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

Abstract

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 (PGI2), as assessed by plasma 6-keto-PGF1α 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 ±8.9kg; BMI, 23.48±2.17kg x m-2; and maximal oxygen uptake (VO2max), 46.1±4.0ml x kg-1 x min-1. Plasma 6-keto-PGF1a concentrations were measured in venous blood samples taken prior to the exercise and at exhaustion (at VO2max) before and after completing the training protocol. On average, the training resulted in a significant increase in VO2max (p=0.03), power output at VO2max (p=0.001) and a significant increase (p=0.05) in the net-exercise-induced increase in plasma 6-keto-PGF1α concentration (Δ6-keto-PGF1α i.e., the difference between the end-exercise and pre-exercise 6-keto-PGF1α concentrations). No effect of training on the basal PGI2 concentration was found. Interestingly, within the study sample (n=12), two subgroups could be defined with a differential pattern of response with respect to Δ6-keto-PGF1α concentrations. In one subgroup (n=7), a significant increase in Δ6-keto-PGF1α concentration after training was found (p<0.02) (responders). This enhancement in the exercise-induced PGI2 release was accompanied by a significant (p<0.05) increase in VO2max after training. In contrast, in another subgroup (n=5), there was no observed effect of training on the Δ6-keto-PGF1a concentration and the VO2max after training (non-responders). In both of these subgroups, training did not influence the basal PGI2 concentration.In conclusion, the endurance training resulted in the adaptive augmentation of the systemic release of PGI2 in response to exercise, which plays a role in the training-induced increase in VO2max in young, healthy men. The impairment of the training-induced augmentation of PGI2 release in response to exercise demonstrated in the non-responders subgroup may predispose them to increased cardiovascular risk during vigorous exercise.