An hour of exercise three times a week.
(on edit: changed the paragraphs I snipped)
http://well.blogs.nytimes.com/2011/03/02/can-exercise-keep-you-young/March 2, 2011, 12:02 am
Can Exercise Keep You Young?
By GRETCHEN REYNOLDS
We all know that physical activity is beneficial in countless ways, but even so, Dr. Mark Tarnopolsky, a professor of pediatrics at McMaster University in Hamilton, Ontario, was startled to discover that exercise kept a strain of mice from becoming gray prematurely.
But shiny fur was the least of its benefits. Indeed, in heartening new research published last week in The Proceedings of the National Academy of Sciences, exercise reduced or eliminated almost every detrimental effect of aging in mice that had been genetically programmed to grow old at an accelerated pace.
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At 8 months, when their sedentary lab mates were bald, frail and dying, the running rats remained youthful. They had full pelts of dark fur, no salt-and-pepper shadings. They also had maintained almost all of their muscle mass and brain volume. Their gonads were normal, as were their hearts. They could balance on narrow rods, the showoffs.
But perhaps most remarkable, although they still harbored the mutation that should have affected mitochondrial repair, they had more mitochondria over all and far fewer with mutations than the sedentary mice had. At 1 year, none of the exercising mice had died of natural causes. (Some were sacrificed to compare their cellular health to that of the unexercised mice, all of whom were, by that age, dead.)
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http://www.pnas.org/content/early/2011/02/18/1019581108.abstractEndurance exercise rescues progeroid aging and induces systemic mitochondrial rejuvenation in mtDNA mutator mice
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Abstract
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.
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