Relative contributions of hypocarbia and hyperpnea as mechanisms in postexercise asthma.
The purpose of this investigation was to assess the relative contributions of hyperpnea and hypocapnia in the induction of postexercise asthma. To achieve these ends, eight young asthmatics were exercised on a treadmill while minute ventilations (VE) and end-tidal CO2 (PET CO2) tensions were continuously recorded. The subjects were then restudied using a partial rebreathing technique that allowed separation of minute and alveolar ventilations so that independent evaluations could be made of the relative effects of bulk airflow on pulmonary mechanics as well as a systematic study of hypocapnia in a dose-response fashion. Sustained hyperpnea with VEidentical to those recorded during exercise was totally without effect when the mean PET CO2 was isocapnic or lowered to approximately 30 Torr. Reduction in PETCO2 to 21.3 +/-0.9 Torr brought about significant changes in mechanics, but in every variable measured, exercise produced the greatest alterations and did so at PETCO2 values that had no effect when studied in a controlled fashion. Consequently, neither high VE per se, nor hypocapnia can be considered as the mechanisms underlying exercise induced asthma.
D000328:Adult; D001249:Asthma / Q000378:metabolism / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000378:metabolism*; D005260:Female; D006801:Humans; D006985:Hyperventilation / Q000503:physiopathology*; D008168:Lung / Q000503:physiopathology; D008297:Male; D005082:Physical Exertion
D002245:Carbon Dioxide