All subjects but one were still in the study after 3 yr of regular exercise. During follow-up, there were further decreases in systolic and diastolic pressures at rest and during exercise. Systolic BP decreased to a total of 16 mm Hg (8.7%) and diastolic to 15 mm Hg (14%) after 3 yr of regular training. This was also true for BP at rest after exercise (Table 1, Fig. 1) and the rate-pressure product at 100 W (Fig. 2). Furthermore, there was a significant reduction (P < 0.01) in the magnitude of exercise-induced diastolic pressure increase (at 100 W) versus resting conditions when compared pretraining (5.7%) with 3 yr of exercise (11.5%), demonstrating an improved exercise induced vasodilatation. No significant changes in body weight were documented during the training period (average increase 0.2 kg). The average training participation rate of the whole group was 86% (134 session) throughout the 3-yr intervention period.
The arterial pressure-lowering effect of endurance training in the present study was more intensive than what we found using various antihypertensive medications. In this regard, it could be demonstrated that the decrease in systolic pressure of 9.2% during ergometric workload (100 W) after 3 yr is more intensive than what we found in hypertensive controls 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 beta-blocking agents (16.6%, N = 473) (14). In contrast, Blumenthal et al. (3) assessed the effects of a moderate aerobic exercise program in patients classified as mild hypertensives, based on resting BP and ambulatory BP monitoring. After 4 months of exercise (3× wk−1, at 70% O2max), subjects in the exercise group did not exhibit greater BP reductions than the controls. So were the results of other studies (10), which observed only mild reductions in pressures at rest. Even in the present study, subjects exhibited a mild and not significant decrease in BP only at rest after 6 months of regular training, but BP continued to decrease in the long-term observation period. Therefore, from our results, it can be concluded that, besides intensity, the duration of exercise intervention may be the more important underlying influential parameter of the BP-lowering effect due to regular exercise.
Endothelial adaptation and endothelium-derived modulators may also display profound changes with regular aerobic training (4). A likely sequence of events to explain the effects of regular exercise includes a primary vascular change in small vessels involving endothelium-mediated vasodilatation, which has been shown to improve after regular cycling (17). Much research has focused on a probable decline in sympathetic autonomic control and a reduction in circulating catecholamines due to conditioning. A recent published animal study suggests that increased venule density is a specific adaptation of skeletal muscle to training. By increasing the venular bed in the exercising muscles and favoring a reduction in blood volume/vascular capacity ratio, it might contribute to the exercise induced pressure-lowering effect (2).
The observations in the present study were based on a small sample size, and there was no control group, which can be seen as a drawback. But the patients were used as their own control with the initial 3–4 months before the onset of training taken as the control period. After this control period, BP during ergometric testing and in the 5th minute after was reproducible with no statistically significant differences, whereas arterial pressure at rest decreased significantly in the respective period. Besides the pressure-lowering effect of regular exercise, one has to ask about the prognostic outcome of such a long-term therapy due to the incidence of cardiovascular diseases and death. In this regard, recently published data of a prospective cohort study (6) support the view that not only men who exercise regularly have lower rate of cardiovascular morbidity and mortality but moreover that this protective effect is enhanced in hypertensive subjects.
The reduction in BP in hypertensive patients seen after long-term aerobic training therefore implies that exercise has a beneficial effect in the management of hypertension and that pharmacological treatment can be deferred or probably prevented in hypertensive subjects who regularly engage in aerobic sports activities. We suggest that exercise should be recommended as an adjunct to proper diet and weight control for the prevention of cardiovascular diseases due to arterial hypertension. Furthermore, these results demonstrate that in men with physician-diagnosed hypertension, exercise is associated with a decrease in arterial pressure at rest as well as during exercise and that this antihypertensive effect of regular training can be improved and maintained for as long as 3 yr.
This paper is dedicated to Prof. Dr. Ingomar-W. Franz for his 60th birthday.
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