Aging and exercise

The most important determinant of cardiovascular health is the age. The incidence and prevalence of clinical and subclinical cardiovascular diseases increase dramatically with age, making cardiovascular disease the most common cause of death among the elderly.

Aging cardiovascular tissues are exemplified by pathological alterations including hypertrophy, altered left ventricular (LV) diastolic function, and diminished LV systolic reverse capacity, increased arterial stiffness, and impaired endothelial function (Lakatta and Levy 2003).

Aging of the vasculature results in increased arterial thickening and stiffness as well as dysfunctional endothelium. At the molecular level, as endothelial cells age, they exhibit a reduction in eNOS activity, reducing the bioavailability of NO, which is a critical vasodilator produced by endothelial cells, regulating vascular tone, in addition to inhibiting vascular inflammation, thrombotic events, and aberrant cellular proliferation. Loss of NO also promotes endothelial cell senescence. With age, cardiomyocytes become more susceptible to stress, including oxidative stress. Therefore the increase in oxidative stress due to the increase in ROS production with age results in an overall increase in the rate of cardiac cell death with age (North and Sinclair 2012). The NF-κB pathway is a critical component of inflammatory processes activated by oxidative stress. Beside the inflammatory processes, antioxidant deficiency is another mechanism which damage during aging.

Increased physical activity reduces the relative risk of death by 20-35% in both men and women. Brown et al. evaluated the relationship between physical activity and risk of all-cause mortality in a large number of elderly (Brown, McLaughlin et al. 2012). Exercise training prevents and restores age-related impairment of endothelial function. Exercise upregulates also antioxidant defense mechanisms to repair the oxidative damage.

Regular physical exercise reduces C-reactive protein (CRP) and the levels of pro-inflammatory cytokines (TNF-α, IL-6) while increasing anti-inflammatory markers (IL-4, IL-10). Exercise also suppresses TNF-α production by an IL-6 independent pathway in IL-6 knockout mice (Keller, Keller et al. 2004).