Endurance training increases exercise-induced prostacyclin release in young, healthy men--relationship with VO2max.

In the present study, we evaluated the effect of 5 weeks of moderate-intensity endurance training on the basal and exercise-induced systemic release of prostacyclin (PGI(2)), as assessed by plasma 6-keto-PGF(1 alpha) concentration. Twelve physically active young men with the following characteristics participated in this study (the mean +/- SD): age, 22.7 +/- 2.0 years; body mass, 76.8 +/- 8.9 kg; BMI, 23.48 +/- 2.17 kg x m(-2); and maximal oxygen uptake (VO(2 max)), 46.1 +/- 4.0 ml x kg(-1) x min(-1). Plasma 6-keto-PGF(1 alpha) concentrations were measured in venous blood samples taken prior to the exercise and at exhaustion (at VO(2 max)) before and after completing the training protocol. On average, the training resulted in a significant increase in VO(2 max) (p = 0.03), power output at VO(2 max) (p = 0.001) and a significant increase (p = 0.05) in the net-exercise-induced increase in plasma 6-keto-PGF(1 alpha) concentration (Delta 6-keto-PGF(1 alpha) i.e., the difference between the end-exercise and pre-exercise 6-keto-PGF(1 alpha) concentrations). No effect of training on the basal PGI(2) concentration was found. Interestingly, within the study sample (n = 12), two subgroups could be defined with a differential pattern of response with respect to Delta 6-keto-PGF(1 alpha) concentrations. In one subgroup (n = 7), a significant increase in Delta 6-keto-PGF(1 alpha) concentration after training was found (p < 0.02) (responders). This enhancement in the exercise-induced PGI(2) release was accompanied by a significant (p < 0.05) increase in VO(2 max) after training. In contrast, in another subgroup (n = 5), there was no observed effect of training on the Delta 6-keto-PGF(1 alpha) concentration and the VO(2 max) after training (non-responders). In both of these subgroups, training did not influence the basal PGI(2) concentration. In conclusion, the endurance training resulted in the adaptive augmentation of the systemic release of PGI(2) in response to exercise, which plays a role in the training-induced increase in VO(2 max) in young, healthy men. The impairment of the training-induced augmentation of PGI(2) release in response to exercise demonstrated in the non-responders subgroup may predispose them to increased cardiovascular risk during vigorous exercise.