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, Des protocoles prospectifs ont corrélé positivement l'amplitude de ces oscillations de la ventilation au débit cardiaque ( c) et au niveau de ventilation ( E), tandis que la période est raccourcie lorsque E et c augmentent. À l'opposé d'une période des apnées d'environ 1 minute chez les patients IC et SAS, nos observations ont permis de mesurer la période des oscillations ventilatoires à l'exercice et en hypoxie entre 11 et 12 secondes. Les sujets montrant une plus forte réponse ventilatoire à l'hypoxie et une sensibilité plus élevée au CO2 exhibent une plus grande instabilité ventilatoire. L'hyperoxie et l'hypercapnie ont des effets opposés : alors que l'inhalation d'O2 ne modifie pas la stabilité du système (vs normoxie), l'hypercapnie hyperoxique exacerbe le phénomène oscillatoire. Un traitement pharmacologique par acétazolamide (ACZ) améliore la stabilité ventilatoire, appuyant ainsi, en regard des données précédentes, le rôle central des chémorécepteurs périphériques dans la survenue des oscillations de la ventilation. Un modèle mathématique du contrôle de la ventilation intégrant, Contrôle ventilatoire à l'exercice et en hypoxie : mise en évidence d'une périodicité constitutionnelle L'instabilité de la ventilation est un phénomène connu chez l'homme. Elle était jusqu'à présent observée chez l'homme sain en altitude et chez les patients souffrant d'insuffisance cardiaque (IC) et de syndrome d'apnées du sommeil (SAS)