The Relationship Between Physical Fitness and Biological Age
Early epigenetic clocks were insensitive to physical fitness, which didn't make much sense given the evident relationship between physical fitness and mortality risk in later life. Later, better epigenetic clocks have shown that physically fit individuals tend towards a lower biological age. To date, near all pharmacological interventions shown to adjust metabolism in ways that modestly slow aging, and for which human data exists, have failed to improve upon the effects of exercise. Exercise remains the low bar to beat for the longevity industry.
In this context, exercise is a powerful "geroprotector" that is well-recognized to extend the human health span. However, the relationship between physical fitness and biological age, based on the DNA methylation (DNAm) aging clock, is poorly understood. Most previous studies investigated the relationship between physical activity and DNAm aging clocks based on questionnaires and accelerometers using a molecular epidemiological approach. Theoretically, physical activity and fitness differ, with physical fitness considered the result of exercise, which is planned and regular physical activity. Considering that various health outcomes can be strongly associated with fitness, especially cardiorespiratory fitness (CRF), rather than with physical activity, CRF can be a stronger geroprotector than physical activity. Therefore, in the field of geroscience, it can be valuable to investigate the relationship between CRF and the DNAm aging clock and determine fitness reference values for delaying aging.
We attempted to determine the relationship between CRF and various lifestyle-related factors associated with biological aging based on DNAm aging clocks. We found that CRF was negatively related to epigenetic age acceleration, even after adjusting for confounders (chronological age, smoking, and alcohol consumption), and that maintenance of CRF above a reference value (i.e., 22.7 mL/kg/min) was associated with lower age acceleration. Collectively, these findings suggest that although the relative contribution of CRF to biological aging is relatively low when compared with lifestyle-related variables, such as smoking, the maintenance of CRF is associated with delayed biological aging in older males.
The central concern of exercise scientists is determining the causal relationship between CRF and biological aging. Several cross-sectional studies, including ours, have only demonstrated the relationship between physical activity, physical fitness, and biological aging; however, the causal relationship between them remains elusive. To prove a causal relationship, it is necessary to conduct longitudinal studies that track age-related changes in both CRF and DNAm aging clocks, as well as endurance exercise training intervention studies. In mouse studies, late-life exercise training could delay epigenetic aging of skeletal muscle. In humans, exercise training reportedly leads to epigenetic patterns toward a younger profile. Another study has reported that the number of subjects with higher baseline levels of epigenetic age acceleration decreased after exercise training
"Moreover, the maintenance of optimal body composition, adequate intake of carbohydrates and micronutrients, and a morning-type chronotype were associated with lower age acceleration.
Conversely, excessive visceral fat accumulation, smoking, excessive alcohol consumption, and dyslipidemia were associated with acceleration of older age. Finally, the relative contribution of each lifestyle-related variable to age acceleration was suggested to be higher for calf circumference, serum triglycerides, carbohydrate intake, and smoking status than for CRF.
Collectively, these findings suggest that although the relative contribution of CRF to biological aging is relatively low when compared with lifestyle-related variables, such as smoking, the maintenance of CRF is associated with delayed biological aging in older males."
hmmm….gotta check my calf circumference….
"To date, near all pharmacological interventions shown to adjust metabolism in ways that modestly slow aging, and for which human data exists, have failed to improve upon the effects of exercise."
Is there a reference for this statement?