INCREASED PROSTACYCLIN PRODUCTION DURING EXERCISE IN UNTRAINED AND TRAINED MEN - EFFECT OF LOW-DOSE ASPIRIN

The in fluence of a submaximal exercise on urinary 2,3-dinor-6-ketoprostaglandin F-1 alpha (2,3-dinor-6-keto-PGF(1 alpha)), 2,3-dinor-thromboxane B-2 (2,3-dinor-TxB(2)), and prostaglandin E(2) excretion and on platelet aggregation was compared in untrained and trained subjects before and after low-dose aspirin administration (50 mg/day, 7 days). 2,3-Dinor-TxB(2) excretion was significantly higher in the athletes at rest (P < 0.05). Submaximal exercise selectively increased 2,3-dinor-6-keto-PGF(1 alpha), excretion without affecting 2,3-dinor-TxB(2) or prostaglandin E(2) excretion rates or platelet aggregation. Low-dose aspirin inhibited platelet aggregation and 2,3-dinor-TxB(2) excretion but reduced 2,3-dinor-6-keto-PGF(1 alpha), by only 24% in the untrained and by 51% in the trained subjects (P < 0.05). After low-dose aspirin administration, the selective stimulatory effect of submaximal exercise on urinary 2,3-dinor-6-keto-PGF(1 alpha), excretion was even more pronounced than before. The ratio of 2,3-diner-6-keto-PGF(1 alpha), to 2,3-dinor-TxB(2) was increased by exercise; this effect was significantly enhanced by low-dose aspirin (P < 0.05). Our results suggest that the stimulatory effect of submaximal exercise on prostacyclin production is mostly due to an activation of prostacyclin synthesis from endogenous precursors rather than the result of an enhanced endoperoxide shift from activated platelets to the endothelium. This effect is potentiated by low-dose aspirin pretreatment, indicating that 50 mg/day of aspirin do not impair exercise-induced endothelial prostacyclin production.