Hypertension in Special Populations: Athletes

Rosa Maria Bruno; Giulia Cartoni; Stefano Taddei

Disclosures

Future Cardiol. 2011;7(4):571-584. 

In This Article

Effects of Exercise on Cardiovascular Risk

Observational & Interventional Studies

Regular physical activity is considered a cornerstone in the prevention and management of hypertension and cardiovascular disease. Observational studies comparing patients with different levels of cardiorespiratory fitness demonstrated that low fitness is an independent predictor of cardiovascular mortality both in the general population[16] and in hypertensive patients.[17] In particular, the impact of low fitness, evaluated by means of a maximal exercise test, on cardiovascular mortality is comparable to that of smoking, whereas moderate fitness is associated with lower death rates both in the presence or absence of classical cardiovascular risk factors.[18] In the Women's Health Study population (27,055 initially healthy women followed up for 11 years), even moderate levels of physical activity (equivalent to just over 2 h/week of brisk walking), evaluated by means of a validated self-administered questionnaire, were associated with substantially lower risk of clinically relevant cardiovascular events (30 to 40% relative risk reduction).[19] This evidence is reinforced by several interventional trials in different populations. A meta-analysis of 72 randomized interventional trials (3936 participants), based on dynamic aerobic exercise training (at least 4 weeks), designed to induce endurance performance training, demonstrated a significant net reduction of resting and daytime ambulatory blood pressure (3.0/2.4 mmHg and 3.3/3.5 mmHg, respectively). Blood pressure reduction was more pronounced in hypertensive patients (6.9/4.9 mmHg) than in normotensive subjects (1.9/1.6 mmHg).[20] Therefore, current guidelines for the management and treatment of arterial hypertension recommend physical exercise in all patients with hypertension, including those with prehypertension and those who require drug treatment.[4,21] The benefits of dynamic aerobic endurance training are effective on a broad range of classical cardiovascular risk factors, consisting not only in blood pressure reduction, but also in body weight, body fat and waist circumference reduction, and increase in insulin sensitivity and HDL-cholesterol.[20] Even low-intensity training is able to significantly reduce blood pressure, while higher intensity exercise is required in order to achieve significant improvements in lipid profile and body weight.[22]

On the other hand, the effect of resistance training on blood pressure and cardiovascular risk are less established. It is well known that heavy weightlifting acutely induces large blood pressure increases.[23] However, a meta-analysis of 9 randomized controlled studies (341 subjects) demonstrated that chronic resistance training, regardless of the kind of protocol followed, induced a small but significant reduction in office blood pressure (3.2 mmHg).[24] Thus moderate intensity resistance training could be safely added to aerobic activity in patients with arterial hypertension, as recommended by the American College of Sports Medicine.[25] Heart failure patients, in which muscle atrophy could greatly impair quality of life, appear to benefit more from combined endurance-resistance training, compared with endurance training, in terms of muscle strength and quality of life, with similar improvements in left ventricular function.[26] It is still unknown whether resistance training is able to reduce cardiovascular mortality.

Mechanistic Aspects

As explained above, dynamic aerobic exercise appears to be strikingly beneficial in reduction of cardiovascular morbidity and mortality. This is, at least in part, independent from the direct impact on classical cardiovascular risk factors, which appear to be of modest, though significant, entity.[19] Thus, other mechanisms are supposed to be involved. In the above mentioned Women's Health Study population, inflammatory/hemostatic biomarkers made a substantial contribution to lowering cardiovascular risk (high-sensitivity C-reactive protein, fibrinogen, and soluble intracellular adhesion molecule-1).[19] Physical activity also appears to counteract sympathetic nervous system activation, which is one of the physiological mechanisms responsible for development of hypertension and target organ damage.[27] A meta-analysis of clinical trials reported that the effects of exercise training on blood pressure, driven by peripheral vascular resistances reduction, are accompanied by reduction in heart rate and norephinephrine levels.[20] These data based on noninvasive and indirect parameters were confirmed in smaller studies using direct neural recordings by microneurography. In hypertensive patients, a program of exercise training consisting of three 60-min exercise sessions per week for 4 months reduced blood pressure and muscle sympathetic nerve activity and restored baroreflex sensitivity.[28] However, the observed increase in vagal tone and bradicardia caused by intense training may also be proarrhythmogenic and has recently been linked to an increased incidence of atrial fibrillation or flutter in athletes.[29]

The endothelium plays a primary role in the modulation of vascular tone and structure through production of the relaxing factor nitric oxide (NO), which acts by protecting the vessel wall against the development of atherosclerosis and thrombosis.[30] A dysfunctioning endothelium is a feature of the majority of cardiovascular risk factors, being a promoter of atherosclerosis and cardiovascular events.[30] Exercise training is known to ameliorate endothelial dysfunction in the presence of well known risk factors[31–33] and established cardiovascular diseases.[34,35] In particular, aerobic exercise is able to counteract hypertension-induced endothelial dysfunction. In untreated patients with mild essential hypertension, as well as in normotensive subjects, 12-week physical training determined an increase in forearm blood flow response to acetylcholine, which was selectively abolished by NO-synthase inhibition.[33]

The benefits of physical activity on vascular function have been clearly demonstrated in patients. However, it is interesting to question what happens in young healthy individuals, such as athletes. In young, trained individuals, endothelial-dependent vasodilation to acetylcholine (Figure 1),[31] as well as flow-mediated dilation,[32] are not different from the situation observed in matched sedentary control subjects, although conflicting results are found in some studies.[36] It is conceivable that in the young age group, endothelial function is preserved and cannot be affected by potentially beneficial interventions such as physical training. However, there is another possible explanation. Goto and coauthors compared the effect of mild, moderate and high intensity (25, 50, and 75% of maximum oxygen consumption established by cardiopulmonary exercise testing) 12-week physical training in 26 healthy young men.[37] This study demonstrated that only moderate-intensity aerobic exercise augments endothelium-dependent vasodilation through increased production of NO. By contrast, mild-intensity physical training had no effect, while high-intensity exercise caused an increase in plasmatic markers of oxidative stress. Thus young competitive athletes who perform sports requiring high intensity physical activity, may not necessarily derive cardiovascular benefit from their exercise. Furthermore, 4-month resistance training was found to have a negative, though reversible, effect on vascular function, worsening large artery compliance.[38] The above-mentioned differences in cardiovascular outcome between different sports categories[10] could be at least in part related to these aspects.

Figure 1.

Forearm vasodilation induced by intra-arterial administration of acetylcholine (0.15, 0.45, 1.5, 4.5 and 15 µg/100 ml/tissue/min) during administration of saline (0.2 ml/min, white circles) or of the inhibitor of nitric oxide synthase L-NMMA (black circles) in young and elderly athletes and age-matched sedentary subjects.
Adapted with permission from [31].

In elderly subjects, on the other hand, long-term physical training appears to preserve a functional endothelium by preventing oxidative stress and thereby preserving NO availability.[31] Forearm blood flow response to acetylcholine, although reduced as compared with young athletes, was significantly greater in elderly athletes than in age-matched sedentary subjects (Figure 1). Conduit artery endothelial function, studied in a similar population, gave analogous results: aging-induced endothelial dysfunction was not present in elderly endurance trained subjects.[32] Flow-mediated dilation appeared to be positively correlated to maximal oxygen uptake and plasma antioxidant capacity, again confirming that the most important mechanism explaining the beneficial effects of exercise on endothelial function is correction of oxidant status.[32]

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