2019-08-222019-08-222015-032015-03-01https://hdl.handle.net/20.500.12503/26416This investigation tested the hypothesis that central and peripheral reactive oxygen species (ROS) mediate hypoxia induced sympathoexcitation, which is a central feature of the Obstructive Sleep Apnea-Hypopnea Syndrome (OSAS). 10 healthy human subjects were recruited. One hour prior to experimentation, each subject randomly ingested either 70 mg.kg-1 of N-Acetyl Cysteine (NAC, n=5) or vehicle placebo (n=5). ECG, BP, muscle sympathetic nerve activity (MSNA) and plasma ROS and catecholamines were measured. Subjects underwent a 20 minute intermittent hypoxia training (IHT) protocol consisting of cyclical end-expiratory apneas with 100% N2. Venous blood was analyzed pre/post IHT for ROS by electron paramagnetic spectroscopy and for catecholamines by ELISA. In the placebo group, MSNA was increased between pre vs. post IHT (P=0.01). In the NAC group, however, MSNA was unchanged (P=0.26). NAC reduced the percent change (% ∆) of ROS observed from pre- vs. post-IHT compared to placebo (P=0.02). The % ∆ of ROS was directly related to increasing MSNA (R2=0.83, p=0.01). The % ∆ of norepinephrine was lower in the NAC vs. placebo group after IHT (P=0.05), whereas the % ∆ of epinephrine was unchanged (P=0.40). These data indicate that NAC reduces central sympathetic outflow in response to IHT, and thereby could reduce cardiovascular risk in OSAS patients.enposter