Abstract
Exercise inevitably induces damages and triggers a brief inflammation in challenged tissues of the human body. Nevertheless, regular exercise is associated with improved physical fitness and lower all-cause mortality among adults in a dose-dependent manner. The paradox between destructive nature of exercise and its anti-aging benefit can be best explained by decreasing aged cell population of the human body in a Darwinian natural selection fashion, resulting in tissue renewal. In this concept, the unfit-to-fit cell ratio of a multicellular system increases during growth (expansion of cell population and size) and decreases after exercise challenges. Inflammation serves as an innate mechanism to recognize cells in danger and triggers clearance mechanism to eliminate unhealthy cells followed by regeneration. A recent finding of decreased p16INK4a+ senescent cells together with CD68+ macrophage infiltration in human skeletal muscle after resistance exercise supports this concept. The senescent cells are mostly stem cells located in capillaries surrounding myofibers, functioning to replace short-lived endothelial cells. They can be found in young men aged 20–25 years. In this context, exercise controls weight gain (i.e. cell number and size) and decrease senescent cell proportion in capillaries of the human body, providing benefits in physical fitness and increasing life expectancy.
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