...
首页> 外文期刊>Scientific reports. >Purine metabolism in sprint- vs endurance-trained athletes aged 20?90 years
【24h】

Purine metabolism in sprint- vs endurance-trained athletes aged 20?90 years

机译:Sprint-VS耐久性运动员的嘌呤新陈代谢训练有素的运动员20岁?90年

获取原文
           

摘要

Purine metabolism is crucial for efficient ATP resynthesis during exercise. The aim of this study was to assess the effect of lifelong exercise training on blood purine metabolites in ageing humans at rest and after exhausting exercise. Plasma concentrations of hypoxanthine (Hx), xanthine (X), uric acid (UA) and the activity of erythrocyte hypoxanthine-guanine phosphoribosyl transferase (HGPRT) were measured in 55 sprinters (SP, 20?90 years), 91 endurance runners (ER, 20?81 years) and 61 untrained participants (UT, 21?69 years). SP had significantly lower levels of plasma purine metabolites and higher erythrocyte HGPRT activity than ER and UT. In all three groups, plasma purine levels (except UA in UT) significantly increased with age (1.8?44.0% per decade). HGPRT activity increased in SP and ER (0.5?1.0%), while it remained unchanged in UT. Hx and X concentrations increased faster with age than UA and HGPRT levels. In summary, plasma purine concentration increases with age, representing the depletion of skeletal muscle adenine nucleotide (AdN) pool. In highly-trained athletes, this disadvantageous effect is compensated by an increase in HGPRT activity, supporting the salvage pathway of the AdN pool restoration. Such a mechanism is absent in untrained individuals. Lifelong exercise, especially speed-power training, limits the age-related purine metabolism deterioration.
机译:嘌呤代谢对于在运动期间有效的ATP重新合成至关重要。本研究的目的是评估终身运动训练对休息时和疲惫运动后老化人类血液嘌呤代谢物的影响。在55个短跑者(SP,20〜90年)中,测量了次黄嘌呤(HX),黄嘌呤(X),尿酸(UA)和红细胞次黄嘌呤 - 鸟嘌呤磷酰基转移酶(HGPRT)的活性的血浆浓度。 ,20?81年)和61名未经训练的参与者(UT,21岁?69岁)。 SP具有比ER和UT更高的血浆嘌呤代谢物和更高的红细胞HGPR活性。在所有三组中,血浆嘌呤水平(UT中的uA除外)随着年龄的增长显着增加(1.8?每十年44.0%)。 HGPR活度在SP和ER中增加(0.5?1.0%),而在UT中保持不变。 HX和x浓度比UA和HGPT水平更快地增加。总之,血浆嘌呤浓度随着年龄的增长而增加,代表骨骼肌腺嘌呤核苷酸(ADN)池的枯竭。在高度训练的运动员中,这种缺点效果是通过HGPR活性的增加来补偿,支持ADN池恢复的救助途径。在未经训练的人中,这种机制不存在。终身运动,特别是速度训练,限制了与年龄相关的嘌呤代谢恶化。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号