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Exercise preserves physical fitness during aging through AMPK and mitochondrial dynamics

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TLDR
In this article , the role of dynamic mitochondrial remodeling in exercise was investigated using Caenorhabditis elegans, and it was found that the dynamic cycle of mitochondrial fission-fusion is critical for physical fitness.
Abstract
Significance Exercise is a powerful anti-aging intervention. In muscle, exercise remodels mitochondrial metabolism and connectiveness, but the role of dynamic mitochondrial remodeling in exercise remains unknown. Using Caenorhabditis elegans, we find that the dynamic cycle of mitochondrial fission–fusion is critical for physical fitness. Exercise induces remodeling of the proteome that depends upon mitochondrial dynamics and delays an aging-associated decline in mitochondrial connectiveness and physical fitness. AMPK, a metabolic regulator that senses low energy availability and controls mitochondrial dynamics, is needed for exercise to maintain physical fitness with age and can recapitulate this exercise benefit. Our data identify the mitochondrial dynamics cycle as an essential mediator of exercise responsiveness and an entry point for interventions to maintain muscle function during aging.

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Mitochondrial dysfunction in aging

TL;DR: In this paper , a review summarizes mechanisms essential for maintaining mitochondrial homeostasis and emphasizes that imbalanced MQC may accelerate cellular senescence and aging, and suggests that appropriate interventions on MQCs may delay the aging process and extend lifespan.
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Twenty-four hour rhythmicity in mitochondrial network connectivity and mitochondrial respiration; a study in human skeletal muscle biopsies of young lean and older individuals with obesity

TL;DR: In this paper , the authors visualized and quantified the mitochondrial network morphology in human skeletal muscle of young healthy lean and older individuals with obesity over the course of 24 hours, with a more fused network coinciding with higher mitochondrial respiratory capacity.
Journal ArticleDOI

A worm’s life: AMPK links muscle mitochondrial dynamics to physical fitness and healthy aging in Caenorhabditis elegans

TL;DR: In this article , a balance between fusion and fission was found to be critical for healthy aging and energy efficiency, as well as for delaying cardiovascular and metabolic diseases in skeletal muscle.
Journal ArticleDOI

Mitochondrial Fission as a Therapeutic Target for Metabolic Diseases: Insights into Antioxidant Strategies

TL;DR: In this article , the authors explore the physiological and pathological roles of mitochondrial fission, its regulation by dynamin-related protein 1 (Drp1), and the interplay between reactive oxygen species (ROS) and mitochondria in health and metabolic diseases.
References
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Journal ArticleDOI

The Hallmarks of Aging

TL;DR: Nine tentative hallmarks that represent common denominators of aging in different organisms are enumerated, with special emphasis on mammalian aging, to identify pharmaceutical targets to improve human health during aging, with minimal side effects.
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The genetics of ageing

TL;DR: The nematode Caenorhabditis elegans ages and dies in a few weeks, but humans can live for 100 years or more, which means that over evolutionary time mutations have increased lifespan more than 2,000-fold.
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AMP-activated protein kinase (AMPK) action in skeletal muscle via direct phosphorylation of PGC-1α

TL;DR: The data indicate that AMPK phosphorylation of PGC-1α initiates many of the important gene regulatory functions of AMPK in skeletal muscle.
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