Abstract 5081: Leukocyte Telomere Length is Preserved with Age in Adults Who Exercise and is Related to Vascular Endothelial Function
Age increases, whereas habitual physical activity and high maximal aerobic capacity decrease cardiovascular disease (CVD) risk. However, the mechanisms involved are incompletely understood. Leukocyte telomere length (LTL), a marker of biological aging and replicative cellular senescence, decreases with age and is associated with increased CVD risk. We tested the hypothesis that LTL is preserved in habitually exercising middle-aged/older adults and is positively related to aerobic exercise capacity and vascular endothelial function, a predictor of CVD risk. Mean LTL (telomere restriction fragment analysis), endothelium-dependent dilation (EDD, brachial artery flow-mediated dilation) and maximal aerobic exercise capacity (treadmill maximal oxygen consumption, VO2max) were measured in three groups of healthy non-obese adults: young sedentary (YS: n = 8; age 24 ± 1 yr; 5 M), older sedentary (OS: n = 9; 65 ± 2 yr; 5 M) and older endurance exercise-trained (OT: n = 12; 64 ± 2 yr; 10 M). LTL was shorter (P < 0.05) in OS (7672 ± 291 bp) vs. YS (9093 ± 335 bp), but was preserved in OT (9007 ± 327 bp). VO2max and EDD were 43% and 47% lower, respectively (both P < 0.05), in OS (26.5 ± 3 ml/kg/min; 4.2 ± 0.6 Δ%) vs. YS (46.5 ± 3 ml/kg/min; 7.9 ± 0.6 Δ%), but were greater in OT (39 ± 2 ml/kg/min; 6.3 ± 0.8 Δ%) vs. OS (both P < 0.05). In the overall sample, LTL (adjusted for age and sex) was positively related to VO2max (r = 0.52, P < 0.05) and EDD (r = 0.41, P < 0.05). LTL was also related to body mass index (r = −0.37, P < 0.05), but no other metabolic risk factor. The relations between LTL and VO2max and EDD remained significant (P < 0.05) after controlling for body mass index. In contrast to their sedentary peers, leukocyte telomere length is preserved with age in adults who regularly perform endurance exercise. In healthy adults, leukocyte telomere length is positively related to maximal aerobic exercise capacity and vascular endothelial function. These results are consistent with the hypothesis that sedentary aging enhances, whereas habitual exercise/high aerobic fitness inhibits replicative cellular senescence. This may play a role in the contrasting effects of aging and physical activity on vascular endothelial function and CVD risk.