O2 Dependent Contributions of Prostaglandins (PGI2 PGE2) to Exercise Hyperaemia in Young (Y) and Older (O) Men

Abstract

We have shown that breathing 40% O2 and cyclooxygenase (COX) inhibition attenuate exercise hyperaemia to similar extents in Y and O men. PGI2 synthesis is generally attributed to endothelium and PGE2, to skeletal muscle fibres. Thus, in recreationally active Y (18‐25 yrs; n=12) and O (60‐76 yrs; n=12) males, we assayed venous efflux of PGs by ELISA following rhythmic and static handgrip contractions (60% MVC for 3 min, or exhaustion), during air breathing, 40%O2, and after COX blockade with aspirin (A) in a cross over design. In Y males, forearm vascular conductance (FVC) increased from 0.06±0.01 to 0.56±0.06 conductance units (CU) after rhythmic contractions in P/air, but to only 0.44±0.04*, 0.44±0.04* and 0.45±0.03* CU in P/O2, A/air and A/O2 (*P < 0.05 vs P/air). Meanwhile, PGI2 increased from 18.0±6.1 to 349.8±61.7 pg/dl/min in P/air, but to 94.3±26.5*, 44.7±18.4* and 50.8±11.2* pg/dl/min in P/O2, A/air and A/O2, while PGE increased from 20.5±6.6 to 559.5±133.4 pg/dl/min in P/air, but to 189.8±33.8*, 165.4±52.9* and 170.3±43.0* pg/dl/min in P/O2, A/air and A/O2. Similarly in O males, FVC increased from 0.08±0.02 to 0.64±0.06 CU in P/air after rhythmic contraction, but to 0.44±0.06*, 0.46±0.05* and 0.52±0.06* CU in P/O2, A/air and A/O2. Meanwhile, PGI2 increased from 14.4±6.8 to 284.4±43.4 in P/air but to 84.6±25.9*, 52.8±20.3* and 74.6±38.1* pg/dl/min in P/O2, A/air and A/O2, while PGE increased from 16.6±6.6 to 781.6±192.5 in P/air, but to 368.8±188.8*, 357.9±106.4* and 382.3±131.0* pg/dl/min in P/O2, A/air and A/O2. Static contractions yielded similar data. Thus, we propose that PGI2 and PGE2 are released in O2‐dependent ways from endothelium and muscle fibres respectively and contribute to exercise hyperaemia in both Y and O men.