Abstract
Obstructive sleep apnea (OSA) patients have increased upper airway muscle activity, including such lingual muscles as the genioglossus (GG), geniohyoid (GH), and hyoglossus (HG). This adaptation partially protects their upper airway against obstructions. Rodents are used to study the central neural control of sleep and breathing but they do not naturally exhibit OSA. We investigated whether, in chronically instrumented, behaving rats, disconnecting the GH and HG muscles from the hyoid (H) apparatus would result in a compensatory increase of other upper airway muscle activity (electromyogram, EMG) and/or other signs of upper airway instability. We first determined that, in intact rats, lingual (GG and intrinsic) muscles maintained stable activity levels when quantified based on 2 h-long recordings conducted on days 6 through 22 after instrumentation. We then studied five rats in which the tendons connecting the GH and HG muscles to the H apparatus were experimentally severed. When quantified across all recording days, lingual EMG during slow-wave sleep (SWS) was modestly but significantly increased in rats with surgically altered upper airway [8.6 ± 0.7% (SE) vs. 6.1 ± 0.7% of the mean during wakefulness; p = 0.012]. Respiratory modulation of lingual EMG occurred mainly during SWS and was similarly infrequent in both groups, and the incidence of sighs and central apneas also was similar. Thus, a weakened action of selected lingual muscles did not produce sleep-disordered breathing but resulted in a relatively elevated activity in other lingual muscles during SWS. These results encourage more extensive surgical manipulations with the aim to obtain a rodent model with collapsible upper airway.
Highlights
Studies of upper airway control in obstructive sleep apnea syndrome (OSA) patients revealed that upper airway narrowing and collapse during sleep is caused by decrements of activity in upper airway dilator muscles [1,2,3]
The rats with GH/HG muscles disconnected from the H apparatus did not exhibit any overt problems with breathing when under anesthesia during instrumentation or thereafter, nor did they appear to have any problems with eating or drinking
Between the day of instrumentation and the last recording day, the rats with GH/HG muscles disconnected from H apparatus gained 112 ± 12 g (SE) in body weight, and the rats with the GH/HG connection intact gained 84.0 ± 8.9 g
Summary
Studies of upper airway control in obstructive sleep apnea syndrome (OSA) patients revealed that upper airway narrowing and collapse during sleep is caused by decrements of activity in upper airway dilator muscles [1,2,3]. Certain breeds of dogs and cats and rabbits under certain experimental conditions exhibit sleep-related upper airway narrowing or collapse [15,16,17], OSA is an almost uniquely human disorder. This is probably due to distinct features of human upper airway anatomy, including the absence of a rigid support for the hyoid (H) apparatus and elongation of the pharyngeal region in association with the development of speech. The scarcity of animal models is a challenge for the studies that attempt to capture the neuromechanical features important for upper airway control in OSA patients and investigate various consequences of sleep-disordered breathing
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