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20 至 90 岁年龄的短跑和耐力运动员的嘌呤代谢。

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

机构信息

Department of Athletics Strength and Conditioning, Poznan University of Physical Education, ul. Królowej Jadwigi 27/39, 61-871, Poznań, Poland.

Department of Biochemistry, Medical University of Gdansk, ul. Dębinki 1, 80-211, Gdańsk, Poland.

出版信息

Sci Rep. 2019 Aug 19;9(1):12075. doi: 10.1038/s41598-019-48633-z.

Abstract

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.

摘要

嘌呤代谢对于运动过程中高效的 ATP 再合成至关重要。本研究旨在评估终身运动训练对静息和力竭运动后衰老人体血液嘌呤代谢物的影响。在 55 名短跑运动员(SP,20-90 岁)、91 名耐力跑运动员(ER,20-81 岁)和 61 名未经训练的参与者(UT,21-69 岁)中,测量了血浆次黄嘌呤(Hx)、黄嘌呤(X)、尿酸(UA)浓度和红细胞次黄嘌呤-鸟嘌呤磷酸核糖转移酶(HGPRT)活性。SP 的血浆嘌呤代谢物水平明显低于 ER 和 UT,而其红细胞 HGPRT 活性更高。在所有三组中,血浆嘌呤水平(UT 中的 UA 除外)随年龄增长显著增加(每十年增加 1.8-44.0%)。SP 和 ER 中的 HGPRT 活性增加(0.5-1.0%),而 UT 中的 HGPRT 活性保持不变。Hx 和 X 浓度随年龄增长的增加速度快于 UA 和 HGPRT 水平。总之,血浆嘌呤浓度随年龄增长而增加,代表骨骼肌腺嘌呤核苷酸(AdN)池的耗竭。在高度训练的运动员中,HGPRT 活性的增加补偿了这种不利影响,支持了 AdN 池恢复的补救途径。在未经训练的个体中,这种机制不存在。终身运动,尤其是速度力量训练,限制了与年龄相关的嘌呤代谢恶化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edec/6700101/e53cb3cc7548/41598_2019_48633_Fig1_HTML.jpg

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