Exercise-induced arterial hypoxemia (EIAH), defined as a significant decrease in oxygen saturation (<95%) during maximal and sub-maximal exercise, is a phenomenon observed in moderately and highly trained athletes. The consequences of EIAH on exercise performance relate to its negative influence on maximal O 2 uptake (VO 2 max ) and impairment of oxygen delivery. The causes of EIAH are yet to be completely elucidated. Proposed mechanisms include ventilation/perfusion inequality, relative

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... r hypoventilation, right-to-left shunt, and diffusion limitation. We hypothesized that development of interstitial pulmonary edema during maximal exercise triggers the physiological mechanisms leading to EIAH. Eleven subjects, who had previously developed EIAH during a similar testing protocol, performed an incremental cycling or running protocol to exhaustion, and pre-and post-exercise lungs scanned using computed tomography. Scans were analyzed both qualitatively and quantitatively for the development of pulmonary edema. We employed two different procedures for lung density assessment, specifically, lung sampling technique (Method A) and whole lung measurements (Method B). The lung density measurements were as follows: 0.088±0.008 g/cm 3 pre-exercise, 0.090±0.008 g/cm 3 post-exercise (p=0.27) with Method A, and 0.190±0.018 g/cm 3 pre-exercise, 0.178±0.010 g/cm 3 post-exercise (p=0.94) with Method B. These results do not support the presence of interstitial pulmonary edema in individuals known to develop EIAH. Development of interstitial pulmonary edema cannot be conclusively identified as a significant cause of EIAH in moderately and highly trained athletes.