| Summary: | 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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