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Titolo:
Effects of exhaustive endurance exercise on pulmonary gas exchange and airway function in women
Autore:
Wetter, TJ; St Croix, C; Pegelow, DF; Sonetti, DA; Dempsey, JA;
Indirizzi:
Univ Wisconsin, John Rankin Lab Pulm Med, Dept Prevent Med, Madison, WI 53705 USA Univ Wisconsin Madison WI USA 53705 pt Prevent Med, Madison, WI 53705 USA
Titolo Testata:
JOURNAL OF APPLIED PHYSIOLOGY
fascicolo: 2, volume: 91, anno: 2001,
pagine: 847 - 858
SICI:
8750-7587(200108)91:2<847:EOEEEO>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED ARTERIAL HYPOXEMIA; MONOXIDE DIFFUSING-CAPACITY; HIGHLY TRAINED CYCLISTS; FORCED OSCILLATION; SMOOTH-MUSCLE; OXYGEN-UPTAKE; LUNG-VOLUMES; COLD-AIR; HISTAMINE; FLOW;
Keywords:
exercise-induced arterial hypoxemia; arterial blood gases; esophageal temperature; respiratory resistance; histamine;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Wetter, TJ POB 53056, Medford, MA 02153 USA POB 53056 Medford MA USA 02153 OB 53056, Medford, MA 02153 USA
Citazione:
T.J. 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

Abstract

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 separate day, airway reactivity was assessed via methacholine challenge. Arterial O-2 saturation decreased from 97.6 +/-0.5% at rest to 95.1 +/-1.9% at1 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 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-aDO(2). Arterial O-2 saturation 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 exercisebut 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-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 orexercise-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-aDO(2), and the degree of gas exchange impairment was not related toindividual differences in small or large airway function or reactivity.

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Documento generato il 21/10/20 alle ore 10:19:11