Vascular Ageing and Aerobic Exercise

Abstract

Impairment of vascular function, in particular endothelial dysfunction and large elastic artery stiffening, represents a major link between ageing and cardiovascular risk. Clinical and experimental studies identified numerous mechanisms responsible for age-related decline of endothelial function and arterial compliance. Since most of these mechanisms are related to oxidative stress or low-grade inflammation, strategies that suppress oxidative stress and inflammation could be effective for preventing age-related changes in arterial function. Indeed, aerobic physical activity, which has been shown to improve intracellular redox balance and mitochondrial health and reduce levels of systemic inflammatory markers, also improves endothelial function and arterial distensibility and reduces risk of cardiovascular diseases. The present paper provides a brief overview of processes underlying age-related changes in arterial function, as well as the mechanisms through which aerobic exercise might prevent or interrupt these processes, and thus attenuate vascular ageing.

Keywords: aerobic exercise; ageing; arterial stiffness; endothelial dysfunction.

Figure 1

Mechanisms through which ageing deteriorates endothelial function (grey rectangles) and mechanisms through which chronic aerobic exercise improves endothelial dysfunction (white rectangles). ROS: reactive oxygen species; NO: nitric oxide; BH4—tetrahydrobiopterin; eNOS: endothelial nitric oxide synthase; NADPH: nicotinamide-adenine-dinucleotide phosphate; SOD: superoxide dismutase; GTH: glutathione; mt: mitochondrial; EPCs: endothelial progenitor cells; NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells; IL: interleukin; TNF-α: tumor necrosis factor-α.

Figure 2

Mechanisms through which ageing deteriorates arterial compliance (grey rectangles) and mechanisms through which chronic aerobic exercise improves arterial compliance (white rectangles). MMP: matrix-metalloproteinase; AGEs: advanced glycation end products; Ang II: angiotensin II; ET-1: endothelin-1; NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells; TGF-β1: transforming growth factor-β1; SMCs: smooth muscle cells; ROS: reactive oxygen species.