Regular aerobic exercise, like calorie restriction, improves near all aspects of health throughout the life span. Unlike calorie restriction, exercise doesn’t slow aging in the sense of improving life span. It does reduce incidence of many age-related diseases, extending the proportion of life spent in good health, however. Aging is a complicated many-faceted web of cause and consequence, and these two very robust metabolic alterations, exercise and calorie restriction, illustrate this point by the different character of the alterations in aging and age-related disease they produce. That it is possible to have less of most age-related disease but not live longer is a peculiarity of the distribution of affected mechanisms. It would be interesting to look at the set of calorie restriction associated mechanisms that are not also touched on by exercise, and vice versa, but that is (a) poorly mapped at this time, and (b) both sets are very large and incompletely understood. The memo for humans is to practice both interventions.
Biological aging is associated with progressive damage accumulation, loss of organ reserves, and systemic inflammation (‘inflammaging‘), which predispose for a wide spectrum of chronic diseases, including several types of cancer. In contrast, aerobic exercise training (AET) reduces inflammation, lowers all-cause mortality, and enhances both health and lifespan. In this study, we examined the benefits of early-onset, lifelong AET on predictors of health, inflammation, and cancer incidence in a naturally aging mouse model.
Lifelong, voluntary wheel-running (O-AET; 26-month-old) prevented age-related declines in aerobic fitness and motor coordination vs. age-matched, sedentary controls (O-SED). AET also provided partial protection against sarcopenia, dynapenia, testicular atrophy, and overall organ pathology, hence augmenting the ‘physiologic reserve‘ of lifelong runners. Systemic inflammation, as evidenced by a chronic elevation in 17 of 18 pro- and anti-inflammatory cytokines and chemokines, was potently mitigated by lifelong AET, including master regulators of the cytokine cascade and cancer progression (IL-1β, TNF-α, and IL-6).
In addition, circulating SPARC, previously known to be upregulated in metabolic disease, was elevated in old, sedentary mice, but was normalized to young control levels in lifelong runners. Remarkably, malignant tumours were also completely absent in the O-AET group, whereas they were present in the brain (pituitary), liver, spleen, and intestines of sedentary mice. Collectively, our results indicate that early-onset, lifelong running dampens inflammaging, protects against multiple cancer types, and extends healthspan of naturally-aged mice.