The aim of this systematic review and meta-analysis was 1) to assess whether master athletes have longer telomeres than age-matched non-athletes and 2) discuss possible underlying mechanisms underlying telomere length preservation in master athletes. A literature search was performed in PubMed, Web of Science, Scopus and SPORTDiscus up to August 2020. Only original articles published in peer-reviewed journals that compared telomere length between master athletes and aged-matched non-athletes were included. Eleven studies fulfilled eligibility criteria and were included in the final analysis. Overall, 240 master athletes (51.9±7.5 years) and 209 age-matched non-athletes (50.1±9.1 years) were analyzed. Master athletes had been participating in high-level competitions for approximately 16.6 years. Pooled analyses revealed that master athletes had longer telomeres than aged-matched non-athletes (SMD=0.89; 95% CI=0.45 to 1.33; p<0.001). Master athletes showed lower pro-oxidant damage (SMD=0.59; 95% CI=0.26 to 0.91; p<0.001) and higher antioxidant capacity (SMD=-0.46; 95% CI=-0.89 to −0.03; p=0.04) than age-matched non-athletes. Further, greater telomere length in master athletes is associated with lower oxidative stress and chronic inflammation, and enhanced shelterin protein expression and telomerase activity. In conclusion, 1) master athletes have longer telomeres than age-matched non-athletes, which may be the result of 2) lower levels of oxidative stress and chronic inflammation, and elevated shelterin expression and telomerase activity.

该系统评价和荟萃分析的目的是：1）评估硕士运动员是否具有比年龄相匹配的非运动员更长的端粒； 2）讨论了保存硕士运动员端粒长度的潜在潜在机制。截至2020年8月，在PubMed，Web of Science，Scopus和SPORTDiscus中进行了文献检索。仅包括在同行评审期刊上发表的比较了主要运动员与年龄匹配的非运动员之间端粒长度的原创文章。符合资格标准的11项研究已纳入最终分析。总体而言，分析了240位大师级运动员（51.9±7.5岁）和209位年龄相匹配的非运动员（50.1±9.1岁）。大师级运动员参加高水平比赛已有大约16.6年的时间。p <0.001）。高水平运动员表现出较低的促氧化剂损伤（SMD = 0.59; 95％CI = 0.26至0.91; p <0.001）和更高的抗氧化能力（SMD = -0.46; 95％CI = -0.89至-0.03; p = 0.04）年龄匹配的非运动员。此外，高手运动员中端粒的长度增加与较低的氧化应激和慢性炎症以及增强的胶体蛋白表达和端粒酶活性有关。总而言之，1）高级运动员比年龄相匹配的非运动员具有更长的端粒，这可能是由于2）氧化应激和慢性炎症水平降低，以及庇护素表达和端粒酶活性升高所致。