It’s well-established that exercise protects against heart disease. Men who exercise vigorously have about half the risk of fatal and non-fatal heart disease compared to men who do not. An older (1980) study reported the same, less than half the risk of coronary heart disease, and one gets the impression from the description of the participants, specifically “[m]en who engaged in vigorous sports, keep-fit, and the like”, that many of them were hardly even trying. That is, probably almost any decently vigorous exercise, no matter how defined, long or short in duration, or infrequent, protected at least somewhat against heart disease. Imagine the protection one gets when one goes about exercising systematically.
Given its other preventive effects on other diseases, the fact is that if exercise were a pill, every doctor would prescribe it to every one of his patients and every one of them would take it.
How does exercise prevent heart disease? Atherosclerosis, or the narrowing of arteries through the deposition of plaques on the artery wall, occurs partly due to oxidative stress in the cells of the lining of the blood vessel, which is a major cause of blood vessel pathology. Exercise, by lowering the level of oxidative stress in the lining of arteries, can prevent this, and it turns out that even older men who exercise regularly “do not demonstrate age-associated vascular endothelial oxidative stress”. The older, exercising men in this study had a level of a marker for oxidative stress a full 50% lower than older, sedentary men, and these values did not differ from young sedentary men.
What’s more, the older exercising men had lower insulin levels, lower body mass index, a similar VO2 Max, and lower heart rate than young sedentary men, so they were actually in better shape than the younger men. They performed about twice the level of exercise as the sedentary young men. (Not sure how that computes, because 2 x 0 = 0. Obviously the young men were not completely sedentary.)
One of the pathologies implicated in coronary artery disease, inflammation, is down-regulated by anti-inflammatory cytokines generated in skeletal muscle, so-called myokines. Muscles release myokines consequent to muscular contraction, and this points to weightlifting as a highly useful exercise in the generation of myokines, lowering of inflammation, and decreased heart disease risk.
By decreasing inflammation, exercise also exerts potent effects against many other diseases, including diabetes and metabolic syndrome, non-alcoholic fatty liver, and cancer.
Now, why would exercise do this, teleologically speaking? One answer is that our evolutionary history has programmed humans to be physically active, and therefore neglect of exercise messes up (science term, that) our physiology by promoting increased oxidative stress and inflammation:
Humans are not programmed to be inactive. The combination of both accelerated sedentary lifestyle and constant food availability disturbs ancient metabolic processes leading to excessive storage of energy in tissue, dyslipidaemia and insulin resistance. As a consequence, the prevalence of Type 2 diabetes, obesity and the metabolic syndrome has increased significantly over the last 30 years. A low level of physical activity and decreased daily energy expenditure contribute to the increased risk of cardiovascular morbidity and mortality following atherosclerotic vascular damage. Physical inactivity leads to the accumulation of visceral fat and consequently the activation of the oxidative stress/inflammation cascade, which promotes the development of atherosclerosis. Considering physical activity as a ‘natural’ programmed state, it is assumed that it possesses atheroprotective properties. Exercise prevents plaque development and induces the regression of coronary stenosis. Furthermore, experimental studies have revealed that exercise prevents the conversion of plaques into a vulnerable phenotype, thus preventing the appearance of fatal lesions. Exercise promotes atheroprotection possibly by reducing or preventing oxidative stress and inflammation through at least two distinct pathways.
Evolution has shaped our genes in such a way that we are adapted to high levels of physical activity, and if we don’t get that activity, our genes conspire to create oxidative stress, inflammation, and heart disease. Our distant ancestors, and even not-so-distant ones, hunted, fought, ran, or walked long distances daily, and they didn’t suffer from heart disease or any of the other diseases of civilization. Failure to be cognizant of this and failure to act on it has in large measure led to an epidemic of heart disease.
Exercise causes a substantial decrease in oxidative stress in blood vessels, which is a major cause of atherosclerosis and heart disease. It is such a potent agent against oxidative stress that older men who exercise regularly show very little of it. It works because our evolutionary heritage has designed us for physical activity, not being a couch potato. Exercise is mandatory for prevention of heart disease in men.