Fitness and physical exercise are among the most neglected means to improve prognosis. They are the healthiest cardiovascular intervention. Even cardiologists focus on pharmacological treatment and evaluate classical risk factors without asking about daily exercise or objective measures of physical capacity. It is surprising considering the strong data that underscores the survival benefit of regular exercise training.
Exercise works for everybody!
Years ago, Ralph Paffenbarger (1) published on a huge observational study, involving 17,000 male alumni from Harvard University. Men, who spend more than 2000 kcal’s on exercise a week, saw their death rate reduced with one third to one quarter as compared to less active men after a follow-up period of 12 to 16 years. More recently, Jonathan Myers (2) demonstrated the independent predictive value of exercise capacity in 6200 men referred for exercise testing. Remarkably, the largest reduction in mortality was observed between the least fit and the next quintile, suggesting that even a limited improvement in fitness has significant results. The “no pain-no gain” principle seems no longer valid. Exercise capacity mattered in both healthy subjects and cardiovascular patients. This finding has been confirmed in several patient groups, such as those with coronary artery disease and high-risk patients with chronic heart failure.
But how does it work?
Is it just a matter of healthier lifestyle? Apparently not, since the observed benefits occur independent of the modulation of coronary risk factors.
Numerous studies have shown that reversal of abnormal function of blood vessels in cardiovascular patients is one of the important mechanisms that link exercise training with improved outcome. In order to allow increased blood flow during exercise, both coronary arteries and arteries supplying working muscles have to increase in size. This dynamic process, called vasodilation, is severely impaired in patients with coronary artery disease and chronic heart failure.
There is a whole body of evidence suggesting that exercise elicits molecular changes at the level of endothelial cells. These cells cover the inner site of blood vessels. Nitric oxide (NO) is the key biological messenger produced by these endothelial cells. It regulates vascular tone, it prevents blood cells from sticking to the vascular wall and it reduces the likelihood of atherosclerotic plaques to develop. Simply stated, improved regulation of blood flow through exercise might be the mechanism.
During exercise, higher pulse rate and contraction of the heart increase the rate of flow in blood vessels. This phenomenon is sensed by endothelial cells and translated into a very complicated process that finally leads to increased production of NO. First of all, this occurs through increased levels and activity of the enzyme that synthesises the molecule (the endothelial nitric oxide synthase or eNOS). Secondly, the production of highly reactive and toxic oxygen radicals, that are capable of NO inactivation, is reduced. In addition, anti-oxidant enzymes that neutralize oxygen radicals are activated through exercise training. Finally, exercise training increases the diameter of large blood vessels, but it also leads to a higher number of small vessels (capillaries) via a process called angiogenesis.