Vascular Ageing and Exercise: Focus on Cellular Reparative Processes

Abstract

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.

Figure 1

The effect of age and exercise on the endothelium. SIRT1: Sirtuin 1, TAC: total antioxidant capacity, NO: nitric oxide, ROS: reactive oxygen species, and EMP: endothelial microparticles.

Figure 2

The effects of age and exercise on EPC-mediated vascular repair and endothelial function. Ageing causes the reduced signaling between CXCR4 and Janus Kinase-2 (JAK-2), as well as being associated with a reduced antioxidant capacity. Exercise mobilizes EPCs from bone marrow and rescues the signaling between CXCR4 and JAK-2, as well as stimulating production of antioxidants Sirtuin 1 (SIRT1) and superoxide dismutase (SOD). EPC-mediated repair of endothelium leads to improved endothelial function.