Key result
Cyclooxygenase inhibition with aspirin attenuated postcontraction increases in forearm vascular conductance by 17-27% and prostaglandin efflux by 50-85% in young and older men (p < 0.05).
Why the study?
The role of prostaglandins in exercise hyperemia remains controversial, specifically regarding whether their release is oxygen-dependent or affected by aging.
Does COX inhibition with aspirin and/or hyperoxia reduce postexercise hyperemia and prostaglandin release in recreationally active men?
Does COX inhibition with aspirin and/or hyperoxia reduce postexercise hyperemia and prostaglandin release in recreationally active men?
Prostaglandins significantly contribute to postcontraction hyperemia in both young and older men, and their generation appears dependent on contraction-induced falls in tissue oxygenation.
Aspirin may blunt postcontraction vasodilation; hypothesis-generating for prostaglandin contributions in exercise hyperemia and requires patient studies.
The role of prostaglandins (PGs) in exercise hyperemia is controversial. We tested their contributions in moderate intensity forearm exercise, whether their release is oxygen (O2)-dependent or affected by aging. A total of 12 young (21 ± 1 years) and 11 older (66 ± 2 years) recreationally active men performed rhythmic and isometric handgrip contractions at 60% maximum voluntary contraction for 3 min during air breathing after placebo, after cyclooxygenase (COX) inhibition with aspirin, while breathing 40% O2 and during their combination (aspirin + 40% O2). Forearm blood flow (FBF) was recorded with venous occlusion plethysmography (forearm vascular conductance (FVC): FBF/mean arterial pressure). Venous efflux of PGI2 and PGE2 were assessed by immunoassay. Postcontraction increases in FVC were similar for rhythmic and isometric contractions in young and older men, and accompanied by similar increases in efflux of PGI2 and PGE2. Aspirin attenuated the efflux of PGI2 by 75%–85%, PGE2 by 50%–70%, (p < .05 within group; p > .05 young versus. older), and postcontraction increases in FVC by 22%–27% and 17%–21% in young and older men, respectively (p < .05 within group and young versus. older). In both age groups, 40% O2 and aspirin + 40% O2 caused similar inhibition of the increases in FVC and efflux of PGs as aspirin alone (p < .05 within group). These results indicate that PGs make substantial contributions to the postcontraction hyperemia of rhythmic and isometric contractions at moderate intensities in recreationally active young and older men. Given PGI2 is mainly released by endothelium and PGE2 by muscle fibers, we propose PG generation is dependent on the contraction-induced falls in O2 at these sites.
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Junejo et al. (2020) studied Healthy (recreationally active) (n=23). Aspirin and 40% O2 breathing vs. Placebo and air breathing was evaluated on Postcontraction increases in forearm vascular conductance (FVC) and venous efflux of PGI2 and PGE2 (p=< .05). Cyclooxygenase inhibition with aspirin attenuated postcontraction increases in forearm vascular conductance by 17-27% and prostaglandin efflux by 50-85% in young and older men (p < 0.05).
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