Below you'll find links to a selection of recent papers and research publicity materials on exercise in the context of aging. Regular moderate exercise is a good plan, the standard issue thirty minutes to an hour a day on most days of the week that is put forward by the experts. Human statistical studies show strong correlations between moderate exercise, a lower incidence of age-related disease, and three to seven years of additional life expectancy. The corresponding animal studies show causation between exercise, health, and longevity, providing solid evidence for exercise to produce these benefits. Of course a piano could tomorrow fall upon even the most health conscious of us, but this is a game of weighting the odds in your favor, and not one of absolute outcomes.
Over the long term, regular exercise can do things for us that no medical technology can presently reproduce. This is a disappointing state of affairs, given that we are in the midst of a revolution in the capabilities of biotechnology, but the dominion of exercise will be slowly gnawed away in the years ahead, its benefits reproduced by medicine. As a first step, we might look at gene therapies and inhibitors to block myostatin for example, approaches that produce a gain in muscle tissue without the need to work for it. That will certainly be useful as a way to compensate for the progressive loss of muscle mass and strength that occurs in aging. Most of the benefits of exercise are more subtle and complex than this, however, involving poorly understood shifts in the operation of cellular metabolism. We might look back at the expensive and so far futile history of research aimed at calorie restriction mimetic drugs to see a preview of future efforts to produce exercise mimetic drugs. Safely adjusting metabolism into even well-known and well-cataloged states is a challenge.
In the long run, the important research in aging has little to do with exercise, however. You can't exercise your way to 100, or even 90 with any reliability. Three quarters of the population, including most of those with the best health, are dead before they see their 90s. Good health practices such as exercise just tend to make the decline somewhat less terrible. The only way to avoid the same trajectory of aging suffered by all of your ancestors is through the development of treatments that can repair the root causes of aging, many of which are actually modestly slowed by exercise: stem cell decline, mitochondrial damage, cellular senescence, metabolic waste products such as lipofusin, amyloids, and cross-links. The difference between modest slowing and actual repair is night and day. Sufficiently comprehensive repair creates rejuvenation, a life of health and vigor for as long as you desire, as the treatment can be repeated as needed. Just when these therapies will arrive is another game of odds: we can help to speed things up in many ways, but it happens when it happens. That we are not there yet is why exercise remains just as important as it ever was, and possibly more so now that it can weight the odds a little towards living long enough to benefit from the first rejuvenation treatments.
The study compared world-class track and field athletes in their 80s with people of the same age who are living independently. There have been few such studies of aging and muscle weakening in masters athletes in this age group. The study found that athletes' legs were 25 per cent stronger on average and had about 14 per cent more total muscle mass. In addition, the athletes had nearly one-third more motor units in their leg muscles than non-athletes. More motor units, consisting of nerve and muscle fibres, mean more muscle mass and subsequently greater strength. With normal aging, the nervous system lose motor neurons, leading to a loss of motor units, reduced muscle mass, less strength, speed and power. That process speeds up substantially past age 60.
Declining muscle mass and function is one of the main drivers of loss of independence in the elderly. Sarcopenia is associated with numerous cellular and endocrine perturbations, and it remains challenging to identify those changes that play a causal role and could serve as targets for therapeutic intervention. In this study, we uncovered a remarkable differential susceptibility of certain muscles to age-related decline. Aging rats specifically lose muscle mass and function in the hindlimbs, but not in the forelimbs. By performing a comprehensive comparative analysis of these muscles, we demonstrate that regional susceptibility to sarcopenia is dependent on neuromuscular junction fragmentation, loss of motor neuron innervation, and reduced excitability. Remarkably, muscle loss in elderly humans also differs in vastus lateralis and tibialis anterior muscles in direct relation to neuromuscular dysfunction. By comparing gene expression in susceptible and non-susceptible muscles, we identified a specific transcriptomic signature of neuromuscular impairment. Importantly, differential molecular profiling of the associated peripheral nerves revealed fundamental changes in cholesterol biosynthetic pathways. Altogether our results provide compelling evidence that susceptibility to sarcopenia is tightly linked to neuromuscular decline in rats and humans, and identify dysregulation of sterol metabolism in the peripheral nervous system as an early event in this process.
Klotho is an anti-aging protein that is predominantly secreted by the kidneys. The aim of the study was to measure and compare the circulating Klotho levels in the serum of trained athletes and in healthy, non-athlete controls. Thirty trained football players were enrolled and their serum Klotho levels were measured the morning after their last evening exercise training. The plasma free Klotho concentration was significantly higher in the athlete group compared to the non-athletes. Regular aerobic exercise could increase plasma Klotho levels, and this could be an explanation for exercise-related anti-aging effects.
There is evidence that an acute bout of exercise confers cognitive benefits, but it is largely unknown what the optimal mode and duration of exercise is and how cognitive performance changes over time after exercise. We compared the cognitive performance of 31 older adults using the Stroop test before, immediately after, and at 30 and 60 minutes after a 10 and 30 minute aerobic or resistance exercise session. Heart rate and feelings of arousal were also measured before, during and after exercise. We found that independent of mode or duration of exercise, the participants improved in the Stroop Inhibition task immediately post-exercise. We did not find the exercise influenced the performance of the Stroop Color or Stroop Word Interference tasks. Our findings suggest that an acute bout of exercise can improve cognitive performance, and in particular the more complex executive functioning, of older adults.
Aging and low physical activity are associated with the development of diseases (hypertension, type 2 diabetes, dyslipidemia, obesity) marked by chronic low-grade inflammation. Cardiovascular disease is the most common cause of death worldwide, while exercising muscle tissue can increase the secretion of myokines that can reestablish a possible inflammatory process in virtue of the anti-inflammatory effect. The objective of this review is to focus on molecular mechanisms involved between different kinds of exercise and cellular oxidative stress, and the emerging therapeutic strategies which have the potential to promote benefits in vascular health.
Regular exercise increases shear stress, mitochondrial biogenesis, and upregulates mitochondrial antioxidant system, inducing anti-inflammatory actions, such as suppression of TNF-α which may offer protection against TNF-α-induced vascular impairment. Exercise training of various durations and intensities appears to prevent and restore the age-related impairment of endothelial function, likely through the restoration of nitric oxide availability, reduction in oxidative stress, and turnover of the apoptotic process in the endothelium, thus minimizing vascular inflammation and decreasing the formation of atherosclerotic plaques.
Exercise causes an increase in the production of free radicals. As a result of a hormetic mechanism antioxidant enzymes are synthesized and the cells are protected against further oxidative stress. Thus, exercise can be considered as an antioxidant. Age-associated frailty is a major medical and social concern as it can easily lead to dependency. In this review we describe that oxidative stress is associated with frailty and the mechanism by which exercise prevents age-associated frailty. We propose that individually tailored multicomponent exercise programmes are one of the best ways to prevent and to treat age-associated frailty.