Exercise-induced arterial hypoxaemia in healthy young women

• Published in: The Journal of physiology Vol. 507; no. 2; pp. 619 - 628
• Main Authors: Harms, Craig A., McClaran, Steven R., Nickele, Glenn A., Pegelow, David F., Nelson, William B., Dempsey, Jerome A.
• Format: Journal Article
• Language: English
• Published: Oxford, UK The Physiological Society 01.03.1998; Blackwell Science Ltd; Blackwell Science Inc
• Subjects: Adolescent; Adult; Blood Gas Analysis; Blood Pressure - physiology; Exercise - physiology; Female; Humans; Hypoxia - blood; Lung - physiology; Male; Original; Oxygen Consumption - physiology; Respiratory Function Tests
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1111/j.1469-7793.1998.619bt.x

We questioned whether exercise-induced arterial hypoxaemia (EIAH) occurs in healthy active women, who have smaller lungs, reduced lung diffusion, and lower maximal O 2 consumption rate ( ) than age- and height-matched men. Twenty-nine healthy young women with widely varying fitness levels ( 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 during the follicular phase of their menstrual cycle. Arterial blood samples were taken at rest and near the end of each workload. Arterial P O 2 ( P a,O 2 ) decreased > 10 mmHg below rest in twenty-two of twenty-nine subjects at ( P a,O 2 , 77.5 ± 0.9 mmHg; range, 67–88 mmHg; arterial O 2 saturation ( S a,O 2 ), 92.3 ± 0.2 %; range, 87–94 %). The remaining seven subjects maintained P a,O 2 within 10 mmHg of rest. P a,O 2 at was inversely related to the alveolar to arterial O 2 difference (A-aDO 2 ) ( r = -0.93; 35–52 mmHg) and to arterial P CO 2 ( P a,CO 2 ) ( r = -0.62; 26–39 mmHg). EIAH was inversely related to ( r = -0.49); however, there were many exceptions. Almost half of the women with significant EIAH had within 15 % of predicted normal values ( 40–55 ml kg −1 min −1 ); among subjects with very high (55–70 ml kg −1 min −1 ), the degree of excessive A-aDO 2 and EIAH varied markedly (e.g. A-aDO 2 , 30–50 mmHg; P a,O 2 , 68–91 mmHg). In the women with EIAH at many began to experience an excessive widening of their A-aDO 2 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-aDO 2 when compared with active, fitter subjects at the same (40–50 ml kg −1 min −1 ). These data demonstrate that many active healthy young women experience significant EIAH, and at a 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 implies that lung structure/function subserving alveolar to arterial O 2 transport is abnormally compromised in many of these habitually active subjects.