Key result
Regular exercise promotes endothelial function, prevents endothelial senescence, and modulates endothelial progenitor cells to offset the vascular ageing process.
Why the study?
Does exercise offset vascular ageing and improve endothelial reparative processes?
Does exercise offset vascular ageing and improve endothelial reparative processes?
Regular exercise offsets vascular ageing by promoting endothelial function and enhancing cellular reparative processes via endothelial progenitor cells.
Supports exercise for vascular health in practice; leaves open need for RCTs to confirm outcomes in ageing.
Ageing is associated with an increased risk of developing noncommunicable diseases (NCDs), such as diabetes and cardiovascular disease (CVD). The increased risk can be attributable to increased prolonged exposure to oxidative stress. Often, CVD is preceded by endothelial dysfunction, which carries with it a proatherothrombotic phenotype. Endothelial senescence and reduced production and release of nitric oxide (NO) are associated with "vascular ageing" and are often accompanied by a reduced ability for the body to repair vascular damage, termed "reendothelialization." Exercise has been repeatedly shown to confer protection against CVD and diabetes risk and incidence. Regular exercise promotes endothelial function and can prevent endothelial senescence, often through a reduction in oxidative stress. Recently, endothelial precursors, endothelial progenitor cells (EPC), have been shown to repair damaged endothelium, and reduced circulating number and/or function of these cells is associated with ageing. Exercise can modulate both number and function of these cells to promote endothelial homeostasis. In this review we look at the effects of advancing age on the endothelium and these endothelial precursors and how exercise appears to offset this "vascular ageing" process.
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Ross et al. (2015) conducted a review in Vascular ageing and cardiovascular disease. Exercise was evaluated. Regular exercise promotes endothelial function, prevents endothelial senescence, and modulates endothelial progenitor cells to offset the vascular ageing process.
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