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-keto-PGF1α 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 exercise-induced 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., J. A. Zoladz ... [et al.]., and Obsahuje seznam literatury
In this experiment we studied the effect of different pedalling rates during cycling at a constant power output (PO) 132±31 W (mean±S.D.), corresponding to 50 % V02 max, on the oxygen uptake and the magnitude of the slow component of V02 kinetics in humans. The PO corresponded to 50 % of V02 max, established during incremental cycling at a pedalling rate of 70 rev.min-1. Six healthy men aged 22.2 ±2.0 years with V02 max 3.89 ±0.92 l.min-1, performed on separate days constant PO cycling exercise lasting 6 min at pedalling rates 40, 60, 80, 100 and 120 rev.min-1, in random order. Antecubital blood samples for plasma lactate [La]pi and blood acid-base balance variables were taken at 1 min intervals. Oxygen uptake was determined breath-by-breath. The total net oxygen consumed throughout the 6 min cycling period at pedalling rates of 40, 60, 80, 100 and 120 rev.min-1 amounted to 7.727± 1.197, 7.705± 1.548, 8.679± 1.262, 9.945± 1.435 and 13.720± 1.862 1, respectively for each pedalling rate. The VO2 during the 6 min of cycling only rose slowly by increasing the pedalling rate in the range of 40-100 rev.min-1. This increase, was 0.142 1 per 20 rev.min-1 on the average. Plasma lactate concentration during the sixth minute of cycling changed little within this range of pedalling rates: the values were 1.83 ±0.70, 1.80 ± 0.48, 2.33 ±0.88 and 2.52 ±0.33 mmoLl-1. The values of [La]pi reached in the 6th minute of cycling were not significantly different from the pre-exercise levels. Blood pH was also not affected by the increase of pedalling rate in the range of 40-100 rev.min-1. However, an increase of pedalling rate from 100 to 120 rev.min-1 caused a sudden increase in the VO2 amounting to 0.747 1 per 20 rev.min-1, accompanied by a significant increase in [La]pj from 1.21 ±0.26 mmol.l-1 in pre-exercise conditions to 5.92±2.46 mmol.l-1 reached in the 6th minute of cycling (P<0.01). This was also accompanied by a significant drop of blood pH, from 7.355 ±0.039 in the pre-exercise period to 7.296 ± 0.060 in the 6th minute of cycling (P<0.01). The mechanical efficiency calculated on the basis of the net VO2 reached between the 4th and the 6th minute of cycling amounted to 26.6 ±2.7, 26.4±2.0, 23.4±3.4, 20.3 ±2.6 and 14.7±2.2 %, respectively for pedalling rates of 40, 60, 80,100 and 120 rev.min-1. No significant increase in the VO2 from the 3rd to the 6th min (representing the magnitude of the slow component of V02 kinetics) was observed at any of the pedalling rates (-0.022±0.056, -0.009±0.029, 0.012±0.073, 0.030±0.081 and 0.122±0.176 l.min-1 for pedalling rates of 40, 60, 80, 100 and 120 rev.min-1, respectively). Thus a significant increase in [La]pi and a decrease in blood pH do not play a major role in the mechanism(s) responsible for the slow component of VO2 kinetics in
humans.