THE ROLE OF SLEEP APNEA INDUCED REACTIVE OXYGEN SPECIES IN SYMPATHOEXCITATION

Purpose: The obstructive sleep apnea (OSA) patient experiences multiple hypopneas and apneas, or intermittent hypoxia (IH) throughout the night. In healthy subjects, one 20s to 30s bout of IH has been reported to increase muscle sympathetic nervous activity (MSNA) for periods of 3hrs. Results from animal and human investigations indicate that apnea induced elevations in reactive oxygen species (ROS) are associated with increases in MSNA. Increases in sympathetic activity result in increases in the operating point of the arterial baroreflex's control of blood pressure. We hypothesized that the IH induced increase in ROS and sympathoexcitation would attenuate arterial baroreflex (ABR) control of stroke volume (SV). Methods: Healthy human subjects (n = 11, 5 female) underwent neck pressure/suction (NP/NS) to assess carotid baroreflex (CBR) function before and after intermittent hypoxia training with or without the antioxidant, N-acetyl cysteine (NAC). During NP/NS, mean arterial pressure and stroke volume were recorded non-invasively using a finometer. Following baseline measurements for hemodynamic variables and CBR function, subjects were asked to ingest a drink containing either NAC or a placebo. One hour after ingestion, hemodynamic variables and ABR function were measured, following which the subjects were intermittently hypoxia trained (IHT) using 20s of intermittently breathing nitrogen and breath holding resulting in IH. After that, measurements of SV were recorded during NP/NS (immediately 30 minutes and 1 hour post IHT). A two way repeated measures analysis of variance (ANOVA) was used to analyze differences between treatment groups across time. Results: Repeated measures (ANOVA) comparing stroke volume between treatment groups identified that there were no differences in SV over time (p = 0.332). There was no difference in CBR function (p = 0.891) between placebo and NAC conditions. Conclusions: These data suggest that there is no significant influence of IHT or ROS on the CBR control of stroke volume.