The weight of scientific evidence tells use that regular moderate exercise is very beneficial; aside from calorie restriction, it is the best thing that basically healthy people can do for themselves. No presently available medical technology surpasses the benefits of exercise and calorie restriction for long term health for the vast majority of the population - which is a strange thing to be saying in the midst of modern medicine and biotechnology. Strange but nonetheless true. This is a state of affairs we'd all like to see change for the better, via the introduction of new biotechnologies of rejuvenation, therapies that can be envisaged in some detail today, and which (if research and development is well funded) lie only a few decades ahead of us.
Near enough to matter, but still out of reach. So at this point exercise and calorie restriction are all that most of us have to work with to increase the odds of you still being alive to benefit from future rejuvenation therapies. It has to be said that the odds are not going to be moved to anywhere near the degree they would if a very large amount of funding arrived at the SENS Research Foundation, thus speeding up progress towards clinical reversal of age-related degeneration, but most of us are not in a position to make that happen.
The benefits of exercise are very broad, much like those offered by calorie restriction. It impacts mechanisms and the speed of change throughout the body and the aging process. On this topic, I recently noticed a couple of papers that note two small aspects of the interaction of exercise and aging, one in mice, and one in we humans. In mouse studies, it's quite possible to show that exercise causes numerous health benefits: mice are short-lived and thus researchers can follow them all the way through their lives:
Fourteen C57Bl/6J mice (seven male and seven female) were individually housed at eight weeks of age in cages with a running wheel, magnetic sensor and digital odometer. Duration, distance and running velocity were recorded daily. Fourteen additional mice C57Bl/6J mice (seven male and seven female) were placed in individual cages without running wheels at eight weeks of age. [Ultrasound techniques] were used to image the left ventricle every four weeks throughout the lifespan.
Lifelong physical activity resulted in greater diastolic filling parameters by the second quarter of the lifespan highlighting the clinical importance of regular aerobic activity in young adulthood as a mechanism for improved left ventricular performance with aging.
In the case of humans a research group must instead work with shorter snapshots of time, drawing data from existing populations with their quirks and histories. Given that, it is much harder to prove the degree to which exercise causes good health and slower aging versus only being associated with these line items.
The study was conducted on a subgroup population of the IKARIA study consisting of 185 middle-aged (40-65 years) and 142 elderly subjects (66-91 years). Endothelial function was evaluated by ultrasound measurement of flow-mediated dilatation (FMD).
In the overall study population FMD was inversely associated with age and middle-aged subjects had higher FMD compared with the elderly. Multiple linear regression analysis revealed that among middle-aged subjects the physically active had higher FMD compared with the physically inactive. Physically active subjects in the middle-aged group showed higher FMD compared with the physically active elderly. However, there was no difference in FMD values between middle-aged inactive subjects and the elderly physically active.
The present study revealed that increased [physical activity] was associated with improved endothelial function in middle-aged subjects and that [physical activity] in elderly subjects can ameliorate the devastating effects of ageing on arterial wall properties.
The full PDF version of the Ikaria study paper quoted above is available, so you can judge for yourself just how justified the authors' conclusion might be. Causation is hard to demonstrate - but the general presumption is that the causation shown in animal studies is also operating in human ones when it comes to things like exercise and cardiovascular health in aging. Proving and then putting numbers to that presumption are the challenges.