Prostaglandins (PGs) Contribute in an O2 Dependent Manner to Reflex Vasoconstriction in Exercise

Abstract

Our previous studies indicated that the contribution of locally released PGs to exercise hyperaemia is O2‐dependent. PGs have also been implicated in triggering the exercise reflex that induces sympathetic vasoconstriction in resting muscle. We have now tested whether this role is O2‐dependent in healthy young males (18‐21 yrs; n=11) who performed two 2‐min periods of isometric handgrip contractions at 60% MVC while breathing air after placebo (P), after COX blockade with 600 mg aspirin p.o. (A), or breathing 40% O2 in a cross‐over design. Contraction was followed by 2‐min post exercise circulatory occlusion (PECO) to trap metabolites, or no occlusion (NO‐PECO). Mean arterial blood pressure (ABP) and heart rate (HR) were monitored by Finometer and ipsilateral calf blood flow (CBF) by venous occlusion plethysmography at approximately 1‐min intervals during and after contraction. Baseline Calf vascular resistance (CVR: ABP/CBF) was not significantly different between conditions. In PECO trials, CVR increased by 17.84±6.84 RU during contraction with air breathing and P, but by only 5.49±1.77* and 6.69±2.64* RU with air/A and 40% O2/P respectively (*P < 0.01; vs. P.; Factorial ANOVA). During PECO the ΔCVR was maintained at 11.30±3.47, 4.34±1.49* and 7.35±2.27 RU (*P < 0.03). In NO‐PECO trials, CVR increased by 17.13±5.97, 5.83±1.92* and 6.23±3.16* RU with air/P, or air/A, and 40% O2/P respectively (*P < 0.03). During NO‐PECO, ΔCVR fell to 4.26±1.55, 4.47±1.64 and 4.74±2.94 RU for air/P, or air/A, and 40% O2/P respectively (P < 0.95). Our findings allow the novel proposal that the contribution of PGs synthesised in exercising muscle to the exercise reflex, notably to vasoconstriction in resting muscle, is O2‐dependent.