The study here measures vascular function in athletic and sedentary older individuals, finding that, as one might expect, long-term exercise produces a slower pace of decline in the ability of blood vessels to respond to circumstances by relaxing or contracting as needed. The molecular damage of aging impairs this function, and blood vessels stiffen, leading to rising blood pressure. Aerobic exercise slows the pace of many of the aspects of aging, this one included, though it doesn't appear to extend overall life span in mouse studies. Rather the period of life spent healthy is extended. Whether or not this holds up in humans is an interesting question; epidemiological studies show correlations between regular exercise and something like five years of additional life expectancy. People are not mice, and these two approaches to scientific discovery can't really be directly compared to one another, unfortunately.
Impaired vascular function as a result of aging occurs due to the coalition of environment, oxidative stress, and inflammation. These factors result in reduced nitric oxide (NO) bioavailability, causing a failure of the vasculature to dilate in response to increases in shear stress during hyperaemia. Furthermore, vascular structure is also compromised with age as wall stiffness increases, reducing flexibility. Therefore, vascular dysfunction promotes cardiovascular disease (CVD) risk and contributes both to a reduction in health span and overall life expectancy. Given this premise there is an increasingly important but unmet need for interventions which aim to reduce inflammation and oxidative stress, while developing an environment conducive to vascular function.
Modifiable lifestyle factors, such as increased physical activity (PA) and/or exercise have been advocated to reduce vascular impairment and restore NO dependent vasodilatation, even in apparently healthy older cohorts. Multiple lines of evidence, including both human and pre-clinical models demonstrate that those individuals who are regularly active enjoy superior vascular function, with lower levels of systemic inflammation and oxidative stress. Vascular function, or specifically endothelial function, is commonly assessed non-invasively using the flow mediated dilation (FMD) technique. As cardiovascular events can be independently predicted by endothelial compliance, FMD has emerged as a conventional method to determine vascular function.
We conducted a systematic review and meta-analysis of controlled studies examining flow mediated dilatation (FMD) of athletic older persons and otherwise healthy sedentary counterparts to (i) compare FMD as a determinant of endothelial function between athletes and sedentary individuals and, (ii) summarize the effect of exercise training on FMD in studies of sedentary aging persons. Studies were identified from systematic search of major electronic databases. Thirteen studies with age ranges from 62 to 75 years underwent quantitative pooling of data. The majority of study participants were male.
Older athletes had more favorable FMD compared with sedentary controls. There was no significant improvement in the vascular function of sedentary cohorts following a period of exercise training. However, there was a significant increase in artery baseline diameter from pre to post intervention. In addition, there was no significant difference in endothelial independent vasodilation between the trained and sedentary older adults, or from pre to post exercise intervention. In conclusion, long-term aerobic exercise appears to attenuate the decline in endothelial vascular function, a benefit which is maintained during chronological aging. However, currently there is not enough evidence to suggest that exercise interventions improve vascular function in previously sedentary healthy older adults.