Edward F. Adolph Distinguished Lecture: The remarkable anti-aging effects of aerobic exercise on systemic arteries

Abstract

Cardiovascular diseases (CVD) remain the leading cause of morbidity and mortality in modern societies, and advancing age is the major risk factor for CVD. Arterial dysfunction, characterized by large elastic artery stiffening and endothelial dysfunction, is the key event leading to age-associated CVD. Our work shows that regular aerobic exercise inhibits large elastic artery stiffening with aging (optimizes arterial compliance) and preserves endothelial function. Importantly, among previously sedentary late middle-aged and older adults, aerobic exercise improves arterial stiffness and enhances endothelial function in most groups and, therefore, also can be considered a treatment for age-associated arterial dysfunction. The mechanisms by which regular aerobic exercise destiffens large elastic arteries are incompletely understood, but existing evidence suggests that reductions in oxidative stress associated with decreases in both adventitial collagen (fibrosis) and advanced glycation end-products (structural protein cross-linking molecules), play a key role. Aerobic exercise preserves endothelial function with aging by maintaining nitric oxide bioavailability via suppression of excessive superoxide-associated oxidative stress, and by inhibiting the development of chronic low-grade vascular inflammation. Recent work from our laboratory supports the novel hypothesis that aerobic exercise may exert these beneficial effects by directly inducing protection to aging arteries against multiple adverse factors to which they are chronically exposed. Regular aerobic exercise should be viewed as a "first line" strategy for prevention and treatment of arterial aging and a vital component of a contemporary public health approach for reducing the projected increase in population CVD burden.

High-Intensity Interval Training Versus Moderate-Intensity Continuous Training in the Prevention/Management of Cardiovascular Disease

“…Reference lists of all articles obtained from this search were also examined for additional relevant articles. The inclusion/exclusion criteria for all articles in this review were such that they needed to provide information 6 relating to the physiological responses induced by HIIT and/or MICT with particular relevance to the prevention and/or management of cardiovascular disease.…”

“…[1][2][3][4][5] Indeed, declines in cardiorespiratory fitness and endothelial function are greatly implicated in the development and progression of CVDs. 6 Low levels of cardiorespiratory fitness are associated with an increased risk for cardiovascular and all-cause mortality in people of all ages, 2 while impaired endothelial function results in a chronic inflammatory process accompanied by a loss of antithrombotic factors and an increase in vasoconstrictor and prothrombotic factors in addition to abnormal vasoreactivity. This sequence leads, leading to atherosclerosis and, in turn, cardiovascular events.…”

The effects of resistance exercise training on arterial stiffness in metabolic syndrome

“…The mechanisms behind these improvements likely reflect enhanced endothelial function (a key component of AS), along with changes in the intrinsic properties of the vessel wall (smooth muscle content, collagen and elastin properties). Such adaptations in elastin and collagen have been confirmed in animal studies after exercise interventions (Fleenor et al 2010; Kingwell et al 1997; Matsuda et al 1993; Seals 2014). Another mechanism, which may influence vascular adaptations to RT, is the increased pressures caused by Valsalva-like maneuvers.…”

Nutrition and other lifestyle influences on arterial aging

“…However, these arteries stiffen progressively with aging (Avolio et al, 1985). This forces the heart to work harder (pushing against stiff arteries), and leads to higher blood pressure, as well as greater pulsatile flow that damages other tissues, especially high-perfusion organs such as the brain, kidneys and eyes (Seals, 2014) (Figure 2). Age-related declines in arterial elasticity result primarily from structural changes that occur in the arterial wall as we age, including increases in collagen (fibrosis), fragmentation and degradation of elastin, and the formation of advanced glycation end-products—all of which reduce elasticity and confer stiffness (Cavalcante et al, 2011).…”