Exercise-induced prostacyclin release positively correlates with VO2max in young healthy men

In this study we have evaluated the effect of maximal incremental cycling exercise (IE) on the systemic release of prostacyclin (PGI2), assessed as plasma 6-keto-PGF1α concentration in young healthy men. Eleven physically active – untrained men (mean ± S.D.) aged 22.7 ± 2.1 years; body mass 76.3 ± 9...

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Veröffentlicht in:Physiological research 2009, p.229-238
Hauptverfasser: Zoladz, JA, Majerczak, J, Duda, K, Chłopicki, S
Format: Artikel
Sprache:eng
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Zusammenfassung:In this study we have evaluated the effect of maximal incremental cycling exercise (IE) on the systemic release of prostacyclin (PGI2), assessed as plasma 6-keto-PGF1α concentration in young healthy men. Eleven physically active – untrained men (mean ± S.D.) aged 22.7 ± 2.1 years; body mass 76.3 ± 9.1 kg; BMI 23.30 ± 2.18 kg · m-2; maximal oxygen uptake (VO2max) 46.5 ± 3.9 ml · kg-1 · min-1, performed an IE test until exhaustion. Plasma concentrations of 6-keto-PGF1α, lactate, and cytokines were measured in venous blood samples taken prior to the exercise and at the exhaustion. The net exercise-induced increase in 6-keto-PGF1α concentration, expressed as the difference between the end-exercise minus pre-exercise concentration positively correlated with VO2max (r=0.78, p=0.004) as well as with the net VO2 increase at exhaustion (r=0.81, p=0.003), but not with other respiratory, cardiac, metabolic or inflammatory parameters of the exercise (minute ventilation, heart rate, plasma lactate, IL-6 or TNF-α concentrations). The exercise-induced increase in 6-ketoPGF1α concentration was significantly higher (p=0.008) in a group of subjects (n=5) with the highest VO2max when compared to the group of subjects with the lowest VO2max, in which no increase in 6-keto-PGF1α concentration was found. In conclusion, we demonstrated, to our knowledge for the first time, that exerciseinduced release of PGI2 in young healthy men correlates with VO2max, suggesting that vascular capacity to release PGI2 in response to physical exercise represents an important factor characterizing exercise tolerance. Moreover, we postulate that the impairment of exercise-induced release of PGI2 leads to the increased cardiovascular hazard of vigorous exercise.
ISSN:0862-8408
1802-9973
DOI:10.33549/physiolres.931403