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Review
. 2021 May 13;13(10):14522-14543.
doi: 10.18632/aging.203051. Epub 2021 May 13.

Effects of exercise on cellular and tissue aging

Affiliations
Review

Effects of exercise on cellular and tissue aging

Priscila Viana Carapeto et al. Aging (Albany NY). .

Abstract

The natural aging process is carried out by a progressive loss of homeostasis leading to a functional decline in cells and tissues. The accumulation of these changes stem from a multifactorial process on which both external (environmental and social) and internal (genetic and biological) risk factors contribute to the development of adult chronic diseases, including type 2 diabetes mellitus (T2D). Strategies that can slow cellular aging include changes in diet, lifestyle and drugs that modulate intracellular signaling. Exercise is a promising lifestyle intervention that has shown antiaging effects by extending lifespan and healthspan through decreasing the nine hallmarks of aging and age-associated inflammation. Herein, we review the effects of exercise to attenuate aging from a clinical to a cellular level, listing its effects upon various tissues and systems as well as its capacity to reverse many of the hallmarks of aging. Additionally, we suggest AMPK as a central regulator of the cellular effects of exercise due to its integrative effects in different tissues. These concepts are especially relevant in the setting of T2D, where cellular aging is accelerated and exercise can counteract these effects through the reviewed antiaging mechanisms.

Keywords: AMPK; aging; exercise; type 2 diabetes.

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Conflict of interest statement

CONFLICTS OF INTEREST: The authors declare that they have no conflicts of interest.

Figures

Figure 1
Figure 1
Effects of exercise upon the aging process of different organs and systems. Created in BioRender.
Figure 2
Figure 2
AMPK as an effector node on the effects of exercise upon the different hallmarks of aging. AMP, adenosine monophosphate; AMPK, AMP- activated protein kinase; ATP, adenosine triphosphate; AGEs, advanced glycation end-products; FoxO3, Forkhead Box O3; LKB1, Liver kinase B1; mTOR, mammalian target of rapamycin; mTORC1, mTOR complex 1; NAD+, Nicotinamide adenine dinucleotide; NADH, Reduced Nicotinamide adenine dinucleotide; NFkB, Nuclear Factor kappa-light-chain-enhancer of activated B cells; NRF2, Nuclear factor erythroid 2-Related Factor 2; p53, Tumor suppressor protein 53; PGC-1, peroxisome proliferator-activated receptor gamma; SIRT1, Silent information regulator. Created in BioRender.
Figure 3
Figure 3
Exercise activated pathways in muscle capable of contributing to improved metabolic control in T2D. AMP, adenosine monophosphate; AMPK, AMP- activated protein kinase; ATP, adenosine triphosphate; Ca2+, divalent cation calcium; CaMKs, calcium/calmodulin dependent protein kinases; GLUT4, glucose transporter type 4; LKB1, liver kinase B1; PGC-1, peroxisome proliferator-activated receptor gamma; ROS, reactive oxygen species. Created in BioRender.
Figure 4
Figure 4
Conceptual overview. Created in BioRender.

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