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间歇性爬梯运动训练对肥胖中年大鼠心肌线粒体生物合成及内质网应激的影响

Effects of intermittent ladder-climbing exercise training on mitochondrial biogenesis and endoplasmic reticulum stress of the cardiac muscle in obese middle-aged rats.

作者信息

Kim Kijin, Ahn Nayoung, Jung Suryun, Park Solee

机构信息

Department of Physical Education, College of Physical Education, Keimyung University, Daegu 42601, Korea.

出版信息

Korean J Physiol Pharmacol. 2017 Nov;21(6):633-641. doi: 10.4196/kjpp.2017.21.6.633. Epub 2017 Oct 30.

Abstract

The aim of this study is to investigate the effects of intermittent ladder-climbing exercise training on mitochondrial biogenesis and ER stress of the cardiac muscle in high fat diet-induced obese middle-aged rats. We induced obesity over 6 weeks of period in 40 male Sprague-Dawley rats around 50 weeks old, and were randomly divided into four experimental groups: chow, HFD, exercise+HFD, and exercise+chow. The exercising groups underwent high-intensity intermittent training using a ladder-climbing and weight exercise 3 days/week for a total of 8 weeks. High-fat diet and concurrent exercise resulted in no significant reduction in body weight but caused a significant reduction in visceral fat weight (p<0.05). Expression of PPARδ increased in the exercise groups and was significantly increased in the high-fat diet+exercise group (p<0.05). Among the ER stress-related proteins, the expression levels of p-PERK and CHOP, related to cardiac muscle damage, were significantly higher in the cardiac muscle of the high-fat diet group (p<0.05), and were significantly reduced by intermittent ladder-climbing exercise training (p<0.05). Specifically, this reduction was greater when the rats underwent exercise after switching back to the chow diet with a reduced caloric intake. Collectively, these results suggest that the combination of intermittent ladder-climbing exercise training and a reduced caloric intake can decrease the levels of ER stress-related proteins that contribute to cardiac muscle damage in obesity and aging. However, additional validation is required to understand the effects of these changes on mitochondrial biogenesis during exercise.

摘要

本研究旨在探讨间歇性爬梯运动训练对高脂饮食诱导的肥胖中年大鼠心肌线粒体生物合成及内质网应激的影响。我们在40只约50周龄的雄性Sprague-Dawley大鼠中诱导肥胖6周,然后将其随机分为四个实验组:正常饮食组、高脂饮食组、运动+高脂饮食组和运动+正常饮食组。运动组每周进行3天的高强度间歇性训练,包括爬梯和负重运动,共持续8周。高脂饮食和同时进行的运动并未导致体重显著下降,但导致内脏脂肪重量显著降低(p<0.05)。运动组中PPARδ的表达增加,在高脂饮食+运动组中显著增加(p<0.05)。在内质网应激相关蛋白中,与心肌损伤相关的p-PERK和CHOP的表达水平在高脂饮食组的心肌中显著更高(p<0.05),而间歇性爬梯运动训练使其显著降低(p<0.05)。具体而言,当大鼠在恢复到热量摄入减少的正常饮食后进行运动时,这种降低更为明显。总体而言,这些结果表明,间歇性爬梯运动训练和减少热量摄入的组合可以降低导致肥胖和衰老过程中心肌损伤的内质网应激相关蛋白水平。然而,需要进一步验证以了解这些变化在运动过程中对线粒体生物合成的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8623/5709480/a65db42436cd/kjpp-21-633-g001.jpg

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