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Exercise not only appears to keep skin younger, it may also even reverse skin aging in people who start exercising late in life, according to surprising new research.
As many of us know from woeful experience, our skin changes as the years advance, resulting in wrinkles, crow’s feet and sagging. This occurs because of changes within our layers of skin. After about age 40, most of us begin to experience a thickening of our stratum corneum, the final, protective, outer layer of the epidermis, itself the top layer of your skin. The stratum corneum is the portion of the skin that you see and feel. Composed mostly of dead skin cells and some collagen, it gets drier, flakier and denser with age.
At the same time, the layer of skin beneath the epidermis, the dermis, begins to thin. It loses cells and elasticity, giving the skin a more translucent and often saggier appearance.
These changes are independent of any skin damage from the sun. They are solely the result of the passage of time.
But recently, researchers at McMaster University in Ontario began to wonder if such alterations were inevitable. Earlier studies at McMaster involving mice that were bred to age prematurely had shown that a steady regimen of exercise could stave off or even undo the signs of early aging in these animals. When members of this breed of mice remained sedentary, they rapidly grew wizened, frail, ill, demented, and graying or bald. But if they were given access to running wheels, they maintained healthy brains, hearts, muscles, reproductive organs, and fur far longer than their sedentary labmates. Their fur never even turned gray.

A causal role for mitochondrial DNA (mtDNA) mutagenesis in mammalian aging is supported by recent studies demonstrating that the mtDNA mutator mouse, harboring a defect in the proofreading-exonuclease activity of mitochondrial polymerase gamma, exhibits accelerated aging phenotypes characteristic of human aging, systemic mitochondrial dysfunction, multisystem pathology, and reduced lifespan. Epidemiologic studies in humans have demonstrated that endurance training reduces the risk of chronic diseases and extends life expectancy. Whether endurance exercise can attenuate the cumulative systemic decline observed in aging remains elusive. Here we show that 5 mo of endurance exercise induced systemic mitochondrial biogenesis, prevented mtDNA depletion and mutations, increased mitochondrial oxidative capacity and respiratory chain assembly, restored mitochondrial morphology, and blunted pathological levels of apoptosis in multiple tissues of mtDNA mutator mice. These adaptations conferred complete phenotypic protection, reduced multisystem pathology, and prevented premature mortality in these mice. The systemic mitochondrial rejuvenation through endurance exercise promises to be an effective therapeutic approach to mitigating mitochondrial dysfunction in aging and related comorbidities.

Source : New York Times

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