Exercise to maintain physical fitness remains one of the most cost-effective approach to slowing aging. It clearly works, and even if the effect size is smaller than we'd all like it to be, it costs little more than time and effort. Of the various other approaches to achieving slowed aging or rejuvenation that have an established body of robust animal data, only calorie restriction, first generation senolytics to clear senescent cells, and mTOR inhibition as a calorie restriction mimetic strategy improve on the results of physical activity.
The dose-response curve for exercise is particularly steep when moving from no physical activity to some physical activity. Human epidemiological data suggests that there is a sizable difference between being sedentary and undertaking 30 minutes of moderate exercise once a week. Today's study is essentially a comparison between (a) people who undertake little to no exercise and (b) people who undertake at least some exercise. The little to no exercise group is evidently worse off.
Epigenetic aging measures or clocks are DNA methylation-based indicators of biological aging, linked to health outcomes and disease risk. Physical activity and exercise may influence epigenetic aging, suggesting a pathway through which it promotes healthier aging and reduces chronic disease burden. In this study, we assessed the association between self-reported moderate-to-vigorous physical activity and epigenetic age acceleration (EAA) in participants of the Health and Retirement Study, followed biennially for 12 years from 2004 to 2016.
Leukocyte DNA methylation was measured from venous blood samples collected in 2016 and second-generation epigenetic clocks (GrimAge, PhenoAge, and DunedinPACE) were used to assess EAA. Physical activity was assessed at each wave, with participants reporting vigorous activity at least once per week or moderate activity more than once per week or more categorized as 'physically active'.
In 2016, 58% of the participants were classified as physically active. In cross-sectional analysis, physically active participants had lower EAA than inactive participants: -1.26 years for GrimAge acceleration, -1.70 years for PhenoAge acceleration, and -0.05 years per chronological year for DunedinPACE.
Our findings highlight physical activity as a robust factor associated with slower epigenetic aging, with both accumulation and concurrent physical activity as the strongest predictors. These results underscore the role of physical activity in promoting healthier biological aging, suggesting its potential as a target for interventions aimed at mitigating age-related health decline.
View the full article at FightAging
