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Progressive augmentation and ventilatory long‐term facilitation are enhanced in sleep apnoea patients and are mitigated by antioxidant administration
Author(s) -
Lee Dorothy S.,
Badr M. Safwan,
Mateika Jason H.
Publication year - 2009
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2009.178053
Subject(s) - medicine , placebo , anesthesia , hypoxia (environmental) , intermittent hypoxia , hypoxic ventilatory response , facilitation , randomized controlled trial , ventilation (architecture) , respiratory system , obstructive sleep apnea , psychology , oxygen , mechanical engineering , chemistry , alternative medicine , organic chemistry , pathology , neuroscience , engineering
Progressive augmentation (PA) and ventilatory long‐term facilitation (vLTF) of respiratory motor output are forms of respiratory plasticity that are initiated during exposure to intermittent hypoxia. The present study was designed to determine whether PA and vLTF are enhanced in obstructive sleep apnoea (OSA) participants compared to matched healthy controls. The study was also designed to determine whether administration of an antioxidant cocktail mitigates PA and vLTF. Thirteen participants with sleep apnoea and 13 controls completed two trials. During both trials participants were exposed to intermittent hypoxia which included twelve 4‐min episodes of hypoxia (, 50 mmHg; , 4 mmHg above baseline) followed by 30 min of recovery. Prior to exposure to intermittent hypoxia, participants were administered, in a randomized fashion, either an antioxidant or a placebo cocktail. Baseline measures of minute ventilation during the placebo and antioxidant trials were not different between or within groups. During the placebo trial, PA was evident in both groups; however it was enhanced in the OSA group compared to control (last hypoxic episode 36.9 ± 2.8 vs. 27.7 ± 2.2 l min −1 ; P ≤ 0.01). Likewise, vLTF was evident during the recovery period in both groups; on the other hand vLTF was greater in the OSA group compared to control (29.3 ± 2.8 vs. 20.4 ± 1.3 l min −1 ; P ≤ 0.01). PA and vLTF were reduced in the OSA group following antioxidant administration compared to the placebo (PA 30.6 ± 2.0 vs. 36.9 ± 2.8 l min −1 , P ≤ 0.01; vLTF 23.3 ± 1.4 vs. 29.3 ± 2.8 l min −1 , P ≤ 0.05). We conclude that PA and vLTF are enhanced in participants with OSA and that these forms of respiratory plasticity are mitigated after treatment with an antioxidant cocktail.