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Aging decreases muscle mass, strength, and functional capacity. High-salt stress seems to promote muscle aging and decrease lifespan. However, exercise delays muscle aging and increases longevity, and it may protect muscle from rapid aging induced by high-salt intake (HSI), but the molecular mechanisms are poorly understood. In this study, the flies were fed a high-salt diet and trained to exercise. Muscle CG2196 (salt) gene and dSir2 gene were over-expressed by building mef2-gal4/UAS system. The results showed that both physical exercise and muscle dSir2 gene overexpression prevented HSI-induced and muscle salt overexpression-induced accelerated age-related decline of climbing index, climbing endurance, muscle NAD+ level, SOD activity level, dSir2 expression, and dFOXO expression, and they also prevented HSI-induced and muscle salt overexpression-induced accelerated age-related increase in muscle ROS level, MDA level, and salt gene expression. Physical exercise improved lifespan decrease induced by HSI and muscle salt overexpression. Therefore, current results indicated that high-salt stress accelerated muscle aging by decreasing muscular NAD+/dSir2/dFOXO pathway activity and increasing oxidative stress. Physical exercise protected muscle from accelerated aging induced by high-salt stress through activating muscle NAD+/dSir2/dFOXO pathway and enhancing muscle oxidation resistance. The combination of exercise and muscle dSir2 overexpression had the best protective effect on muscle aging and lifespan in flies.


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Physical exercise protects muscle from accelerated aging induced by high-salt intake and muscle CG2196 (salt) gene overexpression in Drosophila

Show Author's information Dengtai Wena( )Yiling Chenb( )Xu Tianc( )Wenqi Houa
Department of Physical Education, Ludong University, Yantai 264025, China
College of Physical Education, Yichun University, Yichun 336000, China
School of Exercise and Health, Shanghai University of Sport, Shanghai 200438, China

Peer review under responsibility of KeAi Communications Co., Ltd.

Abstract

Aging decreases muscle mass, strength, and functional capacity. High-salt stress seems to promote muscle aging and decrease lifespan. However, exercise delays muscle aging and increases longevity, and it may protect muscle from rapid aging induced by high-salt intake (HSI), but the molecular mechanisms are poorly understood. In this study, the flies were fed a high-salt diet and trained to exercise. Muscle CG2196 (salt) gene and dSir2 gene were over-expressed by building mef2-gal4/UAS system. The results showed that both physical exercise and muscle dSir2 gene overexpression prevented HSI-induced and muscle salt overexpression-induced accelerated age-related decline of climbing index, climbing endurance, muscle NAD+ level, SOD activity level, dSir2 expression, and dFOXO expression, and they also prevented HSI-induced and muscle salt overexpression-induced accelerated age-related increase in muscle ROS level, MDA level, and salt gene expression. Physical exercise improved lifespan decrease induced by HSI and muscle salt overexpression. Therefore, current results indicated that high-salt stress accelerated muscle aging by decreasing muscular NAD+/dSir2/dFOXO pathway activity and increasing oxidative stress. Physical exercise protected muscle from accelerated aging induced by high-salt stress through activating muscle NAD+/dSir2/dFOXO pathway and enhancing muscle oxidation resistance. The combination of exercise and muscle dSir2 overexpression had the best protective effect on muscle aging and lifespan in flies.

Keywords: Physical exercise, high-salt intake, muscle aging, NAD+/dSir2

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Received: 18 April 2021
Revised: 23 July 2021
Accepted: 02 September 2021
Published: 04 April 2023
Issue date: November 2023

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© 2023 Beijing Academy of Food Sciences.

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Acknowledgements

Thanks to Core Technology Facility of Center for Excellence in Molecular Cell Science. CAS (CEMS) for your service. This work is supported by the National Natural Science Foundation of China (NSFC) (32000832) and Province Natural Science Foundation of Shandong (ZR2020QC096).

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This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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