Regular exercise-induced increased number and activity of circulating endothelial progenitor cells attenuates age-related decline in arterial elasticity in healthy men

Chronic heart failure and aging – effects of exercise training on endothelial function and mechanisms of endothelial regeneration: Results from the Leipzig Exercise Intervention in Chronic heart failure and Aging (LEICA) study

“…16,36 The present results are also comparable to previous trials showing improved vascular function with exercise interventions in sedentary healthy subjects, thus attenuating the age-related decline of circulating EPCs. [37][38][39] In contrast to the mentioned previous studies, we have demonstrated in one study comprising a larger and age-stratified sample size that all subjects with impaired endothelial function and reduced number and function of EPCs at baseline (young and old CHF patients, and in part old RCs), improved these variables through regular supervised exercise for four weeks.…”

Atrial fibrillation is associated with different levels of physical activity levels at different ages in men

“…Exercise has positive effects on traditional cardiovascular risk factors such as hypertension, diabetes, hypercholesterolaemia and obesity 19 20. Furthermore, it has a positive effect on age-related decline in arterial elasticity 21. All these factors protect against AF.…”

Effects of physical activity on endothelial progenitor cells (EPCs)

“…These findings are prominent in sedentary old population (Taddei et al, 1995; Gerhard et al, 1996), since the effects of aging on EPCs disability are related to both the senescence of EPCs and the down-regulation of pro-angiogenic factors like HIF-1 and VEGF (Torella et al, 2004; Leosco et al, 2007a). Interestingly, physical exercise can prevent and reverse age-related endothelial dysfunction, representing a valid strategy to stimulate EPCs in old subjects (DeSouza et al, 2000; Smith et al, 2003; Heiss et al, 2005; Hoetzer et al, 2007; Yang et al, 2013). In addition, physical exercise leads to a significant reduction of myelosuppressive and pro-inflammatory cytokines, like C-reactive protein (CRP) (Szmitko et al, 2003) and tumor necrosis factor-α (TNF-α) (Agnoletti et al, 1999), thus exerting also an anti-inflammatory role.…”