Resveratrol enhances exercise training responses in rats selectively bred for high running performance

Resveratrol enhances exercise training responses in rats selectively bred for high running performance
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DOI:
10.1016/j.fct.2013.01.051
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发表时间:
2013-11-01
影响因子:
4.3
通讯作者:
Radak, Zsolt
Radak, Zsolt
中科院分区:
农林科学2区
文献类型:
--
作者:
Hart, Nikolett;Sarga, Linda;Radak, Zsolt

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高容量跑步者(High Capacity Runner,HCR)大鼠是通过对跑步机耐力跑能力的不同人工选择培育出来的,旨在探索有氧生物与疾病之间的联系。补充白藜芦醇的有益效果已经在耐力跑中得到证实,白藜芦醇的抗氧化能力也得到了证明。在这项研究中,我们研究了12周的跑步机运动训练和/或白藜芦醇是否可以提高HCR的成绩。事实上,白藜芦醇提高了这些大鼠上肢的有氧运动能力和力量。此外,我们还发现白藜芦醇激活了AMP激活的蛋白激酶SIRT1和线粒体转录因子A(p<0.05)。线粒体分裂/融合和Lon蛋白水解酶/HSP78水平的变化表明,运动训练不会引起蛋白质的明显损伤。此外,运动训练和补充白藜芦醇都不会改变蛋白质羰基的含量。叉头转录因子1和SIRT4水平的变化可能意味着脂肪利用率的增加和胰岛素敏感性的改善。这些数据表明,补充白藜芦醇可通过激活AMPK-SIRT1-PGC-1α通路来提高有氧运动能力。(C)2013爱思唯尔有限公司。保留所有权利。
High Capacity Runner (HCR) rats have been developed by divergent artificial selection for treadmill endurance running capacity to explore an aerobic biology-disease connection. The beneficial effects of resveratrol supplementation have been demonstrated in endurance running and the antioxidant capacity of resveratrol is also demonstrated. In this study we examine whether 12 weeks of treadmill exercise training and/or resveratrol can enhance performance in HCR. Indeed, resveratrol increased aerobic performance and strength of upper limbs of these rats. Moreover, we have found that resveratrol activated the AMP-activated protein kinase, SIRT1, and mitochondrial transcription factor A (p < 0.05). The changes in mitochondrial fission/fusion and Lon protease/HSP78 levels suggest that exercise training does not significantly induce damage of proteins. Moreover, neither exercise training nor resveratrol supplementation altered the content of protein carbonyls. Changes in the levels of forkhead transcription factor 1 and SIRT4 could suggest increased fat utilization and improved insulin sensitivity. These data indicate, that resveratrol supplementation enhances aerobic performance due to the activation of the AMPK-SIRT1-PGC-1 alpha pathway. (C) 2013 Elsevier Ltd. All rights reserved.