An Overview of the Molecular Mechanisms by Which Exercise Impacts Aging

Exercise slows many of the degenerations of aging and - much like calorie restriction - this appears to be the result of changes in a multitude of biological processes and systems. In effect exercise adjusts the operation of your metabolism, moving it into a better configuration.

If you'd like a look under the hood, an overview of what is presently known of the biology that links exercise to improved long term health, you might read this recent open access review paper. It focuses on the heart, but the underlying mechanisms are of general interest:

It is generally accepted that regular exercise is an effective way for reducing cardiovascular morbidity and mortality. Physical inactivity and obesity are also increasingly recognized as modifiable behavioral risk factors for a wide range of chronic diseases, including cardiovascular diseases. Furthermore, epidemiologic investigations indicate that the survival rate of heart attack victims is greater in physically active persons compared to sedentary counterparts. Several large cohort studies have attempted to quantify the protective effect of physical activity on cardiovascular and all cause mortality. Nocon et al. in a meta-analysis of 33 studies with 883,372 participants reported significant risk reductions for physically active participants. All-cause mortality was reduced by 33%, and cardiovascular mortality was associated with a 35% risk reduction. Exercise capacity or cardiorespiratory fitness is inversely related to cardiovascular and all-cause mortality, even after adjustments for other confounding factors.

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Physical inactivity is increasingly recognized as modifiable behavioral risk factor for cardiovascular diseases. A partial list of proposed mechanisms for exercise-induced cardioprotection include induction of heat shock proteins, increase in cardiac antioxidant capacity, expression of endoplasmic reticulum stress proteins, anatomical and physiological changes in the coronary arteries, changes in nitric oxide production, adaptational changes in cardiac mitochondria, increased autophagy, and improved function of sarcolemmal and/or mitochondrial ATP-sensitive potassium channels. It is currently unclear which of these protective mechanisms are essential for exercise-induced cardioprotection. ... A better understanding of the molecular basis of exercise-induced cardioprotection will help to develop better therapeutic strategies.

Being sedentary appears to be just as self-sabotaging as letting yourself become obese. It will lower your odds of living in good health for as long as you might like - and that is enormously important in this age of biotechnology. Every additional year is another year of progress in the laboratories, of progress in advocacy for longevity science, of progress towards rejuvenation therapies that could arrive in time for those of us reading this today. Failing to take care of your health will shift the odds against you, and it's already the case that far too many people will die before the advent of repair technologies for the biological damage of aging. Why add to your risk becoming one of them?

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