Key result
Selective inhibition of COX-2 with rofecoxib or COX-1 with aspirin did not affect systemic prostacyclin synthesis after physical exercise in trained healthy volunteers.
Why the study?
Does selective COX-2 inhibition with rofecoxib compared to aspirin affect systemic prostacyclin synthesis and platelet function after exercise in healthy volunteers?
RCT (n=10)
Double-blind
Cross-over
Does selective COX-2 inhibition with rofecoxib compared to aspirin affect systemic prostacyclin synthesis and platelet function after exercise in healthy volunteers?
In healthy volunteers, selective COX-1 or COX-2 inhibition does not alter systemic prostacyclin synthesis following physical exercise, despite differential effects on thromboxane B2 levels.
No effect of COX-1 or COX-2 inhibition on post-exercise prostacyclin in healthy volunteers; extends mechanistic understanding of eicosanoid responses during exercise.
To test the hypothesis that selective inhibition of cyclooxygenase (COX)-2 would result in exercise-induced platelet activation by causing a shift in the endogenous thromboxane (TX)/prostacyclin balance, a double blind, randomized study comparing aspirin (300 mg/d) with rofecoxib (25 mg/d) (cross-over design, 14 days washout between treatments) in n = 10 trained healthy volunteers was carried out. Physical exercise resulted only in a minor platelet activation, as reflected by the expression of basal or ADP-stimulated platelet activation markers or basal plasma concentrations of TXB(2). Aspirin significantly reduced TXB(2) in plasma while rofecoxib significantly increased TXB(2) in urine. Although no increase in systemic prostacyclin concentration was observed, there was a significant exercise-related increase in both platelet cAMP and cGMP without any drug-related effects. It is concluded that, in trained healthy volunteers, selective inhibition of COX-1 (aspirin) or COX-2 (rofecoxib) does not affect systemic prostacyclin synthesis after physical exercise. However, our data do not exclude the possibility that in subjects at risk for atherothrombotic complications (e.g. patients with advanced atherosclerotic disease) COX-2 inhibitors may result in platelet activation by inhibiting endothelial prostacyclin formation.
No takes yet. Share an insight, caveat, or question.
Weber et al. (2007) conducted an RCT in Healthy (n=10). Rofecoxib vs. Aspirin (300 mg/d) was evaluated on Systemic prostacyclin synthesis after physical exercise. Selective inhibition of COX-2 with rofecoxib or COX-1 with aspirin did not affect systemic prostacyclin synthesis after physical exercise in trained healthy volunteers.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: