Regular exercise is good for you, and a great weight of scientific studies back up that statement. Insofar as the degenerations of aging go, the present consensus appears to be that exercise in humans slows aging to around the same degree as calorie restriction in humans. Where else could you go to find a fairly cost-effective way of extending your healthy life expectancy by a decade or so? (Or from the glass half empty perspective, we might add lack of exercise and eating too much to the list of ways to shorten your healthy life expectancy by a decade or so - like smoking, for example). The multiple mechanisms involved in producing the benefits of calorie restriction and exercise are incompletely understood but known to overlap to some degree: hormesis, for example, heat shock proteins, and lower amounts of of visceral body fat. But on either side there are likely distinct processes at work. There is every reason to expect exercise and calorie restriction practiced together to produce greater benefits than just one or the other.
Long-term exercise training activates telomerase and reduces telomere shortening in human leukocytes. The age-dependent telomere loss was lower in the master athletes who had performed endurance exercising for several decades.
"The most significant finding of this study is that physical exercise of the professional athletes leads to activation of the important enzyme telomerase and stabilizes the telomere," said Ulrich Laufs, M.D., the study's lead author and professor of clinical and experimental medicine in the department of internal medicine at Saarland University in Homburg, Germany. "This is direct evidence of an anti-aging effect of physical exercise. Physical exercise could prevent the aging of the cardiovascular system, reflecting this molecular principle."
This is in one cell population amongst thousands, of course - and there still remain questions about telomere biology and its relationship to age-related degeneration. Is it more of a cause of aging or more of a marker of aging - is telomere shortening a consequence of mitochondrial DNA damage, for example? That damage is the villain in the mitochondrial free radical theory of aging. We know that exercise correlates with lower levels of mitochondrial DNA damage, and it looks much as though mitochondrial DNA damage correlates with shorter telomeres. At this point there are all sorts of plausible theories floating around - more plausible on the mitochondrial side of the pool from where I stand - but the telomere researchers and mitochondria researchers haven't hammered in that last stake to prove root causes beyond any reasonable debate.
This is one of the many areas in which the Strategies for Engineered Negligible Senescence approach shines. We have a list of items that change with aging: here (a) mitochondrial DNA, (b) telomere length. We could spend an age working on a complete understanding, or we could instead start work immediately on methods to reverse both changes. It researchers can reverse all the biochemical changes of aging we know of - and there is good reason to believe researchers know of all the important ones in some detail - then it doesn't matter which are secondary, which are primary, or how exactly they work and interconnect. If your goal is to reverse aging, or rather if your goal is primarily accomplishment rather than primarily knowledge accumulation, then you engineer your way though uncertainty towards the most likely and comprehensive fix for the problem at hand.
Consider: just as our ancestors didn't need a formal mathematics of architecture and precision materials science to engineer fine bridges, we who stand at the dawn of the biotech century don't need a complete understanding of human biochemistry in order to reverse the damage of aging. Our longevity therapies will be pretty clunky compared to what will come with complete understanding, but they will work, and billions will be saved from suffering and death because we didn't wait around when we could have been getting the job done.
Werner, C., Furster, T., Widmann, T., Poss, J., Roggia, C., Hanhoun, M., Scharhag, J., Buchner, N., Meyer, T., Kindermann, W., Haendeler, J., Bohm, M., & Laufs, U. (2009). Physical Exercise Prevents Cellular Senescence in Circulating Leukocytes and in the Vessel Wall Circulation DOI: 10.1161/CIRCULATIONAHA.109.861005