Speaker
Description
Recent work suggests a physically active hunting and gathering lifestyle may have played a role in the evolution of long human lifespans. However, the mechanisms linking physical activity (PA) with longevity remain unclear. Moderate PA is associated with longer telomere length (TL), while shorter TL has been associated with increased cellular senescence and functional decline with age. Some research also suggests increased levels of bioinflammatory markers, such as C-reactive protein (CRP), are associated with telomere dysfunction. Here, we tested the hypothesis that CRP levels mediate the association between moderate to vigorous physical activity (MVPA) and TL, providing a potential mechanistic pathway linking PA and longevity. To evaluate this mechanism, we used the UK Biobank, a large-scale biomedical database, and analyzed adjusted T/S ratio (relative telomere to single gene copy), serum CRP, and MVPA measured via device-measured actigraphy data (n=79,839). To examine these relationships we used general linear models controlling for a range of covariates (age, ABSI [body shape index], smoking status, sex, ethnicity, time between data collection, and socioeconomic status). In this sample, MVPA was positively associated with TL (p=0.007). CRP was found inversely associated with TL (p<2.6e-16). Mediation analysis suggests CRP mediates the relationship between MVPA and TL (mediation total effect = 0.001; p=0.004). Our analysis supports the hypothesis that CRP acts as a mediator between MVPA and TL. These results suggest inflammatory markers play a role in cellular aging and may provide insight into how the evolution of high PA levels may have influenced cellular aging in humans.
