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J Appl Physiol 91: 847-858, 2001;
8750-7587/01 $5.00
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Vol. 91, Issue 2, 847-858, August 2001

Effects of exhaustive endurance exercise on pulmonary gas exchange and airway function in women

Thomas J. Wetter, Claudette M. St. Croix, David F. Pegelow, David A. Sonetti, and Jerome A. Dempsey

Department of Preventive Medicine, John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin, Madison, Wisconsin 53705

Seventeen fit women ran to exhaustion (14 ± 4 min) at a constant speed and grade, reaching 95 ± 3% of maximal O2 consumption. Pre- and postexercise lung function, including airway resistance [total respiratory resistance (Rrs)] across a range of oscillation frequencies, was measured, and, on a separate day, airway reactivity was assessed via methacholine challenge. Arterial O2 saturation decreased from 97.6 ± 0.5% at rest to 95.1 ± 1.9% at 1 min and to 92.5 ± 2.6% at exhaustion. Alveolar-arterial O2 difference (A-aDO2) widened to 27 ± 7 Torr after 1 min and was maintained at this level until exhaustion. Arterial PO2 (PaO2) fell to 80 ± 8 Torr at 1 min and then increased to 86 ± 9 Torr at exhaustion. This increase in PaO2 over the exercise duration occurred due to a hyperventilation-induced increase in alveolar PO2 in the presence of a constant A-aDO2. Arterial O2 saturation fell with time because of increasing temperature (+2.6 ± 0.5°C) and progressive metabolic acidosis (arterial pH: 7.39 ± 0.04 at 1 min to 7.26 ± 0.07 at exhaustion). Plasma histamine increased throughout exercise but was inversely correlated with the fall in PaO2 at end exercise. Neither pre- nor postexercise Rrs, frequency dependence of Rrs, nor diffusing capacity for CO correlated with the exercise A-aDO2 or PaO2. Although several subjects had a positive or borderline hyperresponsiveness to methacholine, this reactivity did not correlate with exercise-induced changes in Rrs or exercise-induced arterial hypoxemia. In conclusion, regardless of the degree of exercise-induced arterial hypoxemia at the onset of high-intensity exercise, prolonging exercise to exhaustion had no further deleterious effects on A-aDO2, and the degree of gas exchange impairment was not related to individual differences in small or large airway function or reactivity.

exercise-induced arterial hypoxemia; arterial blood gases; esophageal temperature; respiratory resistance; histamine


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