Exercise‐induced arterial hypoxaemia in healthy young women
- 1 March 1998
- journal article
- clinical trial
- Published by Wiley in The Journal of Physiology
- Vol. 507 (2), 619-628
- https://doi.org/10.1111/j.1469-7793.1998.619bt.x
Abstract
1. We questioned whether exercise-induced arterial hypoxaemia (EIAH) occurs in healthy active women, who have smaller lungs, reduced lung diffusion, and lower maximal O2 consumption rate (VO2,max) than age- and height-matched men. 2. Twenty-nine healthy young women with widely varying fitness levels (VO2,max, 57 +/- 6 ml kg-1 min-1; range, 35-70 ml kg-1 min-1; or 148 +/- 5%; range, 93-188% predicted) and normal resting lung function underwent an incremental treadmill test to VO2,max during the follicular phase of their menstrual cycle. Arterial blood samples were taken at rest and near the end of each workload. 3. Arterial PO2 (Pa,O2) decreased > 10 mmHg below rest in twenty-two of twenty-nine subjects at VO2,max (Pa,O2, 77.5 +/- 0.9 mmHg; range, 67-88 mmHg; arterial O2 saturation (Sa,O2), 92.3 +/- 0.2%; range, 87-94%). The remaining seven subjects maintained Pa,O2 within 10 mmHg of rest. Pa,O2 at VO2,max was inversely related to the alveolar to arterial O2 difference (A-aDO2) (r = -0.93; 35-52 mmHg) and to arterial PCO2 (Pa,CO2) (r = -0.62; 26-39 mmHg). 4. EIAH was inversely related to VO2,max (r = -0.49); however, there were many exceptions. Almost half of the women with significant EIAH had VO2,max within 15% of predicted normal values (VO2,max, 40-55 ml kg-1 min-1); among subjects with very high VO2,max (55-70 ml kg-1 min-1), the degree of excessive A-aDO2 and EIAH varied markedly (e.g. A-aDO2, 30-50 mmHg; Pa,O2, 68-91 mmHg). 5. In the women with EIAH at VO2,max, many began to experience an excessive widening of their A-aDO2 during moderate intensity exercise, which when combined with a weak ventilatory response, led to a progressive hypoxaemia. Inactive, less fit subjects had no EIAH and narrower A-aDO2 when compared with active, fitter subjects at the same VO2 (40-50 ml kg-1 min-1). 6. These data demonstrate that many active healthy young women experience significant EIAH, and at a VO2,max that is substantially less than those in their active male contemporaries. The onset of EIAH during submaximal exercise, and/or its occurrence at a relatively low VO2,max, implies that lung structure/function subserving alveolar to arterial O2 transport is abnormally compromised in many of these habitually active subjects.This publication has 24 references indexed in Scilit:
- Reduced performance of male and female athletes at 580?m altitudeEuropean Journal of Applied Physiology, 1997
- FLOW LIMITATION AFFECTS CONTROL OF BREATHING DURING HEAVY EXERCISE IN HIGHLY TRAINED WOMEN 463Medicine & Science in Sports & Exercise, 1996
- Effect of the Different Phases of the Menstrual Cycle and Oral Contraceptives on Athletic PerformanceSports Medicine, 1993
- Exercise-induced hypoxemia in athletes: Role of inadequate hyperventilationEuropean Journal of Applied Physiology, 1992
- Sex and Race Differences in the Development of Lung FunctionAmerican Review of Respiratory Disease, 1988
- Analysis of Spirometric Data from a National Sample of Healthy 6- to 24-year-olds (NHANES II)American Review of Respiratory Disease, 1988
- Is the lung built for exercise?Medicine & Science in Sports & Exercise, 1986
- Exercise‐induced arterial hypoxaemia in healthy human subjects at sea level.The Journal of Physiology, 1984
- Postnatal human lung growth.Thorax, 1982