Obstructive sleep apnea (OSA) is characterised by cyclical respiratory events followed by hyperpneic breaths that frequently coincide with cortical arousals. Whilst this post-event hyperventilation partly reflects accumulated respiratory stimuli, arousal itself appears to contribute independently through both its presence and its intensity. This study aimed to quantify the relative contributions of arousal presence and arousal intensity to post-event ventilation, independent of chemoreflex-driven responses. Two retrospective polysomnography data sets were analysed: a community-based cohort (Multi-Ethnic Study of Atherosclerosis, MESA; N = 1781 included) and a Physiological Study data set (N = 67). For every obstructive respiratory event, arousal presence (0/1), arousal intensity (range 0 to 9) and post-event ventilation were derived for each event, and mixed-effects linear models were used to examine their associations at both the inter-event and inter-participant levels. At the inter-event level, arousal presence at event termination increased ventilation by 17-30%Eupnea (increase above eupneic baseline) in both data sets, with each step increment in arousal intensity contributing an additional 1-4%Eupnea. At the inter-participant level, each step increment in overnight mean arousal intensity was associated with a 2-4%Eupnea increase in the ventilatory response to arousal in both data sets. These findings demonstrate that arousal presence plays an important role in post-event hyperventilation in OSA, with arousal intensity exerting a modest effect per increment but a substantial cumulative effect across the full 0-9 scale. Consistent across both data sets, the results suggest a mechanistic pathway to post-event hyperventilation distinct from chemoreflex stimulation.

STUDY OBJECTIVES:Central (CSA) and obstructive (OSA) sleep apnea are common in heart failure (HF) patients, and treatment options depend on differential classification. To better characterize CSA vs OSA, we evaluated the discriminative value of established and novel polysomnographic traits in patients with HF. METHODS:We analyzed LOFT-HF trial participants with reduced left ventricular ejection fraction (LVEF) and apnea-hypopnea index (AHI) >15 events/hr. Central versus obstructive events were classified with expert investigator input. Multivariable logistic regression tested whether CSA (>50% of central/mixed events; otherwise OSA) was associated with increased loop gain, and other mechanistic traits (arousal threshold, collapsibility, muscle compensation). Mechanistic traits together with novel clinically-informed traits (e.g. event periodicity, flow limitation) were modeled to provide a probability score "Pr(CSA)" for objective CSA-versus-OSA discrimination. RESULTS:Among 122 HF patients (CSA:OSA=84:38), CSA was associated with higher loop gain (OR=4.4[2.2-9.1]), lower arousal threshold (6.4[2.4-16.9]), and greater muscle compensation (2.5[1.0-6.2]). Novel traits-greater event periodicity, larger event-related drive reduction, and reduced flow limitation-further improved discrimination (likelihood ratio test P=0.013 vs. mechanistic model). The final model (AUC=0.88) identified a subgroup enriched for true CSA (OR=8.4[3.5-20.1]). Sensitivity analyses using stricter central apnea-based definitions yielded similar or stronger associations with loop gain and modestly improved discrimination, although fewer individuals met CSA criteria. CONCLUSIONS:Patients with HF and CSA exhibit a distinct set of polysomnographic characteristics compared to OSA, which may facilitate their objective physiology-based characterization along the CSA-OSA continuum.

Ride-hail drivers often experience working conditions that increase their vulnerability to sleeprelated issues and their exposure to fatigued driving. This exploratory study aimed to identify the factors contributing to sleep duration, sleep quality, and falling asleep, and to examine the relationship between these sleep indices and sleep-related fatigue in ride hail drivers. One hundred drivers (12% female) completed a survey reporting their sleep patterns, work-related factors, and experiences of fatigued driving. Regression analyses were conducted to examine potential contributing factors, including working hours, prioritising money over sleep, income, age, perceived impact of fatigue, working in secondary jobs, and their links to sleep-related measures. The analysis revealed that a substantial proportion of the drivers (44%) slept less than the recommended 7 h per night. Prioritising financial gain over adequate sleep, holding a secondary job, perceived fatigue impact, being younger, and working longer hours were identified as contributing factors to one or more sleep-related issues.A substantial proportion of drivers (22%) who had fallen asleep while driving indicated that they had been involved in a crash. Further analyses indicated that sleep-related fatigue was significantly associated with the frequency of falling asleep at the wheel in the past month, shorter sleep duration, and decreased sleep quality. These data suggest an urgent need for targeted strategies to mitigate the risks of fatigued driving and other sleep-related driving issues. These may include implementing educational programs on fatigue management and the critical role of adequate sleep in safe driving, and promoting policies that support better work-life balance and regulated working hours.

Study Objectives:Emerging evidence indicates that Indigenous peoples experience disproportionately high rates of obstructive sleep apnea (OSA). This systematic review aimed to examine OSA prevalence, contributing factors, and intervention or treatment outcomes among Indigenous peoples worldwide. Materials and Methods:We systematically searched PubMed, Embase, CINAHL, Cochrane CENTRAL, ATSI Health, Web of Science and PsycINFO (last searched June 30, 2025), and grey literature for original research involving Indigenous peoples (≥18 years) diagnosed with OSA via self-report or laboratory-based measures (e.g. polysomnography). Data extraction focused on study characteristics and key findings. Methodological quality was assessed using NIH tools, and cultural appropriateness was evaluated using the CREATE Aboriginal and Torres Strait Islander Quality Appraisal Tool. A narrative synthesis was conducted. Results:From 599 records, 41 studies from six countries were included. OSA prevalence among Indigenous populations varied widely (community-based samples, 6.5%-69%; referred samples, 85%-95%; self-reported diagnosis, 1.2%-8.4%; hospital audit diagnoses, 0.8%-11.4%), with only one study reporting a robust population-based estimate (~6.5% among Māori). Severe cases predominated in referred samples. Factors associated with OSA included male sex, age, BMI, neck circumference, craniofacial and geographic factors, and symptoms such as snoring. Treatment evidence was limited to CPAP, with low adherence. Conclusions:Findings suggests that OSA is common among Indigenous peoples across diverse settings. However, prevalence estimates are heterogeneous and limited by differences in study design, sampling frame, and diagnostic approaches, with most evidence based on referred clinical samples. Improving awareness and culturally responsive screening and management may improve outcomes. Sleep health among Indigenous peoples warrants a higher priority in research, policy and practice. Registration:The protocol for this systematic review was registered with Prospero (CRD42024466932).

Sleep-disordered breathing is incompletely characterized by the apnea-hypopnea index. Although typically viewed as milder disease, snoring and flow limitation can yield major deficits in sleep health for both patients and their bed partners. Here we tested whether a combined noradrenergic and antimuscarinic intervention to activate pharyngeal muscles yields improved snoring loudness and flow limitation severity, plus self-reported outcomes, by snorers and their bed partners. In a randomized placebo-controlled double-blind crossover study, adults with loud habitual snoring took atomoxetine plus oxybutynin for 10 days before bedtime at full adult doses (80 and 5 mg, respectively; half-dose run-in on days 1–3) and at half-doses (40 and 2.5 mg, respectively). Baseline polysomnography with tracheal sound recording established baseline snoring (mean loudness > 75 dB) and an apnea-hypopnea index of < 15 events/h. Mixed models compared full and half-doses to placebo in snoring loudness, flow limitation, and snoring self-evaluation and bed-partner evaluation scores, adjusting for baseline and period effects (intention-to-treat analysis). Fifteen participants were randomly assigned and 13 completed all treatment periods. Snoring loudness was reduced with full dose (−9.3 [−19.6, −2.9] dB; difference [95 Clinical Trial Registration: Registry: ClinicalTrials.gov; Name: Pharmacological Intervention for Symptomatic Snoring; URL: https://clinicaltrials.gov/study/NCT03720353 ; Identifier: NCT03720353. Calianese N, Hess LB, Vena D, et al. Atomoxetine plus oxybutynin for symptomatic snoring and airflow limitation in individuals without moderate-to-severe obstructive sleep apnea. J Clin Sleep Med. 2025;21(9):1579–1590.

Obstructive Sleep Apnea (OSA) is a highly prevalent, yet significantly under-recognized disorder in First Nations Australians. Responding to strong community demand for local capacity building for sleep health equity, this paper outlines the Let's Yarn About Sleep-OSA (LYAS-OSA) program protocol. The LYAS-OSA program will involve the co-design, implementation, and evaluation of a place-based, culturally responsive, nurse-led, and Aboriginal Health Worker-supported model for OSA diagnosis and management for First Nations peoples. This program will partner with health services and organizations across 12 communities in Queensland, Australia. The program will be conducted from 2023 to 2027. During the set up and development stage, an advanced data analytics study of secondary data will examine OSA phenotypes and symptomatology in First Nations Queensland communities. In addition, consumers and healthcare professionals will be engaged in co-design workshops to inform the development of a service delivery model framework. In stage two, local capacity building activities for Aboriginal Health Workers and nurses will be undertaken, with training on OSA diagnosis and management. This work will culminate in delivering and evaluating the co-designed service model. This community-led approach to co-designing, implementing, and evaluating the LYAS-OSA service delivery model will advance knowledge to deliver culturally responsive, context-responsive, OSA diagnosis, and management care for First Nations communities. The LYAS-OSA program outputs will significantly contribute to the evidence base and service delivery provision for OSA care, thereby improving sleep health equity for First Nations Australians.Statement of Significance Obstructive Sleep Apnea (OSA) in First Nations communities is highly prevalent, yet limited community awareness, lack of culturally responsive services, and unavailability of local diagnosis and management hinder timely and effective care. Addressing these gaps is crucial for improving sleep health equity for First Nations Australians. The program offers a community-led, co-designed, place-based model of care that integrates data analytics, co-design, and healthcare providers' capacity building to address service delivery gaps. This approach aims to bridge service delivery gaps in Obstructive Sleep Apnea care for First Nations peoples across Australia. The outputs and outcomes from this program will significantly contribute to the evidence base for improving the quality and accessibility of Obstructive Sleep Apnea care for First Nations Australians.

BACKGROUND:Patient selection for hypoglossal nerve stimulation (HGNS) for obstructive sleep apnoea (OSA) requires assessment of pharyngeal site of collapse using drug-induced sleep endoscopy (DISE). The current study aims to address two key knowledge gaps. First, we prospectively confirm that, among HGNS candidates, reduced HGNS efficacy is associated with oropharyngeal lateral wall (OLW) collapse (Aim 1). Second, given DISE is a resource-intensive procedure and delays treatment, we evaluate whether a recently developed non-invasive method for identifying OLW collapse using airflow shapes is associated with reduced HGNS efficacy (Aim 2). METHODS:Patients who underwent DISE, HGNS implantation and follow-up sleep testing were included in Aim 1 (n=369) as part of an observational cohort study. For Aim 2, airflow data estimating OLW collapse probability were collected during DISE via a pneumotachograph (n=138; DISE Flow cohort) and from a home sleep test (HST) via nasal cannula for validation (n=46; HST cohort). Linear regression quantified associations between HGNS efficacy (percent reduction in apnoea-hypopnoea index (AHI)) and DISE-determined OLW collapse (Aim 1) or flow shape-determined OLW collapse (probability score per 2sd) (Aim 2), adjusting for baseline AHI. RESULTS:Compared to non-OLW collapse, DISE-determined OLW collapse reduced HGNS efficacy by -18.0% (95% CI -31.9- -6.2%). Increased flow shape-determined OLW collapse probability (Δ2sd) was associated with reduced HGNS efficacy in both DISE Flow (-24.8%, 95% CI -40.4- -11.7%) and HST (-22.7%, 95% CI -50.0- -2.6%) cohorts. CONCLUSION:This study prospectively validates OLW collapse as a key factor in HGNS failure and shows that airflow-based identification of OLW collapse can effectively estimate HGNS efficacy, representing a significant advancement in patient selection for HGNS.

STUDY OBJECTIVES:There is substantial night-to-night variability (NtNV) in obstructive sleep apnea (OSA) severity in some individuals; however, predictors for this remain incompletely understood. This study aims to quantify the degree of NtNV in the apnea-hypopnea index (AHI), hypoxic burden, airflow limitation, and OSA endotypes; to determine if a relationship exists between the degree of NtNV in AHI and in endotype expression; to assess whether the degree of flow-limited breathing is predictive of the degree of NtNV of the AHI. METHODS:Seventy-one patients with OSA underwent 2 polysomnograms (PSGs). OSA endotypes, hypoxic burden, and flow limitation frequency were extracted from PSG data. Intraindividual agreement was assessed and associations with the NtNV of the AHI were calculated. Patients were grouped into High Variability vs Low Variability based on the degree of difference in AHI between each night. RESULTS:Despite wide limits of agreement, at the group level most PSG and endotype variables were not statistically different between first and second night. Flow limitation frequency was 7.7% (2.1-13, p < 0.01) higher on the second night compared to baseline. There were weak linear associations between NtNV of endotypes and NtNV of the AHI. In subgroup analysis, there was greater difference between nights for Vactive (5%eupnea, p = 0.01), Vpassive (3.1%eupnea, p = 0.03), Vcomp (3.2%eupnea, p = 0.01), and arousal threshold (4.1%eupnea, p = 0.04) in the High-Variability compared to the Low-Variability group. CONCLUSIONS:There is high NtNV in AHI, OSA endotypes, and flow limitation in some individuals; however, no strong linear relationship exists between these changes. CLINICAL TRIALS:Combined Upper-airway and Breathing Control Therapies for Obstructive Sleep Apnea (https://clinicaltrials.gov/study/NCT03189173?term=NCT03189173&rank=1, NCT03189173). Pharmacological Intervention for Symptomatic Mild Sleep Disordered Breathing (https://clinicaltrials.gov/study/NCT04611750?term=NCT04611750&rank=1, NCT04611750). Combination Pharmacological Interventions for Multiple Mechanisms of Obstructive Sleep Apnea (https://clinicaltrials.gov/study/NCT03892772?term=NCT03892772&rank=1, NCT03892772).

Hypoxic burden (HB) is a measure incorporating frequency, depth and duration of respiratory event-related desaturations. While HB is associated with cardiovascular disease in adults with obstructive sleep apnea (OSA), it has not been assessed in typically developing (TD) children with OSA, nor in children with Down syndrome (DS), who have a higher incidence of OSA with more severe hypoxia. We assessed whether HB in these children was related to heart rate variability (HRV), an indicator of cardiovascular outcomes. Children (3-19 years, n = 44) with DS and TD children matched for OSA severity, age and sex underwent overnight polysomnography and were grouped into primary snoring (PS), Mild or Moderate/Severe (MS) OSA. HRV was analysed using power spectral analysis of the electrocardiograph. Regression analysis determined whether HB was predictive of HRV. Children with MS OSA in both groups had higher HB compared with children with PS (p < 0.001 for both) and Mild OSA (DS, p < 0.001; TD, p < 0.05). Children with DS and PS or Mild OSA had higher HB compared with TD children (PS p < 0.05; Mild OSA p < 0.001). There was no difference between the MS OSA groups. HB predicted dampened sympathetic and parasympathetic activity only in children with DS (R 2 = 0.12, β = -10.6, SE = 4.6, p = 0.03). HB was higher in children with DS and PS or Mild OSA compared to TD children and predicted dampened autonomic function in children with DS. The potential contribution of the adverse effects of HB on autonomic function adds weight to the importance of identifying and treating OSA in children with DS.

Rationale: Both the site of upper airway collapse during drug-induced sleep endoscopy (DISE) and pathophysiological endotypic traits are associated with non-continuous positive airway pressure treatment outcomes for obstructive sleep apnea (OSA). Reduced hypoglossal nerve stimulation treatment efficacy has been associated with complete concentric collapse at the level of the palate (CCCp), lateral wall collapse, lower arousal threshold, and poor dilator muscle compensation. However, these predictors may not be independent. Objective: Assess the relationship between the site of upper airway collapse (structure) and pathophysiological endotypic traits (function). Methods: This retrospective cohort study examined 182 patients (median [95% confidence interval] apnea-hypopnea index, 24.2 [17.6, 32.8]; body mass index, 27.8 [25.2, 30.5]; age, 51.3 [40.4, 58.8] yr) who underwent in-laboratory polysomnography and DISE. All DISE studies were scored by one researcher, thereby avoiding interrater variability. Endotypic traits (loop gain, collapsibility, arousal threshold, and compensation) were estimated using routine polysomnography (Sands et al., Am J Respir Crit Care Med 2018;197:1187-1197). Linear regression quantified differences in traits between DISE categories. Multivariable logistic regression quantified associations between DISE categories (dependent variable, with vs. without a certain collapse type) and individual traits. Analyses were mutually adjusted for other endotypic traits. Results: CCCp was independently associated with greater collapsibility (Δ collapsibility, 9.8 [4.6, 15.0]%; P < 0.001 with vs. without CCCp; odds ratio [OR], 6.9 [95% confidence interval, 2.2, 22.1] per 2-standard deviation [2 SD] increase in collapsibility [SD, 15.9%]) but a lower arousal threshold (Δ arousal threshold, -8.4 [-15.6, -1.2]%; OR, 5.4 [1.2, 24.2] per 2 SD [SD, 24.9%]). Conversely, complete tongue base collapse was associated with less severe collapsibility (Δ collapsibility, -5.9 [-10.2, -1.6]%; OR, 5.0 [1.4, 17.9]) but a higher arousal threshold (Δ arousal threshold, 7.6 [1.6, 13.5]%; OR, 5.7 [1.4, 23.5]). Complete lateral wall collapse was independently associated with reduced compensation (Δ compensation, -8.0 [-14.5, -1.5]%; P = 0.018; OR, 3.6 [1.2, 10.4] per 2 SD [SD, 17.5%]), whereas epiglottic collapse was associated with greater compensation (Δ compensation, 8.1 [1.0, 15.3]%; OR, 5.8 [1.1, 31.2]). Findings persisted with additional adjustment for apnea-hypopnea index and body mass index, except for collapsibility and tongue base collapse. Loop gain was not associated with any site of collapse. Conclusions: Different sites of upper airway collapse manifest distinctly different pathophysiological traits in patients with OSA. The greater collapsibility and lower arousal threshold seen with CCCp and reduced compensation with lateral wall collapse may help explain reduced non-continuous positive airway pressure treatment efficacy in these populations. Clinical trial registered with www.clinicaltrials.gov (NCT04753684).

Rationale:Excessive daytime sleepiness, an important symptom of obstructive sleep apnea (OSA), is commonly quantified using the Epworth Sleepiness Scale score (ESS). Baseline OSA severity measures (ventilatory burden, flow limitation, and hypoxemia) provide insights into OSA pathophysiology and could predict changes in sleepiness (i.e. change-in-ESS) following continuous positive airway pressure (CPAP) treatment. Objectives:We hypothesized that change-in-ESS following CPAP treatment can be predicted from baseline polysomnography. Methods:Associations between OSA severity measures and ESS were evaluated in 2332 participants, adjusting for age, sex, BMI, and total sleep time. Change-in-ESS prediction was evaluated using 213 CPAP treatment studies (HomePAP, BestAIR, and ABC) in three steps: severity measures were compared (adjusted regression, n =64), a prediction model was developed using baseline ventilatory burden and baseline ESS ( n =139), and then evaluated in holdout participants ( n =74). Measurements and Main Results:In cross-sectional analysis, ESS was associated with ventilatory burden (0.45 points/SD; 95% CI 0.23-0.67), hypoxic burden (0.39; 0.17-0.62), the apnea-hypopnea index (AHI) (0.36; 0.14-0.59), and flow limitation severity (0.22; 0.01-0.43). Comparison analysis revealed that change-in-ESS was most strongly associated with baseline ventilatory burden (-1.08 points/SD; -2.13 to -0.05) and baseline ESS (-2.75; -3.83 to -1.69); the AHI association was weaker (-0.97; -2.01-0.05). Predicted change-in-ESS and actual change-in-ESS were correlated in holdout participants (adjusted R² =0.313); median [IQR] actual change-in-ESS of predicted responders (≥2-point ESS improvement, n =54, 73.0%) was -5.0 [-10.0 to -2.0] and non-responders was 0.0 [-1.0-1.0] ( P <0.001). Conclusions:Baseline ventilatory burden and baseline ESS were independently associated with change-in-ESS and could be used together to inform clinicians whether CPAP treatment will likely improve a patient's sleepiness.

Rationale: The physiological factors modulating the severity of snoring have not been adequately described. Airway collapse or obstruction is generally the leading determinant of snore sound generation; however, we suspect that ventilatory drive is of equal importance. Objective: To determine the relationship between airway obstruction and ventilatory drive on snore loudness. Methods: In 40 patients with suspected or diagnosed obstructive sleep apnea (1-98 events/hr), airflow was recorded via a pneumotachometer attached to an oronasal mask, ventilatory drive was recorded using calibrated intraesophageal diaphragm electromyography, and snore loudness was recorded using a calibrated microphone attached over the trachea. "Obstruction" was taken as the ratio of ventilation to ventilatory drive and termed flow:drive, i.e., actual ventilation as a percentage of intended ventilation. Lower values reflect increased flow resistance. Using 165,063 breaths, mixed model analysis (quadratic regression) quantified snore loudness as a function of obstruction, ventilatory drive, and the presence of extreme obstruction (i.e., apneic occlusion). Results: In the presence of obstruction (flow:drive = 50%, i.e., doubled resistance), snore loudness increased markedly with increased drive (+3.4 [95% confidence interval, 3.3-3.5] dB per standard deviation [SD] change in ventilatory drive). However, the effect of drive was profoundly attenuated without obstruction (at flow:drive = 100%: +0.23 [0.08-0.39] dB per SD change in drive). Similarly, snore loudness increased with increasing obstruction exclusively in the presence of increased drive (at drive = 200% of eupnea: +2.1 [2.0-2.2] dB per SD change in obstruction; at eupneic drive: +0.14 [-0.08 to 0.28] dB per SD change). Further, snore loudness decreased substantially with extreme obstruction, defined as flow:drive <20% (-9.9 [-3.3 to -6.6] dB vs. unobstructed eupneic breathing). Conclusions: This study highlights that ventilatory drive, and not simply pharyngeal obstruction, modulates snore loudness. This new framework for characterizing the severity of snoring helps better understand the physiology of snoring and is important for the development of technologies that use snore sounds to characterize sleep-disordered breathing.

Background Differences in the pharyngeal site of collapse influence efficacy of non -continuous positive airway pressure therapies for obstructive sleep apnoea (OSA). Notably, complete concentric collapse at the level of the palate (CCCp) during drug -induced sleep endoscopy (DISE) is associated with reduced efficacy of hypoglossal nerve stimulation, but CCCp is currently not recognisable using polysomnography. Here we develop a means to estimate DISE -based site of collapse using overnight polysomnography. Methods 182 OSA patients provided DISE and polysomnography data. Six polysomnographic flow shape characteristics (mean during hypopnoeas) were identified as candidate predictors of CCCp (primary outcome variable, n=44/182), including inspiratory skewness and inspiratory scoopiness. Multivariable logistic regression combined the six characteristics to predict clear presence (n=22) versus absence (n=128) of CCCp (partial collapse and concurrent tongue base collapse excluded). Odds ratios for actual CCCp between predicted subgroups were quantified after cross -validation. Secondary analyses examined complete lateral wall, tongue base or epiglottis collapse. External validation was performed on a separate dataset (ntotal=466). Results CCCp was characterised by greater scoopiness (f3=1.5 +/- 0.6 per 2SD, multivariable estimate +/- SE) and skewness (f3=11.4 +/- 2.4) compared with non-CCCp. The odds ratio for CCCp in predicted positive versus negative subgroups was 5.0 (95% CI 1.9-13.1). The same characteristics provided significant crossvalidated prediction of lateral wall (OR 6.3, 95% CI 2.4-16.5), tongue base (OR 3.2, 95% CI 1.4-7.3) and epiglottis (OR 4.4, 95% CI 1.5-12.4) collapse. CCCp and lateral wall collapse shared similar characteristics (skewed, scoopy), diametrically opposed to tongue base and epiglottis collapse characteristics. External validation confirmed model prediction. Conclusions The current study provides a means to recognise patients with likely CCCp or other DISEbased site of collapse categories using routine polysomnography. Since site of collapse influences therapeutic responses, polysomnographic airflow shape analysis could facilitate precision site -specific OSA interventions.

The aim of this study was to investigate sleep-wake behavior and gain insights into perceived impairment (sleep, fatigue, and cognitive function) of athletes competing in two international multi-day adventure races. Twenty-four athletes took part across two independent adventure races: Queensland, Australia and Alaska, USA. Individual sleep periods were determined via actigraphy, and racers self-reported their perceived sleep disturbances, sleep impairment, fatigue and cognitive function. Each of these indices was calculated for pre-, during- and post-race periods. Sleep was severely restricted during the race period compared to pre-race (Queensland, 7:46 [0:29] vs. 2:50 [1:01]; Alaska, 7:39 [0:58] vs. 2:45 [2:05]; mean [SD], hh:mm). As a result, there was a large cumulative sleep debt at race completion, which was not 'reversed' in the post-race period (up to 1 week). The deterioration in all four self-reported scales of perceived impairment during the race period was largely restored in the post-race period. This is the first study to document objective sleep-wake behaviors and subjective impairment of adventure racers, in the context of two geographically diverse, multi-day, international adventure races. Measures of sleep deprivation indicate that sleep debt was extreme and did not recover to pre-race levels within 1 week following each race. Despite this objective debt continuing, perceived impairment returned to pre-race levels quickly post-race. Therefore, further examination of actual and perceived sleep recovery is warranted. Adventure racing presents a unique scenario to examine sleep, performance and recovery.

BACKGROUND:Approximately 60% of veterans living with posttraumatic stress disorder (PTSD) experience obstructive sleep apnoea (OSA). Why OSA is so prevalent in individuals with PTSD remains unknown, though PTSD may influence the underlying endotypes known to cause OSA. We examined whether these endotypes (upper airway collapsibility, muscle compensation, loop gain, and the arousal threshold) differ between those with comorbid OSA and PTSD relative to their counterparts with OSA-only. METHODS:Using the ventilatory flow pattern from diagnostic polysomnography, the OSA endotypes were measured in a retrospective cohort of 21 OSA patients with PTSD and 27 OSA-only patients. All participants were trauma exposed elderly male Australian Vietnam War veterans with mild-to-severe OSA (median Apnoea-Hypopnea index: 20.2 vs. 23.6 events/h). Age and BMI were similar between groups (70.7 vs. 71.7 years, and 28.4 vs. 28.4 kg/m2). RESULTS:There were no significant differences in the OSA endotype traits between PTSD + OSA and OSA-only patients for upper airway collapsibility (76.68 [71.53-83.56] vs. 78.35 [72.81-83.82] %Veupnea, median [IQR]), muscle compensation (4.27 [0.34-9.18] vs. 5.41 [1.83-7.21] %Veupnea), loop gain (0.56(0.17) vs. 0.60(0.14)), and arousal threshold (135.76 [126.59-147.54] vs. 146.95 [128.64-151.28] %Veupnea). CONCLUSION:The OSA endotypes in veterans with PTSD were similar to their trauma exposed OSA-only counterparts. PTSD appears to exert little influence on the OSA endotypes beyond the effect that age and trauma exposure may have. The aetiology of increased prevalence of OSA in PTSD remains unclear. Further work examining OSA endotypes using larger and more diverse samples is needed before robust conclusions can be made.

Background Pharyngeal flow limitation during pregnancy may be a risk factor for adverse pregnancy outcomes but was previously challenging to quantify. Our objective was to determine whether a novel objective measure of flow limitation identifies an increased risk of pre-eclampsia (primary outcome) and other adverse outcomes in a prospective cohort: Nulliparous Pregnancy Outcomes Study Monitoring Mothers-to-be (nuMoM2b). Methods Flow limitation severity scores (0%=fully obstructed, 100%=open airway), quantified from breath- by-breath airflow shape, were obtained from home sleep tests during early (6-15 - 15 weeks) and mid (22-31 - 31 weeks) pregnancy. Multivariable logistic regression quantified associations between flow limitation (median overnight severity, both time-points averaged) and pre-eclampsia, adjusting for maternal age, body mass index (BMI), race, ethnicity, chronic hypertension and flow limitation during wakefulness. Secondary outcomes were hypertensive disorders of pregnancy (HDP), gestational diabetes mellitus (GDM) and infant birthweight. Results Of 1939 participants with flow limitation data at both time-points (mean +/- SD SD age 27.0 +/- 5.4 years and BMI 27.7 +/- 6.1 kg m-2), - 2 ), 5.8% developed pre-eclampsia, 12.7% developed HDP and 4.5% developed GDM. Greater flow limitation was associated with increased pre-eclampsia risk: adjusted OR 2.49 (95% CI 1.69-3.69) - 3.69) per 2 SD increase in severity. Findings persisted in women without sleep apnoea (apnoea- - hypopnoea index <5 events h-1). - 1 ). Flow limitation was associated with HDP (OR 1.77 (95% CI 1.33-2.38)) - 2.38)) and reduced infant birthweight (83.7 (95% CI 31.8-135.6) - 135.6) g), but not GDM. Conclusions Greater flow limitation is associated with increased risk of pre-eclampsia, HDP and lower infant birthweight. Flow limitation may provide an early target for mitigating the consequences of sleep disordered breathing during pregnancy.

Driver fatigue significantly impairs performance and is a major risk factor for road crashes. However, fatigue is difficult to objectively measure and quantify. This study aimed to elucidate associations between heart rate variability (HRV) metrics and multidimensional fatigue construct encompassing objective and subjective measures in young drivers with self-reported short sleep. Eighty-four young adults underwent assessments during simulated driving. HRV indices RMSSD and LF/HF ratio were derived from an electrocardiogram, while relative Theta power, oculography drowsiness, lane position variability, and Karolinska Sleepiness Score measured fatigue. RMSSD negatively correlated with Theta power, and LF/HF ratio positively correlated with position variability. Exploratory factor analysis extracted three factors, with RMSSD and LF/HF loading onto one. Structural equation modelling tested the prediction of a latent fatigue construct from HRV. Two models demonstrated an acceptable fit. RMSSD negatively predicted fatigue, explaining 6.4 % of the variance, while the LF/HF ratio positively predicted fatigue, accounting for 3.7 % of the variance. In summary, HRV, particularly RMSSD, showed significant relationships with multidimensional fatigue. Lower RMSSD and higher LF/HF ratio are associated with greater fatigue levels. This study demonstrates that HRV indices exhibit significant relationships within a multidimensional model of fatigue incorporating objective performance, ocular, and subjective measures. The findings provide initial evidence towards using HRV for monitoring complex manifestations of fatigue, rather than single dimensions. Further applied research should investigate translating these findings to naturalistic settings and validating HRV thresholds predictive of on-road impairment.

Rationale: Moderate-severe obstructive sleep apnea (OSA) (apnea-hypopnea index [AHI], >15 events/h) disturbs sleep through frequent bouts of apnea and is associated with daytime sleepiness. However, many individuals without moderate-severe OSA (i.e., AHI <15 events/h) also report sleepiness. Objectives: To test the hypothesis that sleepiness in the AHI <15 events/h group is a consequence of substantial flow limitation in the absence of overt reductions in airflow (i.e., apnea/hypopnea). Methods: A total of 1,886 participants from the MESA sleep cohort were analyzed for frequency of flow limitation from polysomnogram-recorded nasal airflow signal. Excessive daytime sleepiness (EDS) was defined by an Epworth Sleepiness Scale score ⩾11. Covariate-adjusted logistic regression assessed the association between EDS (binary dependent variable) and frequency of flow limitation (continuous) in individuals with an AHI <15 events/h. Results: A total of 772 individuals with an AHI <15 events/h were included in the primary analysis. Flow limitation was associated with EDS (odds ratio, 2.04; 95% confidence interval, 1.17-3.54; per 2-standard deviation increase in flow limitation frequency) after adjusting for age, sex, body mass index, race/ethnicity, and sleep duration. This effect size did not appreciably change after also adjusting for AHI. Conclusions: In individuals with an AHI <15 events/h, increasing flow limitation frequency by 2 standard deviations is associated with a twofold increase in the risk of EDS. Future studies should investigate addressing flow limitation in low-AHI individuals as a potential mechanism for ameliorating sleepiness.

Background CPAP delivered via an oronasal mask is associated with lower adherence, higher residual apnea-hypopnea index (AHI), and increased CPAP therapeutic pressure compared with nasal masks. However, the mechanisms underlying the increased pressure requirements are not well understood. Research Question How do oronasal masks affect upper airway anatomy and collapsibility? Study Design and Methods Fourteen patients with OSA underwent a sleep study with both a nasal and oronasal mask, each for one-half of the night (order randomized). CPAP was manually titrated to determine therapeutic pressure. Upper airway collapsibility was assessed using the pharyngeal critical closing pressure (Pcrit) technique. Cine MRI was done to dynamically assess the cross-sectional area of the retroglossal and retropalatal airway throughout the respiratory cycle with each mask interface. Scans were repeated at 4 cm H2O and at the nasal and oronasal therapeutic pressures. Results The oronasal mask was associated with higher therapeutic pressure requirements (ΔM ± SEM; +2.6 ± 0.5; P < .001) and higher Pcrit (+2.4 ± 0.5 cm H2O; P = .001) compared with the nasal mask. The change in therapeutic pressure between masks was strongly correlated with the change in Pcrit (r2 = 0.73; P = .003). Increasing CPAP increased both the retroglossal and retropalatal airway dimensions across both masks. After controlling for pressure and breath phase, the retropalatal cross-sectional area was moderately larger when using a nasal vs an oronasal mask (+17.2 mm2; 95% CI, 6.2-28.2, P < .001) while nasal breathing. Interpretation Oronasal masks are associated with a more collapsible airway than nasal masks, which likely contributes to the need for a higher therapeutic pressure. CPAP delivered via an oronasal mask is associated with lower adherence, higher residual apnea-hypopnea index (AHI), and increased CPAP therapeutic pressure compared with nasal masks. However, the mechanisms underlying the increased pressure requirements are not well understood. How do oronasal masks affect upper airway anatomy and collapsibility? Fourteen patients with OSA underwent a sleep study with both a nasal and oronasal mask, each for one-half of the night (order randomized). CPAP was manually titrated to determine therapeutic pressure. Upper airway collapsibility was assessed using the pharyngeal critical closing pressure (Pcrit) technique. Cine MRI was done to dynamically assess the cross-sectional area of the retroglossal and retropalatal airway throughout the respiratory cycle with each mask interface. Scans were repeated at 4 cm H2O and at the nasal and oronasal therapeutic pressures. The oronasal mask was associated with higher therapeutic pressure requirements (ΔM ± SEM; +2.6 ± 0.5; P < .001) and higher Pcrit (+2.4 ± 0.5 cm H2O; P = .001) compared with the nasal mask. The change in therapeutic pressure between masks was strongly correlated with the change in Pcrit (r2 = 0.73; P = .003). Increasing CPAP increased both the retroglossal and retropalatal airway dimensions across both masks. After controlling for pressure and breath phase, the retropalatal cross-sectional area was moderately larger when using a nasal vs an oronasal mask (+17.2 mm2; 95% CI, 6.2-28.2, P < .001) while nasal breathing. Oronasal masks are associated with a more collapsible airway than nasal masks, which likely contributes to the need for a higher therapeutic pressure.