Tj. Wetter et al., Effects of exhaustive endurance exercise on pulmonary gas exchange and airway function in women, J APP PHYSL, 91(2), 2001, pp. 847-858
Seventeen fit women ran to exhaustion (14 +/-4 min) at a constant speed and
grade, reaching 95 +/-3% of maximal O-2 consumption. Pre- and postexercise
lung function, including airway resistance [total respiratory resistance (
Rrs)] across a range of oscillation frequencies, was measured, and, on a se
parate day, airway reactivity was assessed via methacholine challenge. Arte
rial O-2 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 O-2 difference (
A-aDO(2)) widened to 27 +/-7 Torr after 1 min and was maintained at this le
vel 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 t
he exercise duration occurred due to a hyperventilation-induced increase in
alveolar PO2 in the presence of a constant A-aDO(2). Arterial O-2 saturati
on fell with time because of increasing temperature (+2.6 +/-0.5 degreesC)
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 capa
city for CO correlated with the exercise A-aDO(2) 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 degre
e of exercise-induced arterial hypoxemia at the onset of high-intensity exe
rcise, prolonging exercise to exhaustion had no further deleterious effects
on A-aDO(2), and the degree of gas exchange impairment was not related to
individual differences in small or large airway function or reactivity.