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 |
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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. |
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ISSN: | 0862-8408 1802-9973 |
DOI: | 10.33549/physiolres.931403 |