| Summary: | The transport of O₂ from alveolus to pulmonary capillary has not typically been
thought of as the limiting step in aerobic performance. It has been demonstrated that fit
athletes are able to, at high workloads, elicit a decreased arterial O₂ saturation to levels
below 90%. This showed that healthy, fit individuals were able to exceed the capacity of
the pulmonary system, and was termed exercise-induced-hypoxemia (ETH). The possible
mechanisms for EIH include veno-arterial shunts, VA/QC mismatch, relative alveolar
hypoventilation, decreased pulmonary transit time, and pulmonary edema. This study
looked for increases in extravascular water (EW) after a 45-minute intense exercise bout
as evidence of pulmonary edema. The subjects were 8 highly trained males (mean ± SD:
age; 26.9 + 3.0 years, height; 179.9 ± 5.7 cm, weight; 76.1 ±6.5 kg) who performed three
tests used to indicate differences pre and post exercise. The testing involved
measurements to ensure normal spirometry (FVC; 6.07 ± 1.141, FEV₁-FVC⁻¹; 79.0 ± 9.2
%) and sufficient fitness (VO₂max = 63.7 ± 2.63 ml-min⁻¹-kg⁻¹). During intervention
testing, subjects completed a 45-minute bout of maximum sustainable cycling activity,
pre and post pulmonary diffusion measures, and pre and post magnetic resonance
imaging. Subjects exercised at 10% below their ventilatory threshold for 45 minutes at a power output of 300 ± 25 watts. Diffusion for carbon monoxide (DLco) and lung
capillary volume (Vc) had decreased one hour post exercise by 12% (p = 0.004) and 21%
(p = 0.017), respectively, but no significant change in membrane diffusing capacity (DM)
was found. The magnetic resonance (MR) scans showed a 9.4% increase (p = .043) in
pulmonary extravascular water after exercise, consistent with the theory that EW produced in well trained subjects. This study was the first to use new MR advances to
show an increase in EW following long duration heavy exercise in trained male subjects. === Education, Faculty of === Kinesiology, School of === Graduate
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