Several epidemiological studies suggest that the incidence of hypertension is less in physically fit or active people than in unfit or sedentary subjects (3,18,43,47). This relationship was independent of baseline BMI or body fat (3,18,47). However, Paffenbarger et al. (43) reported that the inverse relationship between exercise and the incidence of hypertension was more evident for overweight than for lean Harvard alumni.
The results from cross-sectional studies on the associations between physical activity, fitness, and blood pressure are not quite consistent (12,13). Whereas several studies did not observe significant independent relationships, others did find that blood pressure was lower in fitter or more active subjects. On the whole, the differences in blood pressure between the most and the least fit or active rarely exceeded 5 mm Hg after controlling for confounding factors such as age and body size (12,13). It remains difficult, however, to ascribe differences in blood pressure within a population to differences in levels of physical activity or fitness because of the possible confounding factors which cannot be accounted for. Therefore, longitudinal intervention studies are more appropriate to assess the effect of physical exercise on blood pressure. The present meta-analysis of 44 randomized controlled trials involving 68 study groups indicates that dynamic aerobic exercise reduces blood pressure at rest by an average of 3.4 mm Hg for systolic and 2.4 mm Hg for diastolic pressure above blood pressure changes in nonexercising control groups or periods. Baseline BMI did not affect the blood pressure response: the change in blood pressure was indeed similar in overweight and lean participants. However, the lowering of blood pressure was more pronounced in hypertensive subgroups than in the normotensives. The exercise programs led to decreases of BMI (61), particularly in the overweight and obese subjects, but these changes did not determine the blood pressure response.
Although a large number of trials were controlled and applied randomization techniques, other important scientific criteria have not always been observed. The following shortcomings were identified in a variable number of training studies: lack of regular follow-up of the control subjects; no advice to keep diet or lifestyle, or both, constant throughout the study periods; a high number of drop-outs; inadequate statistical analyses and lack of adjustment for confounding variables; failure to blind the person who measured the blood pressure to the treatment or to use stationary or ambulatory automated blood pressure devices; and lack of use of an appropriate cuff size in the obese. Future studies should address these issues. However, it should be realized that it is difficult to blind the participants to the treatment in training studies; the inclusion of low-level exercise as placebo treatment is controversial.
The results on hemodynamic changes in response to dynamic training are conflicting; some authors claim that the lowering of blood pressure is based on a reduction of systemic vascular resistance whereas others observed a decrease of cardiac output. Most studies found a decrease of plasma noradrenaline concentrations suggesting a reduction in autonomic nervous activity. Other possible blood pressure lowering mechanisms have been addressed only rarely in randomized controlled exercise trials. Future studies, particularly in the obese, should not only focus on blood pressure but also on mechanisms involved in blood pressure regulation such as the renin-angiotensin-aldosterone system, prostaglandins, endothelial relaxing factor and endothelin, the sympathetic nervous system, insulin sensitivity and finally, genetic polymorphisms that might influence the blood pressure response to physical training.
The authors gratefully acknowledge the secretarial assistance of N. Ausseloos. R. Fagard is holder of the Prof. A. Amery Chair in Hypertension Research, founded by Merck, Sharp, and Dohme (Belgium).
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