Open AccessExercise-induced prostacyclin release positively correlates with VO2max in young healthy men
Author(s) -
Jerzy A. Żołądź,
Joanna Majerczak,
Krzysztof Duda,
Stefan Chłopicki
Publication year - 2009
Publication title -
physiological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 70
eISSN - 1802-9973
pISSN - 0862-8408
DOI - 10.33549/physiolres.931403
Subject(s) - prostacyclin , medicine , vo2 max , endocrinology , heart rate , anaerobic exercise , venous blood , respiratory exchange ratio , chemistry , blood pressure , physical therapy
In this study we have evaluated the effect of maximalincremental cycling exercise (IE) on the systemic release ofprostacyclin (PGI2), assessed as plasma 6-keto-PGF1αconcentration in young healthy men. Eleven physically active –untrained men (mean ± S.D.) aged 22.7 ± 2.1 years; body mass76.3 ± 9.1 kg; BMI 23.30 ± 2.18 kg · m-2; maximal oxygenuptake (VO2max) 46.5 ± 3.9 ml · kg-1 · min-1, performed an IE testuntil exhaustion. Plasma concentrations of 6-keto-PGF1α, lactate,and cytokines were measured in venous blood samples taken priorto the exercise and at the exhaustion. The net exercise-inducedincrease in 6-keto-PGF1α concentration, expressed as thedifference between the end-exercise minus pre-exerciseconcentration 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 (minuteventilation, heart rate, plasma lactate, IL-6 or TNF-αconcentrations). The exercise-induced increase in 6-ketoPGF1α concentration was significantly higher (p=0.008) in a groupof subjects (n=5) with the highest VO2max when compared to thegroup of subjects with the lowest VO2max, in which no increase in6-keto-PGF1α concentration was found. In conclusion, wedemonstrated, to our knowledge for the first time, that exerciseinduced release of PGI2 in young healthy men correlates withVO2max, suggesting that vascular capacity to release PGI2 inresponse to physical exercise represents an important factorcharacterizing exercise tolerance. Moreover, we postulate thatthe impairment of exercise-induced release of PGI2 leads to theincreased cardiovascular hazard of vigorous exercise.