Reply: The two faces of active expiration: a case of mistaken identity!

Abstract

We are very grateful to Bazilio, Moraes, and Machado (2020) for their letter drawing further attention to the topical and important issue of the mechanism(s) of chronic intermittent hypoxia-induced hypertension. Our colleagues have generated a considerable body of work over the years, contributing, in no small way, to the contemporary understanding of the maladaptive effects of exposure to chronic intermittent hypoxia on cardiorespiratory control. We drew focus in our viewpoint (O'Connor, Lucking & O'Halloran, 2019) to the persistent expression of hypertension across the sleepwake cycle in animals exposed to chronic intermittent hypoxia (CIH), with evidence of active expiration only in wakefulness (Bazilio, Bongamba, Moraes & Machado, 2019). Our intent was to emphasize that active expiration, defined as the motor recruitment of abdominal muscles in support of enhanced pulmonary ventilation, was not obligatory for the continued manifestation of high blood pressure following exposure to CIH. Active expiration increases pulmonary ventilation, enhances mechanoreceptor feedback from the lungs to the brainstem, and alters intrathoracic pressure across the respiratory cycle affecting cardiovascular parameters, changes that can influence None. Experimental Physiology. 2020;105:395-396. wileyonlinelibrary.com/journal/eph 395 396 RESPONSE TO LETTER