The glass half full view on exercise is that it modestly slows aging. The glass half empty view is that being sedentary accelerates age-related decline. Our species evolved in an environment that demanded considerably more physical activity than is the case in today's era of comfort, calories, and machineries of transportation. Lacking that activity, we suffer. There are any number of papers that provide evidence showing that a surprisingly large fraction of cardiovascular and muscle aging, loss of function and loss of strength, is preventable. Exercise can't stop aging, but it can certainly make a meaningful difference to quality of life along the way. If it was expensive, it might not be worth it. But it is free.
Today I'll point out a couple of open access papers that cover aspects of the effects of exercise on function and cellular biochemistry in later life. They are representative of current views on the interaction between physical activity, metabolism, and the progression of aging. As is the case for calorie restriction, one of the interesting puzzles in the matter of exercise and health is how it can manage to be beneficial and yet have a comparatively small effect on life span in our species. Short-lived species have a much more intuitive response: interventions that improve their health tend to lengthen life expectancy to a proportionate degree. Not so in humans.
In fact, I would say that one of our defining features as a species, in comparison to smaller mammals, is just how little our lifestyle affects our life span, even while producing a sizable range in health status. So in mice, just the application of calorie restriction can extend life by 40%, while in humans the overall difference in life expectancy between a terrible lifestyle and an optimal lifestyle is, at best, 15% or so. The scientific understanding of the details of aging and cellular metabolism is not yet at the point that would allow us to do more than speculate as to how this can be the case, even as the short-term benefits of exercise and calorie restriction in mice and humans look very similar.
Central arterial stiffness increases with sedentary aging. While near-daily, vigorous lifelong (more than 25 years) endurance exercise training prevents arterial stiffening with aging, this rigorous routine of exercise training over a lifetime is impractical for most individuals. The aim was to examine whether a less frequent 'dose' of lifelong exercise training (4-5 sessions per week for more than 30 minutes) that is consistent with current physical activity recommendations elicits similar benefits on central arterial stiffening with aging.
A cross-sectional examination of 102 seniors (60 years and older), who had a consistent lifelong exercise history was performed. Subjects were stratified into 4 groups based on exercise frequency as an index of exercise 'dose': sedentary: fewer than 2 sessions per week; casual exercisers: 2-3 sessions per week; committed exercisers: 4-5 sessions per week; Masters athletes: 6-7 sessions per week plus regular competitions. Detailed measures of arterial stiffness and left ventricular afterload were collected.
Biological aortic age and central pulse wave velocity were younger in committed exercisers and athletes compared to sedentary seniors. TACi (total arterial compliance) was lower, while carotid β-stiffness index and Eai (effective arterial elastance) were higher in sedentary seniors compared to the other groups. There appeared to be a dose-response threshold for carotid β-stiffness index and TACi. Peripheral arterial stiffness was not significantly different among the groups. This suggest that 4-5 weekly exercise sessions over a lifetime is associated with reduced central arterial stiffness in the elderly. A less frequent dose of lifelong exercise (2-3 sessions/wk) is associated with decreased ventricular afterload and peripheral resistance, while peripheral arterial stiffness is unaffected by any dose of exercise.
Regular exercise improves the physical capacity and reduces the risk of developing chronic and age-related diseases by improving the metabolic state, antioxidant protection, and redox regulation. Lifelong training was reported to slow down aging-associated skeletal muscle fiber atrophy and prevent the reduction in muscular strength. Notably, acute intensive exercise induces the production of reactive oxygen species (ROS) that can evoke macromolecular damage, oxidative stress, endoplasmic reticulum (ER) stress, and activation of the unfolded protein response (UPR).
On the other hand, regular exercise training results in adaptations in antioxidant defense and improves redox signaling to protect cells against stress-related diseases, thus delaying the aging processes. In addition, the UPR, which is activated by exercise in skeletal muscles, may exert protective effects against ER stress and can promote metabolic adaptation to physical activity. Long-term exercise was reported to upregulate heat shock protein (HSP) production in skeletal muscle, which would be beneficial in coping with oxidative stress, ER stress, and ER stress-related apoptosis. Nevertheless, the ability to induce HSPs in aged skeletal muscle is compromised, which may impair the exercise-mediated adaptation processes.
There is only limited information available on the association of aging and exercise training concerning oxidative stress, ER (SR) stress, UPR, and/or ER stress-related apoptosis in skeletal muscle. Our hypothesis is based on the fact that there is an age-induced disruption of redox regulation, increased redox ER stress, and ER stress-related apoptosis, and that long-term exercise can exert protective effects against these processes. We investigated the key molecular markers associated with redox state, ER stress, and apoptosis in skeletal muscle of old animals in a life-long running model and compared them to young animals. Our data demonstrated that aging induced oxidative stress and activated ER stress-related apoptosis signaling in skeletal muscle, whereas long-term wheel-running improved redox regulation, ER stress adaptation and attenuated ER stress-related apoptosis signaling. These findings suggest that life-long exercise can protect against age-related cellular stress.