Contribution of oxygen-dependent mechanisms to vascular responses of exercise in young and older men: the role of prostaglandins and adenosine

Previous work suggests vasodilating prostaglandins (PGs) are released during isometric handgrip exercise in an O$_2$-dependent manner in young men. This project investigates their contribution to the exercise hyperaemia of isometric and rhythmic handgrip contraction performed by healthy, recreationally-active young and older men. Hyperoxia (40% O$_2$), aspirin, and their combination equally attenuated exercise and post-exercise hyperaemia, and venous efflux of PGE$_2$ and PGI$_2$ in both age groups: efflux of these PGs was not attenuated with age, but their contribution to the hyperaemic response was. Further, the release of COX products evoked reflex vasoconstriction in an O$_2$-dependent manner. Moreover, 40% O$_2$, aspirin, and their combination equally inhibited the exercise-evoked vasoconstriction in both age groups. However, both the exercise-evoked attenuation in perfusion of resting skeletal muscles and the contribution of COX products were attenuated with age. Additional experiments showed that adenosine contributes to the hyperaemia of electrically evoked isometric twitch contractions in an O$_2$-dependent manner; adenosine may contribute to the increase in the concentrations of vasodilating PGs. Importantly, unlike 60% and 100% O$_2$, 40% O$_2$ did not attenuate acetylcholine-evoked endothelium-dependent dilatation in either age group, supporting the argument that the effect of 40% O$_2$ during exercise is independent of hyperoxia-related oxidative stress