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有氧运动通过促进骨骼肌微循环和增加肌肉量来减轻压力超负荷诱导的心脏功能障碍。

Aerobic Exercise Attenuates Pressure Overload-Induced Cardiac Dysfunction through Promoting Skeletal Muscle Microcirculation and Increasing Muscle Mass.

作者信息

Yuan Ling-Yan, Du Pei-Zhao, Wei Min-Min, Zhang Qi, Lu Le, Tian Xu, Fu Shao-Ting, Zeng Xiao-Li

机构信息

Department of Kinesiology, Institute of Physical Education, Shanghai Normal University, Shanghai, China.

Department of Cardiovascular Medicine, Shanghai Baoshan Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai, China.

出版信息

Evid Based Complement Alternat Med. 2021 Nov 15;2021:8279369. doi: 10.1155/2021/8279369. eCollection 2021.

DOI:10.1155/2021/8279369
PMID:34819985
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8608514/
Abstract

BACKGROUND

Aerobic exercise has been proven to have a positive effect on cardiac function after hypertension; however, the mechanism is not entirely clarified. Skeletal muscle mass and microcirculation are closely associated with blood pressure and cardiac function.

OBJECTIVE

This study was designed to investigate the effects of aerobic exercise on the skeletal muscle capillary and muscle mass, to explore the possible mechanisms involved in exercise-induced mitigation of cardiac dysfunction in pressure overload mice.

METHODS

In this study, 60 BALB/C mice aged 8 weeks were randomly divided into 3 groups: control (CON), TAC, and TAC plus exercise (TAE) group and utilized transverse aortic constriction (TAC) to establish hypertensive model; meanwhile, treadmill training is used for aerobic exercise. After 5 days of recovery, mice in the TAE group were subjected to 10-week aerobic exercise. Carotid pressure and cardiac function were examined before mice were executed by Millar catheter and ultrasound, respectively. Muscle mass of gastrocnemius was weighed; cross-sectional area and the number of capillaries of gastrocnemius were detected by HE and immunohistochemistry, respectively. The mRNA and protein levels of VEGF in skeletal muscle were determined by RT-PCR and western blot, respectively.

RESULTS

We found that ① 10-week aerobic exercise counteracted hypertension and attenuated cardiac dysfunction in TAC-induced hypertensive mice; ② TAC decreased muscle mass of gastrocnemius and resulted in muscle atrophy, while 10-week aerobic exercise could reserve transverse aortic constriction-induced the decline of muscle mass and muscle atrophy; and ③ TAC reduced the number of capillaries and the protein level of VEGF in gastrocnemius, whereas 10-week aerobic exercise augmented the number of capillaries, the mRNA and protein levels of VEGF in mice were subjected to TAC surgery.

CONCLUSIONS

This study indicates that 10-week aerobic exercise might fulfill its blood pressure-lowering effect via improving skeletal muscle microcirculation and increasing muscle mass.

摘要

背景

有氧运动已被证明对高血压后的心脏功能有积极影响;然而,其机制尚未完全阐明。骨骼肌质量和微循环与血压及心脏功能密切相关。

目的

本研究旨在探讨有氧运动对骨骼肌毛细血管和肌肉质量的影响,以探究运动诱导压力超负荷小鼠心脏功能障碍减轻的可能机制。

方法

本研究将60只8周龄的BALB/C小鼠随机分为3组:对照组(CON)、主动脉缩窄组(TAC)和TAC加运动组(TAE),采用横向主动脉缩窄(TAC)建立高血压模型;同时,使用跑步机训练进行有氧运动。恢复5天后,TAE组小鼠进行10周的有氧运动。在处死小鼠前,分别通过Millar导管和超声检查颈动脉压力和心脏功能。称量腓肠肌的肌肉质量;分别通过苏木精-伊红(HE)染色和免疫组化检测腓肠肌的横截面积和毛细血管数量。分别通过逆转录-聚合酶链反应(RT-PCR)和蛋白质免疫印迹法检测骨骼肌中血管内皮生长因子(VEGF)的mRNA和蛋白水平。

结果

我们发现,①10周的有氧运动可抵消TAC诱导的高血压小鼠的高血压并减轻心脏功能障碍;②TAC降低了腓肠肌的肌肉质量并导致肌肉萎缩,而10周的有氧运动可保留横向主动脉缩窄引起的肌肉质量下降和肌肉萎缩;③TAC减少了腓肠肌中的毛细血管数量和VEGF蛋白水平,而10周的有氧运动增加了接受TAC手术小鼠的毛细血管数量、VEGF的mRNA和蛋白水平。

结论

本研究表明,10周的有氧运动可能通过改善骨骼肌微循环和增加肌肉质量来实现其降压作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6832/8608514/d79916f66762/ECAM2021-8279369.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6832/8608514/d1f0cdd76ff5/ECAM2021-8279369.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6832/8608514/c3624c594b7d/ECAM2021-8279369.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6832/8608514/6efac561ccf7/ECAM2021-8279369.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6832/8608514/0aae066ad520/ECAM2021-8279369.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6832/8608514/1181d433d1ae/ECAM2021-8279369.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6832/8608514/d79916f66762/ECAM2021-8279369.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6832/8608514/d1f0cdd76ff5/ECAM2021-8279369.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6832/8608514/c3624c594b7d/ECAM2021-8279369.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6832/8608514/6efac561ccf7/ECAM2021-8279369.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6832/8608514/0aae066ad520/ECAM2021-8279369.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6832/8608514/1181d433d1ae/ECAM2021-8279369.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6832/8608514/d79916f66762/ECAM2021-8279369.006.jpg

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