| Summary: | In order to determine if transient pulmonary oedema occurs after strenuous exercise, 10
well trained male athletes were challenged in normoxic and hypoxic conditions. To
determine the minimal tolerable F₁O₂ for hypoxia, ten aerobically trained male athletes
(VC^max = 57.2 ± 7.95mL-kg⁻¹•min⁻¹) performed graded cycling work to maximal effort
under four conditions of varying FT02 (21%, 18%, 15%, 12%). Mean VChmax was
significantly reduced while breathing 15 and 12% oxygen (VC^max = 48.2 ± 7.9 and
31.5 ± 7.4 mL-kg⁻¹•min⁻¹ respectively). In the 12% oxygen condition, the majority of the
subjects were not able to complete maximal exercise without SaO"2 falling below 70%.
Ten highly trained males (V02max = 65.0 ± 7.5mL- kg⁻¹•min⁻¹) then underwent
assessment of lung density by quantified magnetic resonance imaging prior to and 54.0 ±
17.2 and 100.7 ± 15.1 min following 60 min of cycling exercise (61.6 ± 9.5% VO₂max).
The same subjects underwent an identical measure prior to and 55.6 ± 9.8 and 104.3 ±
9.1 min following 60 min cycling exercise (65.4 ± 7.1% hypoxic VChmax) in hypoxia
(F₁O₂ = 15.0%). Two subjects demonstrated mild exercise-induced arterial hypoxaemia
(EIAH) (minSa0₂ = 94.5 & 93.8%), and 7 demonstrated moderate EIAH (minSa0₂ =
91.4 ± 1.1%) during a preliminary VC^max test in normoxia. No significant differences
(p<0.05) were found in lung density following exercise in either condition. Mean lung
densities, measured once pre- and twice post-exercise, were 0.177 ± 0.019, 0.181 ± 0.019
and 0.173 ± 0.019g•mL⁻¹ in the normoxic condition, and 0.178 ± 0.021, 0.174 ± 0.022
and 0.176 ± 0.019g•mL⁻¹ in hypoxic condition. These results indicate that transient
interstitial pulmonary oedema does not occur following sustained steady-state cycling
exercise in normoxia or hypoxia. This diminishes the likelihood of transient oedema as a
mechanism for changes in SaO₂ during sustained exercise. === Education, Faculty of === Kinesiology, School of === Graduate
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