Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2016 Sep;5(3):182-186.
doi: 10.1016/j.imr.2016.07.003. Epub 2016 Jul 22.

Age-related changes in skeletal muscle mitochondria: the role of exercise

Dae Yun Seo  1   2 , Sung Ryul Lee  1   3   2 , Nari Kim  1   3   2 , Kyung Soo Ko  1   3   2 , Byoung Doo Rhee  1   3   2 , Jin Han  1   3   2
Affiliations
Review

Age-related changes in skeletal muscle mitochondria: the role of exercise

Dae Yun Seo et al. Integr Med Res. 2016 Sep.

Abstract

Aging is associated with mitochondrial dysfunction, which leads to a decline in cellular function and the development of age-related diseases. Reduced skeletal muscle mass with aging appears to promote a decrease in mitochondrial quality and quantity. Moreover, mitochondrial dysfunction adversely affects the quality and quantity of skeletal muscle. During aging, physical exercise can cause beneficial adaptations to cellular energy metabolism in skeletal muscle, including alterations to mitochondrial content, protein, and biogenesis. Here, we briefly summarize current findings on the association between the aging process and impairment of mitochondrial function, including mitochondrial biogenesis and reactive oxygen species in skeletal muscle. We also discuss the potential role of exercise in the improvement of aging-driven mitochondrial dysfunctions.

Keywords: aging; exercise; mitochondria; skeletal muscle.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
The effects of sedentary aging. Note. From “Mitochondrial and skeletal muscle health with advancing age” by Adam R. Konopka, K. Sreekumaran Nair, 2013, Mol Cell Endocrinol, 379, p. 19–29. Copyright 2016, https://s100.copyright.com/CustomerAdmin/PLF.jsp?ref=a1ee97ca-af28-4e18-867c-413e399da8a7. Reprinted with permission.
Fig. 2
Fig. 2
Mitochondria biogenesis in aging. Note. From “Regulation of SIRT1 in aging: Roles in mitochondrial function and biogenesis” by Yujia Yuan, Vinicius Fernandes Cruzat, Philip Newsholme, Jingqiu Cheng, Younan Chen, Yanrong Lu, 2016, Mech Ageing Dev, 155, p. 10–21. Copyright 2016, https://s100.copyright.com/CustomerAdmin/PLF.jsp?ref=49996877-41b8-4243-b610-53e2aa846bff. Reprinted with permission. OXPHOS, oxidative phosphorylation; ROS, reactive oxygen species.
Fig. 3
Fig. 3
Mitochondrial changes in aging. Note. From “Skeletal muscle aging and the mitochondrion” by Matthew L. Johnson, Matthew M. Robinson, K. Sreekumaran Nair, 2013, Trends Endocrinol Metab, 24. Copyright 2016, https://s100.copyright.com/CustomerAdmin/PLF.jsp?ref=5ee2ebdc-2005-4f44-9706-d53fb96db265. Reprinted with permission. AMPK, AMP-activated protein kinase; ATP, adenosine triphosphate; PGC-1α, peroxisome proliferator-activated receptor-g coactivator 1α; ROS, reactive oxygen species; SIRT1, sirtuin 1; SOD, superoxide dismutase, VO2 max, the maximum rate of oxygen consumption.
See this image and copyright information in PMC

References

    1. Power G.A., Dalton B.H., Rice C.L. Human neuromuscular structure and function in old age: A brief review. J Sport Health Sci. 2013;2:215–226. - PMC - PubMed
    1. Cano A. Physical activity and healthy aging. Menopause. 2016;23:477–478. - PubMed
    1. Granacher U., Hortobagyi T. Exercise to improve,mobility in healthy aging. Sports Med. 2015;45:1625–1626. - PMC - PubMed
    1. Carter H.N., Chen C.C., Hood D.A. Mitochondria, muscle health, and exercise with advancing age. Physiology (Bethesda) 2015;30:208–223. - PubMed
    1. McBride H.M., Neuspiel M., Wasiak S. Mitochondria: more than just a powerhouse. Curr Biol. 2006;16:R551–R560. - PubMed

LinkOut - more resources