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通过停训对跑步者脂肪组织和肌肉脂蛋白脂肪酶的调节。

The regulation of adipose tissue and muscle lipoprotein lipase in runners by detraining.

作者信息

Simsolo R B, Ong J M, Kern P A

机构信息

Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California 90048.

出版信息

J Clin Invest. 1993 Nov;92(5):2124-30. doi: 10.1172/JCI116813.

Abstract

To study the mechanism of lipoprotein lipase (LPL) regulation by exercise, we recruited 16 healthy athletes to undergo a 2-wk period of detraining. Fasting fat and muscle biopsies were performed both before and after the detraining period. In muscle, detraining resulted in a decrease in LPL activity in both the heparin-releasable (HR) (-45%, P < 0.05) and cellular (extractable [EXT]) (-75%, P < 0.005) fractions, with no significant changes in LPL immunoreactive mass and mRNA levels. However, several subjects demonstrated parallel decreases in LPL mass and mRNA levels with detraining, suggesting that there is some degree of heterogeneity in response. In adipose tissue, detraining had the opposite effects on LPL activity. In the HR fraction, detraining resulted in an 86% increase (P < 0.005) in LPL activity, which was paralleled by a 100% (P = 0.02) increase in HR mass. However, there was no significant change in EXT LPL activity or EXT LPL mass. There were no changes in adipose LPL synthetic rate or LPL mRNA levels with detraining. The ratio of adipose tissue/muscle LPL, which may be an important indicator of the tendency for storage of circulating lipids in adipose tissue, increased significantly after detraining. The adipose/muscle LPL ratio was 0.51 +/- 0.17 in the exercising runners, and 4.45 +/- 2.46 in the same runners after detraining (P < 0.05). Thus, detraining of athletes resulted in a decrease in muscle LPL that occurred through post-translational mechanisms, whereas adipose tissue LPL increased, also due to posttranslational changes. This decrease in muscle LPL, coupled with an increase in adipose LPL, yielded a condition favoring adipose tissue storage.

摘要

为研究运动对脂蛋白脂肪酶(LPL)的调节机制,我们招募了16名健康运动员,让他们经历为期2周的停训期。在停训期前后均进行了空腹脂肪和肌肉活检。在肌肉中,停训导致肝素可释放(HR)部分(-45%,P<0.05)和细胞(可提取[EXT])部分(-75%,P<0.005)的LPL活性降低,而LPL免疫反应性质量和mRNA水平无显著变化。然而,一些受试者在停训时LPL质量和mRNA水平呈平行下降,表明反应存在一定程度的异质性。在脂肪组织中,停训对LPL活性有相反的影响。在HR部分,停训导致LPL活性增加86%(P<0.005),同时HR质量增加100%(P=0.02)。然而,EXT LPL活性或EXT LPL质量无显著变化。停训时脂肪LPL合成率或LPL mRNA水平无变化。脂肪组织/肌肉LPL比值(可能是循环脂质在脂肪组织中储存倾向的重要指标)在停训后显著增加。运动的跑步者中脂肪/肌肉LPL比值为0.51±0.17,同一跑步者停训后为4.45±2.46(P<0.05)。因此,运动员停训导致肌肉LPL通过翻译后机制降低,而脂肪组织LPL也因翻译后变化而增加。肌肉LPL的这种降低,加上脂肪LPL的增加,产生了有利于脂肪组织储存的状况。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f65a/288390/9ff9ad765009/jcinvest00043-0048-a.jpg

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