Pulmonary oedema following exercise in humans

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) per...

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Main Author: Hodges, Alastair Neil Hugh
Language:English
Published: 2010
Online Access:http://hdl.handle.net/2429/18445
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spelling ndltd-UBC-oai-circle.library.ubc.ca-2429-184452018-01-05T17:39:28Z Pulmonary oedema following exercise in humans Hodges, Alastair Neil Hugh 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 2010-01-16T20:23:42Z 2010-01-16T20:23:42Z 2006 2006-05 Text Thesis/Dissertation http://hdl.handle.net/2429/18445 eng For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.
collection NDLTD
language English
sources NDLTD
description 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
author Hodges, Alastair Neil Hugh
spellingShingle Hodges, Alastair Neil Hugh
Pulmonary oedema following exercise in humans
author_facet Hodges, Alastair Neil Hugh
author_sort Hodges, Alastair Neil Hugh
title Pulmonary oedema following exercise in humans
title_short Pulmonary oedema following exercise in humans
title_full Pulmonary oedema following exercise in humans
title_fullStr Pulmonary oedema following exercise in humans
title_full_unstemmed Pulmonary oedema following exercise in humans
title_sort pulmonary oedema following exercise in humans
publishDate 2010
url http://hdl.handle.net/2429/18445
work_keys_str_mv AT hodgesalastairneilhugh pulmonaryoedemafollowingexerciseinhumans
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