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Relationship between exhaled and inhaled nitric oxide and exercise-induced hypoxemia Sheel, Andrew William


The consensus in the literature is that exercise-induced hypoxemia (EIH) occurs secondary to ventilation-perfusion (VA/Q) inequalities and diffusion limitations resulting from elevated pulmonary pressures causing the development of interstitial pulmonary edema, or decreased pulmonary transit time in the pulmonary vasculature. Endogenously produced pulmonary nitric oxide (NO) has been hypothesized to have several physiological functions including VA/Q matching and maintenance of low pulmonary vascular resistance. Respiratory derived NO is detectable in exhaled gases. Inhaled NO, a selective pulmonary vasodilator is used in the treatment of diseases characterized by pulmonary hypertension and hypoxemia. Short-term inhalation of NO causes selective pulmonary vasodilation without any systemic effects. Given that athletes with EIH are thought to have altered pulmonary hemodynamics during exercise, the relationship between endogenously produced and exogenously delivered NO and EIH was examined in two separate studies. It was hypothesized that subjects with EIH would have a decreased production rate of NO (VNO) compared to subjects who maintained normal oxyhemoglobin saturation (SaO2) and that SaO2 would be correlated with VNO. A group of highly-trained male cyclists (n = 18), some of whom develop EIH performed a maximal cycle test. VNO was determined during the cycle test. No significant differences were observed between those with and those without EIH. There was also no observed linear relationship between delta SaO2 and delta VNO. It can be concluded that NO present in exhaled air is not related to the etiology o f EIH. In a subsequent study, delivery of NO was accomplished using highly trained male cyclists (n = 7) with EIH who performed four 5-min cycle tests at VO2max under conditions of normoxia (N), normoxia + 20 ppm nitric oxide (N/NO), hypoxia (H), and hypoxia + 20 ppm nitric oxide (H/NO). It was hypothesized that: (i) inhaled NO would reverse EIH during normoxia, and (ii) inhaled NO would improve arterial oxygenation during hypoxia. Inhalation of NO during normoxic or hypoxic conditions did not significantly affect gas exchange, cardiorespiratory variables, or power output. These findings imply that pulmonary capillary blood volume reaches a maximal morphological limit during exercise and further dilation is not possible.

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