Denham Joshua, O'Brien Brendan J, Prestes Priscilla R, Brown Nicholas J, Charchar Fadi J
School of Science and Technology, University of New England, Armidale, New South Wales, Australia; Australian Centre for Research into Injury in Sport and Its Prevention (ACRISP), Federation University Australia, Mount Helen, Victoria, Australia.
Faculty of Health, Federation University Australia, Mount Helen, Victoria, Australia;
J Appl Physiol (1985). 2016 Jan 15;120(2):148-58. doi: 10.1152/japplphysiol.00587.2015. Epub 2015 Nov 19.
Leukocyte telomeres shorten with age, and excessive shortening is associated with age-related cardiometabolic diseases. Exercise training may prevent disease through telomere length maintenance although the optimal amount of exercise that attenuates telomere attrition is unknown. Furthermore, the underlying molecular mechanisms responsible for the enhanced telomere maintenance observed in endurance athletes is poorly understood. We quantified the leukocyte telomere length and analyzed the expression of telomere-regulating genes in endurance athletes and healthy controls (both n = 61), using quantitative PCR. We found endurance athletes have significantly longer (7.1%, 208-416 nt) leukocyte telomeres and upregulated TERT (2.0-fold) and TPP1 (1.3-fold) mRNA expression compared with controls in age-adjusted analysis. The telomere length and telomere-regulating gene expression differences were no longer statistically significant after adjustment for resting heart rate and relative V̇O(2 max) (all P > 0.05). Resting heart rate emerged as an independent predictor of leukocyte telomere length and TERT and TPP1 mRNA expression in stepwise regression models. To gauge whether volume of exercise was associated with leukocyte telomere length, we divided subjects into running and cycling tertiles (distance covered per week) and found individuals in the middle and highest tertiles had longer telomeres than individuals in the lowest tertile. These data emphasize the importance of cardiorespiratory fitness and exercise training in the prevention of biological aging. They also support the concept that moderate amounts of exercise training protects against biological aging, while higher amounts may not elicit additional benefits.
白细胞端粒长度随年龄增长而缩短,过度缩短与年龄相关的心脏代谢疾病有关。运动训练可能通过维持端粒长度来预防疾病,尽管能减缓端粒损耗的最佳运动量尚不清楚。此外,耐力运动员中观察到的端粒维持增强的潜在分子机制也知之甚少。我们使用定量PCR对耐力运动员和健康对照者(两者n = 61)的白细胞端粒长度进行了量化,并分析了端粒调节基因的表达。我们发现,在年龄调整分析中,与对照组相比,耐力运动员的白细胞端粒显著更长(7.1%,208 - 416 nt),且TERT(2.0倍)和TPP1(1.3倍)mRNA表达上调。在调整静息心率和相对最大摄氧量后,端粒长度和端粒调节基因表达差异不再具有统计学意义(所有P > 0.05)。在逐步回归模型中,静息心率成为白细胞端粒长度以及TERT和TPP1 mRNA表达的独立预测因子。为了评估运动量是否与白细胞端粒长度相关,我们将受试者分为跑步和骑行三分位数组(每周覆盖的距离),发现处于中间和最高三分位数组的个体比最低三分位数组的个体端粒更长。这些数据强调了心肺适能和运动训练在预防生物衰老中的重要性。它们还支持了适度运动训练可预防生物衰老,而运动量更大可能不会带来额外益处的观点。