Exercise‐induced arterial hypoxaemia in healthy young women

Abstract

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 (V̇O2,max) than age‐ and height‐matched men. Twenty‐nine healthy young women with widely varying fitness levels (V̇O2,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 V O2,max during the follicular phase of their menstrual cycle. Arterial blood samples were taken at rest and near the end of each workload. Arterial PO2 (Pa,O2) decreased > 10 mmHg below rest in twenty‐two of twenty‐nine subjects at V̇O2,max (Pa,O2, 77.5 ± 0.9 mmHg; range, 67‐88 mmHg; arterial O 2 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 V O2,max was inversely related to the alveolar to arterial O 2 difference (A‐aDO 2) (r= ‐0.93; 35‐52 mmHg) and to arterial PCO2 (Pa,CO2) (r= ‐0.62; 26‐39 mmHg). EIAH was inversely related to V̇O2,max (r= ‐0.49); however, there were many exceptions. Almost half of the women with significant EIAH had V O2,max within 15 % of predicted normal values (V O2,max, 40‐55 ml kg−1 min−1); among subjects with very high V O2,max (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; Pa,O2, 68‐91 mmHg). In the women with EIAH at V̇O2,max, 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 V O2 (40‐50 ml kg−1 min−1). These data demonstrate that many active healthy young women experience significant EIAH, and at a V O2,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 V̇O2,max, implies that lung structure/function subserving alveolar to arterial O 2 transport is abnormally compromised in many of these habitually active subjects.