Document Detail


Exercise-induced hypoxaemia in highly trained cyclists at 40% peak oxygen uptake.
MedLine Citation:
PMID:  10090636     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A group of 15 competitive male cyclists [mean peak oxygen uptake, VO2peak 68.5 (SEM 1.5 ml x kg(-1) x min(-1))] exercised on a cycle ergometer in a protocol which began at an intensity of 150 W and was increased by 25 W every 2 min until the subject was exhausted. Blood samples were taken from the radial artery at the end of each exercise intensity to determine the partial pressures of blood gases and oxyhaemoglobin saturation (SaO2), with all values corrected for rectal temperature. The SaO2 was also monitored continuously by ear oximetry. A significant decrease in the partial pressure of oxygen in arterial blood (PaO2) was seen at the first exercise intensity (150 W, about 40% VO2peak). A further significant decrease in PaO2 occurred at 200 W, whereafter it remained stable but still significantly below the values at rest, with the lowest value being measured at 350 W [87.0 (SEM 1.9) mmHg]. The partial pressure of carbon dioxide in arterial blood (PaCO2) was unchanged up to an exercise intensity of 250 W whereafter it exhibited a significant downward trend to reach its lowest value at an exercise intensity of 375 W [34.5 (SEM 0.5) mmHg]. During both the first (150 W) and final exercise intensities (VO2peak) PaO2 was correlated significantly with both partial pressure of oxygen in alveolar gas (P(A)O2, r = 0.81 and r = 0.70, respectively) and alveolar-arterial difference in oxygen partial pressure (P(A-a)O2, r = 0.63 and r = 0.86, respectively) but not with PaCO2. At VO2peak PaO2 was significantly correlated with the ventilatory equivalents for both oxygen uptake and carbon dioxide output (r = 0.58 and r = 0.53, respectively). When both P(A)O2 and P(A-a)O2 were combined in a multiple linear regression model, at least 95% of the variance in PaO2 could be explained at both 150 W and VO2peak. A significant downward trend in SaO2 was seen with increasing exercise intensity with the lowest value at 375 W [94.6 (SEM 0.3)%]. Oximetry estimates of SaO2 were significantly higher than blood measurements at all times throughout exercise and no significant decrease from rest was seen until 350 W. The significant correlations between PaO2 and P(A)O2 with the first exercise intensity and at VO2peak led to the conclusion that inadequate hyperventilation is a major contributor to exercise-induced hypoxaemia.
Authors:
A J Rice; G C Scroop; C J Gore; A T Thornton; M A Chapman; H W Greville; M D Holmes; R Scicchitano
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European journal of applied physiology and occupational physiology     Volume:  79     ISSN:  0301-5548     ISO Abbreviation:  Eur J Appl Physiol Occup Physiol     Publication Date:  1999 Mar 
Date Detail:
Created Date:  1999-05-11     Completed Date:  1999-05-11     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0410266     Medline TA:  Eur J Appl Physiol Occup Physiol     Country:  GERMANY    
Other Details:
Languages:  eng     Pagination:  353-9     Citation Subset:  IM    
Affiliation:
Department of Thoracic Medicine, Royal Adelaide Hospital, Australia.
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MeSH Terms
Descriptor/Qualifier:
Adult
Anoxia / etiology*
Arteries
Carbon Dioxide / blood
Exercise / physiology*
Humans
Male
Osmolar Concentration
Oximetry
Oxygen / blood,  metabolism
Oxygen Consumption* / physiology
Oxyhemoglobins / analysis
Partial Pressure
Physical Education and Training*
Pulmonary Alveoli / metabolism
Chemical
Reg. No./Substance:
0/Oxyhemoglobins; 124-38-9/Carbon Dioxide; 7782-44-7/Oxygen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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