Regular, intense exercise training as a healthy aging lifestyle strategy: preventing DNA damage, telomere shortening and adverse DNA methylation changes over a lifetime

Sellami, Maha and Bragazzi, Nicola and Prince, Mohammad Shoaib and Denham, Joshua ORCID: https://orcid.org/0000-0001-5804-4960 and Elrayess, Mohamed (2021) Regular, intense exercise training as a healthy aging lifestyle strategy: preventing DNA damage, telomere shortening and adverse DNA methylation changes over a lifetime. Frontiers in Genetics, 12:652497. pp. 1-12.

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Abstract

Exercise training is one of the few therapeutic interventions that improves health span by delaying the onset of age-related diseases and preventing early death. The length of telomeres, the 5 '-TTAGGG(n)-3 ' tandem repeats at the ends of mammalian chromosomes, is one of the main indicators of biological age. Telomeres undergo shortening with each cellular division. This subsequently leads to alterations in the expression of several genes that encode vital proteins with critical functions in many tissues throughout the body, and ultimately impacts cardiovascular, immune and muscle physiology. The sub-telomeric DNA is comprised of heavily methylated, heterochromatin. Methylation and histone acetylation are two of the most well-studied examples of the epigenetic modifications that occur on histone proteins. DNA methylation is the type of epigenetic modification that alters gene expression without modifying gene sequence. Although diet, genetic predisposition and a healthy lifestyle seem to alter DNA methylation and telomere length (TL), recent evidence suggests that training status or physical fitness are some of the major factors that control DNA structural modifications. In fact, TL is positively associated with cardiorespiratory fitness, physical activity level (sedentary, active, moderately trained, or elite) and training intensity, but is shorter in over-trained athletes. Similarly, somatic cells are vulnerable to exercise-induced epigenetic modification, including DNA methylation. Exercise-training load, however, depends on intensity and volume (duration and frequency). Training load-dependent responses in genomic profiles could underpin the discordant physiological and physical responses to exercise. In the current review, we will discuss the role of various forms of exercise training in the regulation of DNA damage, TL and DNA methylation status in humans, to provide an update on the influence exercise training has on biological aging.


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Item Type: Article (Commonwealth Reporting Category C)
Refereed: Yes
Item Status: Live Archive
Additional Information: Copyright © 2021 Sellami, Bragazzi, Prince, Denham and Elrayess. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Faculty/School / Institute/Centre: No Faculty
Faculty/School / Institute/Centre: No Faculty
Date Deposited: 11 Oct 2021 01:25
Last Modified: 09 Nov 2021 00:05
Uncontrolled Keywords: physical activity, epigenetics, telomerase, gene, oxidative stress, epigenetic clock, skeletal muscle
Fields of Research (2008): 06 Biological Sciences > 0604 Genetics > 060499 Genetics not elsewhere classified
11 Medical and Health Sciences > 1106 Human Movement and Sports Science > 110602 Exercise Physiology
Fields of Research (2020): 31 BIOLOGICAL SCIENCES > 3105 Genetics > 310599 Genetics not elsewhere classified
42 HEALTH SCIENCES > 4207 Sports science and exercise > 420702 Exercise physiology
Identification Number or DOI: https://doi.org/10.3389/fgene.2021.652497
URI: http://eprints.usq.edu.au/id/eprint/43778

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