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Abstract

We tested the hypothesis that decrements in arterial oxyhaemoglobin saturation could be related to elevations in circulating endothelin-1 following 30 minutes of exercise at ventilatory threshold. Eight aerobically trained males (mean ± SEM: age 26.14 ± 1.77 years, height 182.36 ± 1 . 5 1 cm, mass 72.89 ± 2.62 kg) completed 2 maximal exercise tests (mean ± SEM: normoxia (n) 68.56 ± 2.06 mL.kg-¹min-¹; hypoxia (Fi02 0.14)(h) 53.88 ± 1.35 mL.kg-¹.min-¹), and two 30-minute steady state exercise protocols at the power achieved at threshold during maximal exercise tests (mean ± SEM: power (Watts) 257.14 ± 21.57 (n) 191.25 ± 10.79 (Fi02 0.14)(h); HR (bpm) 161.7 ± 5.34 (n) 156.6 ± 3.45 (h)). When participants exercised for 30 minutes at ventilatory threshold inspiring 14%02, a significant decrease in oxygen saturation (as measured by pulse oximetry) was observed, when compared to values in normoxia (80.2 ± 1.17 % (h) vs 94.12 ± 0.24 % (n); p<0.001). This desaturation was not accompanied by significant changes in plasma endothelin-1 (ET-1), big endothelin-1 (BigET-1) or nitric oxide (NO). Both pulmonary artery pressure (PAP) and oscillatory compliance (OC) were significantly greater following exercise (F[superscript omitted] = 4.74 p< 0.05), compared to pre-exercise values. These outcome variables were not different between normoxia and hypoxia. Plasma ET-1 or BigET-1 levels did not differ significantly over time or across conditions F[superscript omitted] = 4.74 p> 0.05). In conclusion, plasma ET-1 levels following 30-minutes of steady state exercise at ventilatory threshold are unrelated to decrements in oxyhaemoglobin saturation.