Exercise modestly slows aging. In humans epidemiological data only allows for the establishment of correlation between physical activity and measures of aging and mortality. Animal data, however, shows that regular exercise modestly slows aging to an extent that improves long-term health, increasing healthspan without extending maximum life span. It is not as impressive as the effects of calorie restriction on life span, but the effects on health along the way are not all that dissimilar in nature.
In today’s open access paper, the authors present a view of exercise and aging that is essentially hormetic in nature. They suggest that exercise slows aging because the short-term stresses generated by exercise overlap to some degree with the long-term stresses generated by the aging of tissues, and adaptation to the former grants greater resistance to the latter. This really need not be the case for exercise to slow aging, however. All that is needed is for the stresses of exercise to trigger generally beneficial responses. Or for exercise to correlate with reduced visceral fat burden, or reduced frailty, or reduced overall calorie intake.
Hormesis is used to describe situations in which mild stress and damage can produce a net gain in function by spurring a lasting increase in maintenance, repair, and defensive activities among the cells making up our tissues. Many forms of stress have this effect, such as reduced nutrient intake, exposure to toxins, heat, cold, and so forth. Exercise evidently stresses tissues via increased energy demands and pushes mitochondria to greater activity, generating oxidative stress as a side-effect, which cells must respond to with greater maintenance, but it also produces a range of other stress mechanisms, such as via inflammatory signaling.
Preventive lifestyle strategies such as exercise have emerged as potent, cost-effective means of reducing chronic disease risk. Exercise has a critical role in disease prevention and has been proposed as a form of “medicine”. The protective effects of exercise on chronic disease risk are ultimately accumulated over time through physiological adaptations to the stress of exercise. Acute exercise causes widespread physiological disruptions that require a complex, integrated response from the major physiological systems (autonomic, cardiovascular, metabolic, musculoskeletal, etc.) to meet the substantial requirements of human locomotion. Repeated exposure to the physiological disruptions incurred by acute exercise (through exercise training) stimulate physiological adaptations that act to attenuate stress during subsequent exercise bouts. These exercise adaptations provide the foundation through which individuals can adapt and improve their ability to perform physical work (e.g., increase muscular power, endurance, aerobic capacity, etc.) and also prevent development of age-related chronic disease.
Thus, physiologic adaptations to exercise are the latent mechanisms through which exercise acts as medicine and reduces chronic disease risk. Despite seminal work that has identified several key mechanisms underlying the protective effects of exercise, there has yet to be an overarching hypothesis that explains broadly why or how it is that exercise protects against age-related chronic disease. We posit that exercise prevents age-related chronic disease because it acutely elicits physiological responses that mimic physiological changes seen with aging, the greatest contributing risk factor to all chronic disease. Thus, we propose the hypothesis that exercise is “medicine” that protects against age-related chronic diseases because exercise can effectively simulate “aging.”
Acute exercise transiently disrupts cardiovascular, musculoskeletal, and brain function and triggers a substantial inflammatory response in a manner that mimics aging/age-related chronic disease. Data indicate that select acute exercise responses may be similar in magnitude to changes seen with an added 10-50 years of aging. The initial insult of the age-mimicking effects of exercise induces beneficial adaptations that serve to attenuate disruption to successive “aging” stimuli (i.e., exercise). Ultimately, these exercise-induced adaptations reduce the subsequent physiological stress incurred from aging and protect against age-related chronic disease. To further examine this hypothesis, future work should more intricately describe the physiological signature of different types/intensities of acute exercise in order to better predict the subsequent adaptation and chronic disease prevention with exercise training in healthy and at-risk populations.