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Journal of Human Hypertension (2005) 19, 585–587 & 2005 Nature Publishing Group All rights reserved 0950-9240/05 $30.00 www.nature.com/jhh 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 1 Boreham C, Riddoch C. The physical activity, fitness and health of children. J Sports Sci 2001; 19: 915–929. 2 He FJ, MacGregor GA. Cost of poor pressure control in the UK: 62 000 unnecessary deaths per year. J Hum Hypertens 2003; 17: 455–457. 3 Gustavsen PH, Hoegholm A, Bang LE, Kristensen KS. White coat hypertension is a cardiovascular risk factor: a 10-year follow-up study. J Hum Hypertens 2003; 17(12): 811–817. 4 Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. JAMA 2002; 287: 356–359. 5 Willaims B et al, British Hypertension Society. Guidelines for management of hypertension: report of the fourth working party of the British Hypertension Society, 2004-BHS IV. J Hum Hypertens 2004; 18(3): 139–185. 6 Thompson PD et al. Exercise and physical activity in the prevention and treatment of atherosclerotic cardiovascular disease: a statement from the Council on Clinical Cardiology (Subcommittee on Exercise, Rehabilitation, and Prevention) and the Council on Nutrition, Physical Activity, and Metabolism (Subcommittee on Physical Activity). Circulation 2003; 107: 3109–3116. 7 Albert CM et al. Triggering of sudden death from cardiac causes by vigorous exertion. N Engl J Med 2000; 343: 1355–1361. 8 Halbert JA, Silagy CA, Finucane P. The effectiveness of exercise training in lowering blood pressure: a metaanalysis of randomised controlled trials of 4 weeks or longer. J Hum Hypertens 1997; 11: 641–649. 9 Whelton SP et al. Effect of aerobic exercise on blood pressure: a meta-analysis of randomized, controlled trials. Ann Intern Med 2002; 136: 493–503. 10 Lee KW, Lip GYH. Effects of lifestyle on hemostasis, fibrinolysis, and platelet reactivity: a systematic review. Arch Intern Med 2003; 163: 2368–2392. 11 Lee KW, Lip GYH. Acute versus habitual exercise, thrombogenesis and exercise intensity. Thromb Haemost 2004; 91: 416–419. 12 Anonymous. At Least Five a Week: Evidence on the Impact of Physical Activity and Its Relation to Health. Department of Health: London, UK, 2004. 13 Hinderliter A et al. Reduction of left ventricular hypertrophy after exercise and weight loss in overweight patients with mild hypertension. Arch Intern Med 2002; 162: 1333–1339. 14 Tsai JC et al. The beneficial effect of regular endurance exercise training on blood pressure and quality of life in patients with hypertension. Clin Exp Hypertens 2004; 26: 255–265. 15 Roberts CK et al. Effect of diet and exercise intervention on blood pressure, insulin, oxidative stress, and nitric oxide availability. Circulation 2002; 106: 2530–2532. 16 Hagberg JM, Park JJ, Brown MD. The role of exercise training in the treatment of hypertension. Sports Med 2000; 30: 193–206. 17 Nami R et al. Aerobic exercise training fails to reduce blood pressure in nondipper-type hypertension. Am J Hypertens 2000; 13: 593–600. 18 Mansoor GA. Sleep actigraphy in hypertensive patients with the ’non-dipper’ blood pressure profile. J Hum Hypertens 2002; 16: 237–242. 19 Verdecchia P, Clement D, Fagard R. Blood Pressure Monitoring. Task force III: Target-organ damage, morbidity and mortality. Blood Press Monit 1999; 4: 303–317. 20 Cuspidi C et al. Cardiovascular target organ damage in essential hypertensives with or without reproducible nocturnal fall in blood pressure. J Hypertens 2004; 22: 273–280. 21 Liu M et al. Non-dipping is a potent predictor of cardiovascular mortality and is associated with autonomic dysfunction in haemodialysis patients. Nephrol Dial Transplant 2003; 18: 563–569. 22 Park S, Jastremski CA, Wallace J. Time of day for exercise on blood pressure reduction in dipping and nondipping hypertension. J Hum Hypertens 2005; 19(8): 597–605 (this issue). 23 Lehmkuhl LA et al. Reproducibility of postexercise ambulatory blood pressure in stage 1 hypertension. J Hum Hypertens 2005; 19(8): 589–595 (this issue). 24 Barengo NC et al. Low physical activity as a predictor for total and cardiovascular disease mortality in middle-aged men and women in Finland. Eur Heart J 2004; 25: 2204–2211. 25 Hu G et al. Joint effects of physical activity, body mass index, waist circumference and waist-to-hip ratio with the risk of cardiovascular disease among middleaged Finnish men and women. Eur Heart J 2004; 25: 2212–2219. 26 Fleischmann EH et al. Intensive training of patients with hypertension is effective in modifying lifestyle risk factors. J Hum Hypertens 2004; 18: 127–131. Journal of Human Hypertension