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Asian J Kinesiol > Volume 25(2); 2023 > Article
Ling: Exercise to Promote Healthy Mitochondria and Improve Lifestyle of Aging Society
Mitochondria produce ATP that provides readily releasable energy to cells [1]. In order to maintain proper function, the mitochondrial network undergoes fission to separate damaged mitochondrial fragments from the healthy, and fusion to reduce mitochondrial dysfunction [2,3]. Dynamin-related proteins that are known to regulate mitochondrial fusion include Mitofusin 1 (Mfn1), Mitofusin 2 (Mfn2) and Optic atrophy gene 1 (Opa1), whereas the major effector of fission is Dynamin-related protein 1 (Drp1) which has been most frequently associated with pathological conditions [4].
During aging, mitochondrial performance declines as the balance between fusion and fission is often compromised [5,6]. This imbalance has been implicated in neurodegenerative diseases [6], sarcopenic muscles [2] and various other pathological conditions [2,4]. Exercise has been reported to increase mitochondrial biogenesis, remove damaged mitochondria, stimulate mitochondrial function [5,7] and delay aging associated decline in physical fitness [8-10] and cognitive function [11]. Exercise in the elderly has also been reported to improve mitochondrial efficiency as observed with the increase in Ser637 phosphorylation in Drp1 [12].
Therefore, promoting exercise is a promising strategy to improve lifestyle of the current aging society, requiring further research to better understand the mechanisms of mitochondrial dynamics.

References

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2. Romanello V. The interplay between mitochondrial morphology and myomitokines in aging sarcopenia. International Journal of Molecular Sciences. 2021; 22(1): 91.
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4. Rosdah AA, Smiles WJ, Oakhill JS, et al. New perspectives on the role of Drp1 isoforms in regulating mitochondrial pathophysiology. Pharmacology & Therapeutics. 2020; 213:107594.
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7. Chen PB, Yang JS, Park Y. Adaptations of skeletal muscle mitochondria to obesity, exercise, and polyunsaturated fatty acids. Lipids. 2018; 53(3): 271–8.
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8. Moore TM, Zhou Z, Cohn W, et al. The impact of exercise on mitochondrial dynamics and the role of Drp1 in exercise performance and training adaptations in skeletal muscle. Molecular Metabolism. 2019; 21:51–67.
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9. Picca A, Calvani R. Molecular mechanism and pathogenesis of sarcopenia: An overview. International Journal of Molecular Sciences. 2021; 22(6): 3032.
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10. Campos JC, Bozi LHM, Krum B, et al. Exercise preserves physical fitness during aging through AMPK and mitochondrial dynamics. 2023; 120(2): e2204750120.
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11. Bernardo TC, Marques-Aleixo , Beleza J, Oliveira PJ, Ascensão A, Magalhães J. Physical Exercise and Brain Mitochondrial Fitness: The Possible Role Against Alzheimer’s Disease. Brain Pathology. 2016; 26(5): 648–63.
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12. Casuso RA, Huertas JR. The emerging role of skeletal muscle mitochondrial dynamics in exercise and ageing. Ageing Research Reviews. 2020; 58:101025.
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