Perfusion of Intrapulmonary Arteriovenous Anastomoses Is Not Related to VO2max in Hypoxia and Is Unchanged by Oral Sildenafil.

Abstract

Background: Perfusion of intrapulmonary arteriovenous anastomoses (IPAVA) is increased during exercise and in hypoxia and is associated with variations in oxygen saturation (SPO2), resulting in blood bypassing the pulmonary microcirculation. Sildenafil is a pulmonary vasodilator that improves SPO2 and endurance performance in hypoxia. The purpose of this study was to determine if 50 mg sildenafil would reduce IPAVA perfusion (QIPAVA) and if the decrement in maximal exercise capacity (VO2max) in hypoxia is related to QIPAVA. We hypothesized that during progressive levels of hypoxia at rest (FIO2 = 0.21, 0.14, 0.12), sildenafil would increase SPO2 and reduce bubble score (estimate of QIPAVA) compared to placebo, and that the decrement in VO2max in hypoxia would be positively correlated with bubble score at rest in hypoxia. Materials and Methods: Fourteen endurance-trained men performed a graded maximal exercise test at sea level and at a simulated altitude of 3000 m, followed by two experimental visits where, after randomly ingesting sildenafil or placebo, they underwent agitated saline contrast echocardiography during progressive levels of hypoxia at rest. Results: All participants experienced a decrement in power output in hypoxia that ranged from 9% to 19% lower than sea level values. Compared to normoxia, bubble score increased significantly in hypoxia (p < 0.001) with no effect of sildenafil (p = 0.580). There was a negative correlation between SPO2 and bubble score (p < 0.001). The decrement in peak power output at VO2max in hypoxia was unrelated to IPAVA perfusion in resting hypoxia (p = 0.32). Several participants demonstrated QIPAVA greater than zero in room air, indicating that arterial hypoxemia may not be the sole mechanism for QIPAVA. Conclusion: These results indicate that the VO2max decrement caused by hypoxia is not related to QIPAVA and that sildenafil does not improve VO2max in hypoxia through modulation of QIPAVA.