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High activity of upper airway dilator muscles is thought to be critical in preventing sleep-related upper airway collapse. To date, most of the research regarding upper airway dilator muscles has focused on the genioglossus muscle, which protrudes the tongue and opens the retroglossal airway. However, collapse commonly occurs in the retropalatal region. We, therefore, aimed to examine the motor control of the palatoglossus muscle as well as investigate breathing route-related changes in genioglossus and palatoglossus motor units. Single motor unit recordings of the genioglossus and palatoglossus were made simultaneously in healthy individuals during wakefulness while breathing through the nose with the mouth closed (NMC), nose with mouth open (NMO), or orally (OMO). The palatoglossus was found to have all five motor unit firing patterns that have been observed in other upper airway dilator muscles, but during nasal breathing had a higher proportion of tonically active but inspiratory modulated motor units as compared with the genioglossus (67% vs. 30%). When still breathing nasally but with the mouth open, the units with an expiratory firing pattern in genioglossus, and all firing patterns in palatoglossus, increased their firing rates compared with nasal breathing with the mouth closed [genioglossus (GG): 17.8 ± 4.9 vs. 23.1 ± 4.8 Hz, palatoglossus (PG): 17.0 ± 4.0 vs. 19.3 ± 4.0 Hz]. Finally, oral breathing resulted in dramatic reductions in the number of palatoglossal motor units that were firing (35 units vs. 92 during nasal breathing). Palatoglossal activity may contribute importantly to airway collapsibility and may provide an alternate pathway for preventing sleep-related airway collapse. NEW & NOTEWORTHY: The firing patterns of motor units in the palatoglossus have until now not been investigated, and how they and motor units in the genioglossus change with breathing route alteration was not known. This study has shown that the palatoglossus contains motor units with all the firing patterns observed in the genioglossus but in different proportions. Furthermore, breathing route changes alter units with different firing patterns differentially in the two muscles. [ABSTRACT FROM AUTHOR]

Obstructive sleep apnea (OSA) is a chronic sleep-related breathing disorder that is highly prevalent in individuals with posttraumatic stress disorder (PTSD). The reason for this high prevalence remains unclear. We hypothesized that breathing instability, one of the key contributors to OSA, may be altered in PTSD and predispose OSA. Healthy participants (214 females, 98 males) aged 17 to 42 (M = 19.92; SD = 2.85) completed online questionnaires measuring PTSD symptomatology, sleep disturbances, and self-reported breathlessness. A subset of these participants (16 females, 14 males) aged 18 to 42 (M = 23.50; SD = 7.18) completed an in-lab breathing instability assessment, whereby they performed a series of 20-second and maximal duration breath-holds. PTSD severity positively predicted subjective perceptions of breathlessness (P < 0.001) but not objective measures of breathing instability, namely ventilation following 20-s breath-holds (P = 0.93) and maximal breath-hold duration (P = 0.41). These results suggest that breathing instability may not be the driving factor behind the high prevalence of OSA in PTSD. Instead, other factors such as a low arousal threshold, elevated ventilatory responses to arousal, or coexisting insomnia may explain the high rates of OSA in PTSD. One explanation for the discrepancy between subjective breathlessness and breathing stability measures relating to PTSD severity may be that hypervigilance and increased anxiety impacted self-perceptions of breathlessness while not altering breathing instability per se. NEW & NOTEWORTHY: Obstructive sleep apnea (OSA) is more common in individuals with posttraumatic stress disorder (PTSD) than the general population for unknown reasons. This study assessed one of the key contributors to OSA, respiratory control instability, in young students with a range of posttraumatic stress symptoms. Although individuals with high PTSD symptoms reported increased subjective breathlessness, objectively measured breathing instability was not altered, suggesting respiratory instability is unlikely to increase the risk of OSA in PTSD. [ABSTRACT FROM AUTHOR]

Study objectivesUpper airway collapsibility is a key determinant of obstructive sleep apnea (OSA) which can influence the efficacy of certain non-continuous positive airway pressure (CPAP) treatments for OSA. However, there is no simple way to measure this variable clinically. The present study aimed to develop a clinically implementable tool to evaluate the collapsibility of a patient's upper airway.MethodsCollapsibility, as characterized by the passive pharyngeal critical closing pressure (Pcrit), was measured in 46 patients with OSA. Associations were investigated between Pcrit and data extracted from patient history and routine polysomnography, including CPAP titration.ResultsTherapeutic CPAP level, demonstrated the strongest relationship to Pcrit (r2=0.51, p < .001) of all the variables investigated including apnea-hypopnea index, body mass index, sex, and age. Patients with a mildly collapsible upper airway (Pcrit ≤ -2 cmH2O) had a lower therapeutic CPAP level (6.2 ± 0.6 vs. 10.3 ± 0.4 cmH2O, p < .001) compared to patients with more severe collapsibility (Pcrit > -2 cmH2O). A therapeutic CPAP level ≤8.0 cmH2O was sensitive (89%) and specific (84%) for detecting a mildly collapsible upper airway. When applied to the independent validation data set (n = 74), this threshold maintained high specificity (91%) but reduced sensitivity (75%).ConclusionsOur data demonstrate that a patient's therapeutic CPAP requirement shares a strong predictive relationship with their Pcrit and may be used to accurately differentiate OSA patients with mild airway collapsibility from those with moderate-to-severe collapsibility. Although this relationship needs to be confirmed prospectively, our findings may provide clinicians with better understanding of an individual patient's OSA phenotype, which ultimately could assist in determining which patients are most likely to respond to non-CPAP therapies.

Upper airway muscle activity is reportedly elevated during slow-wave sleep (SWS) when compared with lighter sleep stages. To uncover the possible mechanisms underlying this elevation, we explored the correlation between different indices of central and reflex inspiratory drive, such as the changes in airway pressure and end-expiratory CO2 and the changes in the genioglossus (GG) and tensor palatini (TP) muscle activity accompanying transitions from the lighter N2 to the deeper N3 stage of non-rapid eye movement (NREM) sleep in healthy young adult men. Forty-six GG and 38 TP continuous electromyographic recordings were obtained from 16 men [age: 20 ± 2.5 (SD) yr; body mass index: 22.5 ± 1.8 kg/m2] during 32 transitions from NREM stages N2 to N3. GG but not TP activity increased following transition into N3 sleep, and the increase was positively correlated with more negative airway pressure, increased end-tidal CO2, increased peak inspiratory flow, and increased minute ventilation. None of these correlations was statistically significant for TP. Complementary GG and TP single motor unit analysis revealed a mild recruitment of GG units and derecruitment of TP units during the N2 to N3 transitions. These findings suggest that, in healthy individuals, the increased GG activity during SWS is driven primarily by reflex stimulation of airway mechanoreceptors and central chemoreceptors.NEW & NOTEWORTHY The characteristic increase in the activity of the upper airway dilator muscle genioglossus during slow-wave sleep (SWS) in young healthy individuals was found to be related to increased stimulation of airway mechanoreceptors and central chemoreceptors. No evidence was found for the presence of a central SWS-specific drive stimulating genioglossus activity in young healthy individuals. However, it remains to be determined whether a central drive exists in obstructive sleep apnea patients.

Study objectivesBoth anatomical and nonanatomical traits are important in obstructive sleep apnea (OSA) pathogenesis. We have previously described a model combining these traits, but have not determined its diagnostic accuracy to predict OSA. A valid model, and knowledge of the published effect sizes of trait manipulation, would also allow us to predict the number of patients with OSA who might be effectively treated without using positive airway pressure (PAP).Design, participants and interventionFifty-seven subjects with and without OSA underwent standard clinical and research sleep studies to measure OSA severity and the physiological traits important for OSA pathogenesis, respectively. The traits were incorporated into a physiological model to predict OSA. The model validity was determined by comparing the model prediction of OSA to the clinical diagnosis of OSA. The effect of various trait manipulations was then simulated to predict the proportion of patients treated by each intervention.Measurements and resultsThe model had good sensitivity (80%) and specificity (100%) for predicting OSA. A single intervention on one trait would be predicted to treat OSA in approximately one quarter of all patients. Combination therapy with two interventions was predicted to treat OSA in ∼50% of patients.ConclusionsAn integrative model of physiological traits can be used to predict population-wide and individual responses to non-PAP therapy. Many patients with OSA would be expected to be treated based on known trait manipulations, making a strong case for the importance of non-anatomical traits in OSA pathogenesis and the effectiveness of non-PAP therapies.

RationaleBody habitus is a major determinant of obstructive sleep apnea (OSA). However, many individuals do not have OSA despite being overweight/obese (body mass index > 25 kg/m(2)) for reasons that are not fully elucidated.ObjectivesTo determine the key physiologic traits (upper-airway anatomy/collapsibility, upper-airway muscle responsiveness, chemoreflex control of ventilation, arousability from sleep) responsible for the absence of OSA in overweight/obese individuals.MethodsWe compared key physiologic traits in 18 overweight/obese subjects without apnea (apnea-hypopnea index < 15 events per hour) with 25 overweight/obese matched patients with OSA (apnea-hypopnea index ≥ 15 events per hour) and 11 normal-weight nonapneic control subjects. Traits were measured by repeatedly lowering continuous positive airway pressure to subtherapeutic levels for 3 minutes during non-REM sleep.Measurements and main resultsOverweight/obese subjects without apnea exhibited a less collapsible airway than overweight/obese patients with apnea (critical closing pressure: -3.7 ± 1.9 vs. 0.6 ± 1.2 cm H2O; P = 0.003; mean ± 95% confidence interval), but a more collapsible airway relative to normal-weight control subjects (-8.8 ± 3.1 cm H2O; P < 0.001). Notably, overweight/obese subjects without apnea exhibited a threefold greater upper-airway muscle responsiveness than both overweight/obese patients with apnea (Δgenioglossus EMG/Δepiglottic pressure: -0.49 [-0.22 to -0.79] vs. -0.15 [-0.09 to -0.22] %max/cm H2O; P = 0.008; mean [95% confidence interval]) and normal-weight control subjects (-0.16 [-0.04 to -0.30] %max/cm H2O; P = 0.02). Loop gain was elevated (more negative) in both overweight/obese groups and normal-weight control subjects (P = 0.02). Model-based analysis demonstrated that overweight/obese individuals without apnea rely on both more favorable anatomy and collapsibility and enhanced upper-airway dilator muscle responses to avoid OSA.ConclusionsOverweight/obese individuals without apnea have a moderately compromised upper-airway structure that is mitigated by highly responsive upper-airway dilator muscles to avoid OSA. Elucidating the mechanisms underlying enhanced muscle responses in this population may provide clues for novel OSA interventions.

Study objectivesRapid eye movement (REM)-induced hypotonia of the major upper airway dilating muscle (genioglossus) potentially contributes to the worsening of obstructive sleep apnea that occurs during this stage. No prior human single motor unit (SMU) study of genioglossus has examined this possibility to our knowledge. We hypothesized that genioglossus SMUs would reduce their activity during stable breathing in both tonic and phasic REM compared to stage N2 sleep. Further, we hypothesized that hypopneas occurring in REM would be associated with coincident reductions in genioglossus SMU activity.DesignThe activity of genioglossus SMUs was studied in (1) neighboring epochs of stage N2, and tonic and phasic REM; and (2) during hypopneas occurring in REM.SettingSleep laboratory.Participants29 subjects (38 ± 13 y) (17 male).InterventionNatural sleep, including REM sleep and REM hypopneas.Measurement and resultsSubjects slept overnight with genioglossus fine-wire intramuscular electrodes and full polysomnography. Forty-two SMUs firing during one or more of stage N2, tonic REM, or phasic REM were sorted. Twenty inspiratory phasic (IP), 17 inspiratory tonic (IT), and five expiratory tonic (ET) SMUs were characterized. Fewer units were active during phasic REM (23) compared to tonic REM (30) and stage N2 (33). During phasic REM sleep, genioglossus IP and IT SMUs discharged at slower rates and for shorter durations than during stage N2. For example, the SMU peak frequency during phasic REM 5.7 ± 6.6 Hz (mean ± standard deviation) was less than both tonic REM 12.3 ± 9.7 Hz and stage N2 16.1 ± 10.0 Hz (P < 0.001). The peak firing frequencies of IP/IT SMUs decreased from the last breath before to the first breath of a REM hypopnea (11.8 ± 10.9 Hz versus 5.7 ± 9.4 Hz; P = 0.001).ConclusionGenioglossus single motor unit activity is significantly reduced in REM sleep, particularly phasic REM. Single motor unit activity decreases abruptly at the onset of REM hypopneas.

Obstructive sleep apnoea is an increasingly common disorder of repeated upper airway collapse during sleep, leading to oxygen desaturation and disrupted sleep. Features include snoring, witnessed apnoeas, and sleepiness. Pathogenesis varies; predisposing factors include small upper airway lumen, unstable respiratory control, low arousal threshold, small lung volume, and dysfunctional upper airway dilator muscles. Risk factors include obesity, male sex, age, menopause, fluid retention, adenotonsillar hypertrophy, and smoking. Obstructive sleep apnoea causes sleepiness, road traffic accidents, and probably systemic hypertension. It has also been linked to myocardial infarction, congestive heart failure, stroke, and diabetes mellitus though not definitively. Continuous positive airway pressure is the treatment of choice, with adherence of 60-70%. Bi-level positive airway pressure or adaptive servo-ventilation can be used for patients who are intolerant to continuous positive airway pressure. Other treatments include dental devices, surgery, and weight loss.

New Findings: What is the central question of this study?How does alcohol intake, which worsens obstructive sleep apnoea, alter motor control of the genioglossus muscle, an upper airway dilator, in healthy awake human volunteers, and does alcohol alter genioglossus muscle afterdischarge?What is the main finding and its importance?Alcohol consumption had a very minor effect on the activity of the genioglossus in healthy young individuals studied during wakefulness and did not alter afterdischarge, leaving open the possibility that alcohol worsens obstructive sleep apnoea via other mechanisms. Alcohol worsens obstructive sleep apnoea (OSA). This effect is thought to be due to alcohol's depressant effect on upper airway dilator muscles such as the genioglossus, but how alcohol reduces genioglossal activity is unknown. The aim of this study was to investigate the effect of alcohol consumption on genioglossus muscle single motor units (MUs). Sixteen healthy individuals were studied on two occasions (alcohol: breath alcohol concentration ∼0.07% and placebo). They were instrumented with a nasal mask, four intramuscular genioglossal EMG electrodes, and an ear oximeter. They were exposed to 8–12 hypoxia trials (45–60 s of 10% O2 followed by one breath of 100% O2) while awake. MUs were sorted according to their firing patterns and quantified during baseline, hypoxia and recovery. For the alcohol and placebo conditions, global muscle activity (mean ± SD peak inspiratory EMG = 119.3 ± 44.1 and 126.5 ± 51.9 μV, respectively, P = 0.53) and total number of MUs recorded at baseline (68 and 67, respectively) were similar. Likewise, the peak discharge frequency did not differ between conditions (21.2 ± 4.28 vs. 22.4 ± 4.08 Hz, P = 0.09). There was no difference between conditions in the number (101 vs. 88, respectively) and distribution of MU classes during hypoxia, and afterdischarge duration was also similar. In this study, alcohol had a very minor effect on genioglossal activity and afterdischarge in these otherwise healthy young individuals studied while awake. If similar effects are observed during sleep, it would suggest that the worsening of OSA following alcohol may be related to increased upper airway resistance/nasal congestion or arousal threshold changes. [ABSTRACT FROM AUTHOR]

The relationship between sex and post-concussion symptom (PCS) reporting after mild traumatic brain injury (mTBI) is not well understood. Subjective sleep disturbance and fatigue impact PCS reporting after mTBI and show sex differences in the normal population. This study investigated whether sex had a relationship with PCS reporting after mTBI, independently of self-reported sleep disturbance and fatigue. Ninety-two premorbidly healthy adults in the post-acute period after mTBI completed the Rivermead Post-Concussion Symptoms Questionnaire, the Pittsburgh Sleep Quality Index, the Multidimensional Fatigue Inventory and measures of depression, anxiety and post-traumatic stress symptomatology. Females (n = 23) demonstrated higher levels of fatigue (p =.019) and greater psychological distress (p =.001) than males (n = 69), but equivalent levels of sleep disturbance (p =.946). Bootstrapping analyses were undertaken because PCS responses were not normally distributed. Female sex predicted greater PCS reporting (p =.001), independently of subjective sleep disturbance, fatigue, psychological distress and litigation status. The current findings support and extend previous work showing premorbidly healthy females are at higher risk of experiencing elevated PCS after mTBI than males in the post-acute period after mTBI. It may be beneficial for clinicians to be particularly sensitive to increased symptom reporting after mTBI in females, irrespective of sleep quality, fatigue or psychological status. [ABSTRACT FROM AUTHOR]

Introduction: An association between the increased risk of late stillbirth and the maternal supine sleeping position has been recently established. The risk of stillbirth following supine sleep has been suspected to occur as a result of aortocaval compression by the gravid uterus. A number of studies conducted during wakefulness have reported compromised cardiovascular function during supine rest, as demonstrated by reductions in cardiac output, blood pressure and utero-placental blood flow. It remains unclear whether similar effects are also present during sleep, due to the presence of key sleep-specific changes in cardiovascular function.Objective: To investigate the changes in maternal cardiovascular function between the supine and left-lateral positions during wakefulness and non-rapid eye movement (NREM) sleep in late pregnancy.Methods: Twenty-nine women with a singleton pregnancy between 24.7 and 36.7 weeks' gestation participated in a single overnight sleep study. Physiological measures (blood pressure, heart rate, heart rate variability - HRV, and pulse arrival time - PAT) were measured and recorded throughout the night using standard polysomnography equipment and the Portapres Model-2 device. As the present study evaluated cardiovascular changes during natural rest and sleep in pregnancy, participants were not given explicit instructions on which position to adopt. Body position was continuously recorded using a position monitor and verified with video recording.Results: No changes in systolic, diastolic or mean arterial blood pressure were observed between the left-lateral and supine positions during wakefulness or sleep. However, heart rate was significantly higher in the supine position compared to the left during wakefulness (p= .03), with a similar trend present during sleep (p= .11). A significantly shorter PAT was measured in the supine position (compared to the left) during wakefulness (p= .01) and sleep (p= .01). No change in HRV measures was observed between the left and supine positions in either state.Conclusion: Blood pressure did not appear to differ significantly between the left-lateral and supine positions during wakefulness and sleep. The lack of blood pressure differences may reflect elevated sympathetic activity during rest and sleep in the supine position (compared to the left), suggesting that some degree of compensation for aortocaval compression may still be possible during sleep. [ABSTRACT FROM AUTHOR]

Our aim was to evaluate cardiac changes evoked by spontaneous and sound-induced arousals from sleep. Cardiac responses to spontaneous and auditory-induced arousals were recorded during overnight sleep studies in 28 young healthy subjects (14 males, 14 females) during non-rapid eye movement sleep. Computerized analysis was applied to assess beat-to-beat changes in heart rate, atrio-ventricular conductance, and ventricular repolarization from 30 s before to 60 s after the auditory tone. During both types of arousals, the most consistent change was the increase in the heart rate (in 62% of spontaneous and in 89% of sound-induced arousals). This was accompanied by an increase or no change in PR interval and by a decrease or no change in QT interval. The magnitude of all cardiac changes was significantly higher for tone-induced vs. spontaneous arousals (mean [+ or -] SD for heart rate: +9 [+ or -] 8 vs. + 13 [+ or -] 9 beats per min; for PR prolongation: 14 [+ or -] 16 vs. 24 [+ or -] 22 ms; for QT shortening: -12 [+ or -] 6 vs. -20 [+ or -] 9 ms). The prevalence of transient tachycardia and PR prolongation was also significantly higher for tone-induced vs. spontaneous arousals (tachycardia: 85% vs. 57% of arousals, P < 0.001; PR prolongation: 51% vs. 25% of arousals, P < 0.001). All cardiac responses were short-lasting (10-15 s). We conclude that cardiac pacemaker region, conducting system, and ventricular myocardium may be under independent neural control. Prolongation of atrio-ventricular delay may serve to increase ventricular filling during arousal from sleep. Whether prolonged atrio-ventricular conductance associated with increased sympathetic outflow to the ventricular myocardium contributes to arrhythmogenesis during sudden arousal from sleep remains to be evaluated. autonomic; atrio-ventricular node; QT; sympathetic