reduction in
dipping and nondipping hypertension. Their classification of patients into dipping and nondipping
Journal of Human Hypertension
hypertension was based on two ambulatory blood
pressure monitoring readings, and they find that
evening exercise significantly reduced the nighttime
blood pressure in nondippers. Furthermore, nondippers exhibited similar daytime systolic blood
pressure reduction as dippers, irrespective of a
morning or evening exercise period. Even morning
exercise seemed to cause a notable reduction of
nighttime blood pressure among nondippers. However, neither morning nor evening exercise resulted
in any significant reduction in nighttime blood
pressure in dippers, which was perhaps not unexpected. Of note, both forms of exercise did result
in significant reduction in daytime and average 24-h
blood pressure in dippers. Thus, the effect of postexercise blood pressure reduction lasted more than
12 h and especially so among nondippers.
These findings are in contrast to previous studies
exhibiting lack of blood pressure reduction with
aerobic exercise in nondipping hypertension,17 but
this might be due to the difference in subject
demography in the studies. Further studies reproducing these observations would be vital before
drawing any definitive conclusions. It should also
be remembered that the effect of an exercise training
programme on blood pressure reduction might be
different from that of a single bout of exercise per se.
The study by Park et al22 also raises the possibility
that ambulatory blood pressure measurement technology helps in further risk stratification of patients
with hypertension and points towards the possibility of individualised exercise programme for low
responders and nonresponders. Indeed, a paper
from the same group in the current issue of the
Journal of Human Hypertension by Lehmkuhl et al23
reports the accuracy and reproducibility of postexercise ambulatory blood pressure in assessing the
effect of exercise in stage 1 hypertension.
Recently published large prospective epidemiological studies have reported physical inactivity as a
predictor of not only cardiovascular but also total
mortality in middle-aged men and women.24,25 This
association is strong, independent of other major
risk factors, and illustrates the enormous preventative potential of regular exercise, especially given
the high prevalence of a sedentary lifestyle in most
communities. It also implies that physical activity
has a protective effect on noncardiovascular mortality too, although all the beneficial mechanisms are
not totally understood.
Given these consistent observations and considering the increasing prevalence of sedentary lifestyle
in most communities, the implementation of recommendations regarding physical activity given by
expert committees should receive high priority.
Though this will involve the whole community,
the evidence shows that short-term intensive programmes motivate patients to change lifestyle risk
factors, leading not only to greater reduction of
blood pressure but also to an improvement in their
overall metabolic profile.26 If only population
Exercise and hypertension
A Choudhury and GYH Lip
587
exercise levels can be improved and sustained, the
cardiovascular risk burden can only improve.
References
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