Abstract
In healthy young volunteers, acquisition of blood oxygen level-dependent (BOLD) magnetic resonance (MR) and muscle sympathetic nerve (MSNA) signals during simulation of obstructive or central sleep apnea identified cortical cardiovascular autonomic regions in which the BOLD signal changed synchronously with acute noradrenergic excitation. In the present work, we tested the hypothesis that such Mueller maneuvers (MM) and breath-holds (BH) would elicit greater concomitant changes in mean efferent nerve firing and BOLD signal intensity in patients with moderate to severe obstructive sleep apnea (OSA) relative to age- and sex-matched individuals with no or only mild OSA (Apnea Hypopnea Index, AHI, <15 events/h). Forty-six participants, 24 with OSA [59 ± 8 years; AHI 31 ± 18 events/h (mean ± SD); seven women] and 22 without (58 ± 11 years; AHI 7 ± 4; nine women), performed a series of three MM and three BH, in randomly assigned order, twice: during continuous recording of MSNA from the right fibular nerve and, on a separate day, during T2∗-weighted echo planar functional MR imaging. MSNA at rest was greater in those with OSA (65 ± 19 vs. 48 ± 17 bursts per 100 heart beats; p < 0.01). MM and BH elicited similar heart rate, blood pressure, and MSNA responses in the two cohorts; group mean BOLD data were concordant, detecting no between-group differences in cortical autonomic region signal activities. The present findings do not support the concept that recurring episodes of cyclical apnea during sleep alter cortical or peripheral neural responsiveness to their simulation during wakefulness by volitional Mueller maneuvers or breath-holds.
Highlights
Initiated by occlusion of the upper airway, obstructive sleep apnea (OSA) is characterized by recurring pauses in breathing, which, if sustained, beget progressive hypoxia and hypercapnia until arousal from sleep causing ventilation to resume
[breath-holds (BH)] (Bradley et al, 2003; Kimmerly et al, 2013), we identified cortical and cerebellar cardiovascular autonomic regions in which the blood oxygen level-dependent (BOLD) signal either increased or decreased profoundly and synchronously with acute sympathetic excitation
After blinded analysis and extraction of those BOLD signal recordings that did not meet prespecified stringent head movement artifact exclusion criteria during Mueller maneuvers (MM) and BHs, acceptable data were collated in 10 participants classified as having OSA and in 14 control subjects for comparative analysis
Summary
Initiated by occlusion of the upper airway, obstructive sleep apnea (OSA) is characterized by recurring pauses in breathing, which, if sustained, beget progressive hypoxia and hypercapnia until arousal from sleep causing ventilation to resume. The latter interrupt, cyclically, the reductions in blood pressure and heart rate typical of normal sleep (Somers et al, 1995; Bradley and Floras, 2003; Floras, 2018) These acute disturbances induce, over time, increased peripheral chemoreceptor reflex sensitivity (Mateika et al, 2004; Mahamed et al, 2005), upward resetting of central sympathetic outflow during wakefulness, and thickening and thinning of specific gray matter constituents of a cortical autonomic network (CAN) engaged in the generation or modulation of cardiovascular autonomic tone (Taylor et al, 2016a, 2018; Floras, 2018). The magnitude of efferent post-ganglionic muscle sympathetic nerve firing recorded during wakefulness is directly proportional to the frequencies of nocturnal breathing cessation and arousal from sleep; the magnitude of subsequent arterial oxygen desaturation; and structural changes within the CAN, left midcingulate cortex thickness and thalamic volume (Taylor et al, 2016a,b, 2018; Floras, 2018)
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