Abstract
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.
Highlights
There is substantial evidence that prostaglandins (PGs) contribute to exercise hyperemia, but there is conflicting evidence
The observation that the attenuating effect of COX inhibition on hyperemia during rhythmic contraction was transient, whereas that of NOS inhibition was sustained led to the proposal that the contribution of PGs to exercise hyperemia is independent of nitric oxide (NO), and can be compensated for by other dilator/s (Schrage, Joyner, & Dinenno, 2004)
We report the novel finding that venous effluxes of PGI2 and PGE2 are increased in older men following both rhythmic and isometric contraction at 60% maximum voluntary contraction (MVC)
Summary
There is substantial evidence that prostaglandins (PGs) contribute to exercise hyperemia, but there is conflicting evidence. A possible explanation for these disparities is that they reflect differences between studies in exercise intensity and a possible fall in partial pressure of O2 (PO2) within muscles For, those which suggested a relatively minor contribution of PGs to exercise hyperemia used exercise intensities of ≤20% maximum (Mortensen et al, 2007; Schrage et al, 2004; Shoemaker et al, 1996), whereas those suggesting a substantial contribution used intensities of ≥60% maximum (Kilbom & Wennmalm, 1976; Win & Marshall, 2005). As muscle blood flow is limited persistently during isometric, but intermittently during rhythmic contractions (Kagaya & Homma, 1997; McNeil, Allen, Olympico, Shoemaker, & Rice, 2015; Van Beekvelt, Shoemaker, Tschakovsky, Hopman, & Hughson, 2001), the fall in tissue PO2 during isometric contraction may have greater effects on PG synthesis
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