ORCID Profile
0000-0002-9372-6788
Current Organisation
Flinders University
Does something not look right? The information on this page has been harvested from data sources that may not be up to date. We continue to work with information providers to improve coverage and quality. To report an issue, use the Feedback Form.
In Research Link Australia (RLA), "Research Topics" refer to ANZSRC FOR and SEO codes. These topics are either sourced from ANZSRC FOR and SEO codes listed in researchers' related grants or generated by a large language model (LLM) based on their publications.
Respiratory Diseases | Cardiorespiratory Medicine and Haematology | Cardiology (incl. Cardiovascular Diseases) | Sensory Systems |
Cardiovascular System and Diseases | Respiratory System and Diseases (incl. Asthma) | Application Tools and System Utilities
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 05-2023
DOI: 10.1161/HYPERTENSIONAHA.122.20513
Abstract: Irregularities in sleep duration and sleep timing have emerged as potential risk factors for hypertension. This study examined associations between irregularity in sleep duration and timing with hypertension in a large, global s le over multiple months. Data from 12 287 adults, who used an under-mattress device to monitor sleep duration and timing and also provided blood pressure recordings on ≥5 separate occasions, were analyzed. Sleep duration irregularity was assessed as the SD in total sleep time across the ≈9-month recording period. Sleep timing irregularity was assessed as SDs in sleep onset time, sleep midpoint, and sleep offset time. Logistic regressions were conducted to investigate associations between sleep irregularity and hypertension, defined as median systolic blood pressure ≥140 mm Hg or median diastolic blood pressure ≥90 mm Hg. Participants were middle-aged (mean±SD, 50±12 years), mostly men (88%) and overweight (body mass index, 28±6 kg/m −2 ). Sleep duration irregularity was consistently associated with an ≈9% to 17% increase in hypertension independently of the total sleep time. A ≈34-minute increase in sleep onset time irregularity was associated with a 32% increase in hypertension (1.32 [1.20–1.45]). A 32-minute increase in sleep midpoint irregularity was associated with an 18% increase in hypertension (1.18 [1.09–1.29]), while a 43-minute increase in sleep offset time irregularity was associated with an 8.9% increase in hypertension (1.09 [1.001–1.18]). These findings support that sleep irregularity, both in duration and timing, is a risk marker for poor cardiovascular health. Further mechanistic investigations of temporal relationships between day-to-day fluctuations in sleep duration and timing, next-day blood pressure, and other cardiovascular outcomes are warranted.
Publisher: American Thoracic Society
Date: 03-2006
Publisher: Oxford University Press (OUP)
Date: 04-03-2022
Abstract: To determine if a novel EEG-derived continuous index of sleep depth/alertness, the odds ratio product (ORP), predicts self-reported daytime sleepiness and poor sleep quality in two large population-based cohorts. ORP values which range from 0 (deep sleep) to 2.5 (fully alert) were calculated in 3s intervals during awake periods (ORPwake) and NREM sleep (ORPNREM) determined from home sleep studies in the HypnoLaus (N = 2162: 1106 females, 1056 males) and men androgen inflammation lifestyle environment and stress (MAILES) cohorts (N = 754 males). Logistic regression was used to examine associations between ORPwake, ORPNREM, and traditional polysomnography measures (as comparators) with excessive sleepiness (Epworth sleepiness scale & ) and poor sleep quality (Pittsburgh sleep quality index & ) and insomnia symptoms. High ORPwake was associated with a ~30% increase in poor sleep quality in both HypnoLaus (odds ratio, OR, and 95% CI) 1.28 (1.09, 1.51), and MAILES 1.36 (1.10, 1.68). High ORPwake was also associated with a ~28% decrease in excessive daytime sleepiness in the MAILES dataset. ORPNREM was associated with a ~30% increase in poor sleep quality in HypnoLaus but not in MAILES. No consistent associations across cohorts were detected using traditional polysomnography markers. ORP, a novel EEG-derived metric, measured during wake periods predicts poor sleep quality in two independent cohorts. Consistent with insomnia symptomatology of poor perceived sleep in the absence of excessive daytime sleepiness, ORPwake may provide valuable objective mechanistic insight into physiological hyperarousal.
Publisher: Elsevier BV
Date: 12-2021
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 19-07-2022
Abstract: Poor sleep quality is associated with increased incident hypertension. However, few studies have investigated the impact of objective sleep structure parameters on hypertension. This study investigated the association between sleep macrostructural and microstructural parameters and incident hypertension in a middle‐ to older‐aged s le. Participants from the HypnoLaus population‐based cohort without hypertension at baseline were included. Participants had at‐home polysomnography at baseline, allowing assessment of sleep macrostructure (nonrapid eye movement sleep stages 1, 2, and 3 rapid eye movement sleep stages and total sleep time) and microstructure including power spectral density of electroencephalogram in nonrapid eye movement sleep and spindles characteristics (density, duration, frequency, litude) in nonrapid eye movement sleep stage 2. Associations between sleep macrostructure and microstructure parameters at baseline and incident clinical hypertension over a mean follow‐up of 5.2 years were assessed with multiple‐adjusted logistic regression. A total of 1172 participants (42% men age 55±10 years) were included. Of these, 198 (17%) developed hypertension. After adjustment for confounders, no sleep macrostructure features were associated with incident hypertension. However, low absolute delta and sigma power were significantly associated with incident hypertension where participants in the lowest quartile of delta and sigma had a 1.69‐fold (95% CI, 1.00–2.89) and 1.72‐fold (95% CI, 1.05–2.82) increased risk of incident hypertension, respectively, versus those in the highest quartile. Lower spindle density (odds ratio, 0.87 95% CI, 0.76–0.99) and litude (odds ratio, 0.98 95% CI, 0.95–1.00) were also associated with higher incident hypertension. Sleep microstructure is associated with incident hypertension. Slow‐wave activity and sleep spindles, 2 hallmarks of objective sleep continuity and quality, were inversely and consistently associated with incident hypertension. This supports the protective role of sleep continuity in the development of hypertension.
Publisher: Elsevier BV
Date: 11-2018
DOI: 10.1016/J.IJCARD.2018.04.076
Abstract: Sleep disordered breathing (SDB) is highly prevalent in patients with atrial fibrillation, heart failure and hypertension and is associated with increased risk of mortality, cardiovascular (CV) events and arrhythmias. Current assessment of the severity of SDB is mainly based on the apnea-hypopnea index (AHI) representing the number of hypopneas and apneas per hour of sleep. However, this event-based parameter alone may not sufficiently reflect the complex pathophysiological mechanisms underlying SDB potentially contributing to CV outcome risk. In this review article, we highlight important limitations and pitfalls of current assessment, quantification and interpretation of SDB-severity in patients with CV disease and will discuss pathophysiological considerations from preclinical and clinical mechanistic studies and possible clinical implications.
Publisher: Oxford University Press (OUP)
Date: 09-2004
Abstract: Partial sleep deprivation and alcohol consumption are a common combination, particularly among young drivers. We hypothesized that while low blood alcohol concentration (<0.05 g/dL) may not significantly increase crash risk, the combination of partial sleep deprivation and low blood alcohol concentration would cause significant performance impairment. Experimental Sleep Disorders Unit Laboratory 20 healthy volunteers (mean age 22.8 years 9 men). Subjects underwent driving simulator testing at 1 am on 2 nights a week apart. On the night preceding simulator testing, subjects were partially sleep deprived (5 hours in bed). Alcohol consumption (2-3 standard alcohol drinks over 2 hours) was randomized to 1 of the 2 test nights, and blood alcohol concentrations were estimated using a calibrated Breathalyzer. During the driving task subjects were monitored continuously with electroencephalography for sleep episodes and were prompted every 4.5 minutes for answers to 2 perception scales-performance and crash risk. Mean blood alcohol concentration on the alcohol night was 0.035 +/- 0.015 g/dL. Compared with conditions during partial sleep deprivation alone, subjects had more microsleeps, impaired driving simulator performance, and poorer ability to predict crash risk in the combined partial sleep deprivation and alcohol condition. Women predicted crash risk more accurately than did men in the partial sleep deprivation condition, but neither men nor women predicted the risk accurately in the sleep deprivation plus alcohol condition. Alcohol at legal blood alcohol concentrations appears to increase sleepiness and impair performance and the detection of crash risk following partial sleep deprivation. When partially sleep deprived, women appear to be either more perceptive of increased crash risk or more willing to admit to their driving limitations than are men. Alcohol eliminated this behavioral difference.
Publisher: Oxford University Press (OUP)
Date: 2023
Publisher: Oxford University Press (OUP)
Date: 10-2021
DOI: 10.1093/SLEEPADVANCES/ZPAB014.169
Abstract: Most studies examining associations between sleep and health outcomes focus on sleep duration or efficiency, ignoring in idual differences in sleep need. We investigated whether sleep need is a more influential correlate of self-rated daytime function and health than sleep duration. This study is a secondary analysis of the 2019 Sleep Health Foundation online survey of adult Australians (N=2,044, aged 18–90 years). Hierarchical multiple linear regressions assessed variance explained by demographics (Model 1: age, sex, BMI), self-reported sleep duration (Model 2: Model 1 + weighted variable of weekday/weekend sleep duration), and in idual sleep need (Model 3: Model 2+ how often they get enough sleep to feel their best the next day, on a 5-point scale) on daytime function items for fatigue, concentration, motivation, and overall self-rated health (EQ-5D, VAS 0–100). Sleep need explained an additional 17.5–18.7% of the variance in fatigue, concentration, motivation, and health rating (all p & 0.001 for R² change) in Model 3. Model 2 showed that sleep duration alone only explained 2.0–4.1% of the variance in these outcomes. Findings were similar when stratified by sex. Sleep need also explained greater variance for older adults than for younger and middle-aged adults, especially on health rating (Model 3: R² change = 0.11 for ages 18-24y, 0.14 for 45-54y, 0.27 for 75y+). Sleep need explains more variance in daytime function and self-rated health than sleep duration. The role of sleep need on other daytime consequences, and in clinical populations, needs further exploration.
Publisher: Wiley
Date: 04-09-2014
DOI: 10.1111/JSR.12079
Publisher: Wiley
Date: 15-02-2022
DOI: 10.1111/JSR.13563
Abstract: Insomnia and obstructive sleep apnea commonly co‐occur (co‐morbid insomnia and sleep apnea), and their co‐occurrence has been associated with worse cardiometabolic and mental health. However, it remains unknown if people with co‐morbid insomnia and sleep apnea are at a heightened risk of incident cardiovascular events. This study used longitudinal data from the Sleep Heart Health Study ( N = 5803) to investigate potential associations between co‐morbid insomnia and sleep apnea and cardiovascular disease prevalence at baseline and cardiovascular event incidence over ~11 years follow‐up. Insomnia was defined as self‐reported difficulties initiating and/or maintaining sleep AND daytime impairment. Obstructive sleep apnea was defined as an apnea–hypopnea index ≥ 15 events per hr sleep. Co‐morbid insomnia and sleep apnea was defined if both conditions were present. Data from 4160 participants were used for this analysis. The prevalence of no insomnia/obstructive sleep apnea, insomnia only, obstructive sleep apnea only and co‐morbid insomnia and sleep apnea was 53.2%, 3.1%, 39.9% and 1.9%, respectively. Co‐morbid insomnia and sleep apnea was associated with a 75% (odd ratios [95% confidence interval] 1.75 [1.14, 2.67]) increase in likelihood of having cardiovascular disease at baseline after adjusting for pre‐specified confounders. In the unadjusted model, co‐morbid insomnia and sleep apnea was associated with a twofold increase (hazard ratio, 95% confidence interval: 2.00 [1.33, 2.99]) in risk of cardiovascular event incidence. However, after adjusting for pre‐specified covariates, co‐morbid insomnia and sleep apnea was not significantly associated with incident cardiovascular events (hazard ratio 1.38 [0.92, 2.07]). Comparable findings were obtained when an alternative definition of insomnia (difficulties initiating and/or maintaining sleep without daytime impairment) was used.
Publisher: BMJ
Date: 06-2002
Abstract: Intrinsic positive end expiratory pressure (PEEPi) constitutes an inspiratory threshold load on the respiratory muscles, increasing work of breathing. The role of continuous positive airway pressure (CPAP) in alleviating PEEPi in patients with severe stable chronic obstructive pulmonary disease is uncertain. This study examined the effect of CPAP on the inspiratory threshold load, muscle effort, and lung volume in this patient group. Nine patients were studied at baseline and with CPAP increasing in increments of 1 cm H(2)O to a maximum of 10 cm H(2)O. Breathing pattern and minute ventilation (I), dynamic PEEPi, expiratory muscle activity, diaphragmatic (PTPdi/min) and oesophageal (PTPoes/min) pressure-time product per minute, integrated diaphragmatic (EMGdi) and intercostal EMG (EMGic) and end expiratory lung volume (EELV) were measured. Expiratory muscle activity was present at baseline in one subject. In the remaining eight, PEEPi was reduced from a mean (SE) of 2.9 (0.6) cm H(2)O to 0.9 (0.1) cm H(2)O (p<0.05). In two subjects expiratory muscle activity contributed to PEEPi at higher pressures. There were no changes in respiratory pattern but I increased from 9.2 (0.6) l/min to 10.7 (1.1) l/min (p<0.05). EMGdi remained stable while EMGic increased significantly. PTPoes/min decreased, although this did not reach statistical significance. PTPdi/min decreased significantly from 242.1 (32.1) cm H(2)O.s/min to 112.9 (21.7) cm H(2)O.s/min). EELV increased by 1.1 (0.3) l (p<0.01). High levels of CPAP reduce PEEPi and indices of muscle effort in patients with severe stable COPD, but only at the expense of substantial increases in lung volume.
Publisher: Faculty Opinions Ltd
Date: 23-09-2010
DOI: 10.3410/M2-70
Publisher: American Academy of Sleep Medicine (AASM)
Date: 15-08-2011
DOI: 10.5664/JCSM.1194
Publisher: Springer Science and Business Media LLC
Date: 20-09-2010
Publisher: American Academy of Sleep Medicine (AASM)
Date: 15-12-2009
DOI: 10.5664/JCSM.27651
Publisher: American Physiological Society
Date: 07-2000
DOI: 10.1152/JAPPL.2000.89.1.47
Abstract: The sensation of increased respiratory resistance or effort is likely to be important for the initiation of alerting or arousal responses, particularly in sleep. Hypoxia, through its central nervous system-depressant effects, may decrease the perceived magnitude of respiratory loads. To examine this, we measured the effect of isocapnic hypoxia on the ability of 10 normal, awake males (mean age = 24.0 ± 1.8 yr) to magnitude-scale five externally applied inspiratory resistive loads (mean values from 7.5 to 54.4 cmH 2 O · l −1 · s). Each subject scaled the loads during 37 min of isocapnic hypoxia (inspired O 2 fraction = 0.09, arterial O 2 saturation of ∼80%) and during 37 min of normoxia, using the method of open magnitude numerical scaling. Results were normalized by modulus equalization to allow between-subject comparisons. With the use of peak inspiratory pressure (PIP) as the measure of load stimulus magnitude, the perception of load magnitude (Ψ) increased linearly with load and, averaged for all loaded breaths, was significantly lower during hypoxia than during normoxia (20.1 ± 0.9 and 23.9 ± 1.3 arbitrary units, respectively P = 0.048). Ψ declined with time during hypoxia ( P = 0.007) but not during normoxia ( P= 0.361). Our result is remarkable because PIP was higher at all times during hypoxia than during normoxia, and previous studies have shown that an elevation in PIP results in increased Ψ. We conclude that sustained isocapnic hypoxia causes a progressive suppression of the perception of the magnitude of inspiratory resistive loads in normal subjects and could, therefore, impair alerting or arousal responses to respiratory loading.
Publisher: American Academy of Sleep Medicine (AASM)
Date: 15-08-2007
DOI: 10.5664/JCSM.8424
Publisher: Acoustical Society of America (ASA)
Date: 12-2022
DOI: 10.1121/10.0016499
Abstract: This study tested for differences in perceived annoyance and loudness between road traffic noise (RTN) and wind farm noise (WFN) with litude modulation (AM) and tonality. Twenty-two participants, who were primarily university students with no previous exposure to WFN and aged between 19 and 29 (mean, 22 years old standard deviation, 2) years old with normal hearing, underwent a laboratory-based listening test. Each participant rated perceived annoyance and loudness of WFN and RTN s les played at sound pressure levels (SPLs) ranging from 33 to 48 dBA. Probability modeling revealed that participants were the largest source of variability in ratings of perceived annoyance and loudness while noise type and SPL were relatively minor sources. Overall, no differences were found between WFN and RTN perceived annoyance or loudness ratings. On the other hand, no substantial differences in annoyance were found between low-frequency tonal AM and mid-to-high-frequency AM or “swish” WFN.
Publisher: American Physiological Society
Date: 03-2007
DOI: 10.1152/AJPREGU.00642.2006
Abstract: 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 ± SD for heart rate: +9 ± 8 vs. +13 ± 9 beats per min for PR prolongation: 14 ± 16 vs. 24 ± 22 ms for QT shortening: −12 ± 6 vs. −20 ± 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.
Publisher: SPIE
Date: 20-02-2020
DOI: 10.1117/12.2545282
Publisher: American Academy of Sleep Medicine (AASM)
Date: 03-2021
DOI: 10.5664/JCSM.8944
Publisher: Elsevier BV
Date: 09-2019
Publisher: Springer Science and Business Media LLC
Date: 1992
DOI: 10.1007/BF00868132
Publisher: Oxford University Press (OUP)
Date: 06-2013
DOI: 10.5665/SLEEP.2698
Publisher: Oxford University Press (OUP)
Date: 11-2005
Abstract: It has been suggested that the Maintenance of Wakefulness Test (MWT) may be clinically useful to assess fitness to drive, yet little is known about the actual relationship between sleep latency and driving performance. This study examined the ability of 2 MWT trials to predict driving-simulator performance in healthy in iduals. Experimental. NA. Twenty healthy volunteers (mean age 22.8 years 9 men). NA. The MWT and driving-simulator performance were examined under 2 conditions-partial sleep deprivation and a combination of partial sleep deprivation and alcohol consumption. Each subject was studied a week apart, with the order randomly assigned. Subjects completed a nighttime 70-minute AusEd driving simulation task and two 40-minute MWT trials, 1 before (MWT1) and 1 after (MWT2) the driving task. In the sleep-deprived condition, the MWT1 sleep latency was inversely correlated with braking reaction time. During the partial sleep deprivation and alcohol condition, the number of microsleeps during the driving task, steering deviation, braking reaction time, and crashes all negatively correlated with the MWT1 sleep latency. Additionally, construction of a receiver-operator characteristic curve revealed that MWT1 sleep latency in the partial sleep deprivation plus alcohol condition significantly discriminated subjects who had a crash from those who did not. These results indicate that sleep latency on the MWT is a reasonable predictor of driving simulator performance in sleepy, alcohol-impaired, normal subjects. Further research is needed to examine the relationship between daytime MWT results and driving simulator performance in sleepy patients (eg, those with obstructive sleep apnea) and in experimentally sleep-deprived normal subjects.
Publisher: Springer Science and Business Media LLC
Date: 10-2006
Publisher: Elsevier BV
Date: 12-2021
DOI: 10.1016/J.SMRV.2021.101519
Abstract: Insomnia and obstructive sleep apnea (OSA) commonly co-occur. Approximately 30-50% of patients with OSA report clinically significant insomnia symptoms, and 30-40% of patients with chronic insomnia fulfil diagnostic criteria for OSA. Compared to either insomnia or OSA alone, co-morbid insomnia and sleep apnea (COMISA) is associated with greater morbidity for patients, complex diagnostic decisions for clinicians, and reduced response to otherwise effective treatment approaches. Potential bi-directional causal relationships between the mechanisms and manifestations of insomnia and OSA could play an integral role in the development and management of COMISA. A greater understanding of these relationships is required to guide personalized diagnostic and treatment approaches for COMISA. This review summarizes the available evidence of bi-directional relationships between COMISA, including epidemiological research, case studies, single-arm treatment studies, randomized controlled treatment trials, and objective sleep study data. This evidence is integrated into a conceptual model of COMISA to help refine the understanding of potential bi-directional causal relationships between the two disorders. This theoretical framework is essential to help guide future research, improve diagnostic tools, determine novel therapeutic targets, and guide tailored sequenced and multi-faceted treatment approaches for this common, complex, and debilitating condition.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 08-1997
DOI: 10.1097/00005768-199708000-00016
Abstract: The complete calibration of indirect calorimetry systems involves simultaneous checks of gas analyzers, volume device, and software, and this requires a machine that can mimic accurately and precisely the ventilation and expired gases of an athlete. While previous calibrators have been built successfully, none have matched the ventilatory flows produced by athletes during high intensity exercise. A calibrator able to simulate high aerobic power (VO2max calibrator) was fabricated and tested against conventional indirect calorimetry systems that use chain-compensated gasometers to measure expired volume (VE systems) and calibrated electronic gas analyzers. The calibrator was also checked against a system that measures inspired volume (VI system) with a turbine ventilometer. The pooled data from both VE and VI systems for predicted VO2 ranging from 2.9 to 7.9 L.min-1 and ventilation ranging from 89 to 246 L.min-1 how that the absolute accuracy (bias) of values measured by conventional indirect calorimetry systems compared with those predicted by the calibrator was excellent. The bias was < 35 mL.min-1 for VO2 and carbon dioxide production, < 0.50 L.min-1 for ventilator (VE BTPS), -0.02% absolute for the percentage of expired O2 and +0.02% absolute for the percentage of expired CO2. Overall, the precision of the measured VO2, VCO2, and VE BTPS was approximately 1%. This VO2max calibrator is a versatile device that can be used for routine calibration of most indirect calorimetry systems that assess the ventilation and aerobic power of athletes.
Publisher: Oxford University Press (OUP)
Date: 12-2009
Publisher: Elsevier BV
Date: 09-2020
Publisher: American Physiological Society
Date: 2002
DOI: 10.1152/JAPPLPHYSIOL.00461.2001
Abstract: 10.1152/japplphysiol.00461.2001.—Obstructive sleep apnea (OSA) is more common in men than in women for reasons that are not clearly understood. An underlying difference between men and women in the respiratory-related neural control of upper airway dilator muscles has been suggested as a possible reason for the gender difference. We have compared three aspects of upper airway dilator muscle function in healthy men and women: 1) resting inspiratory genioglossus electromyogram (EMGgg) activity, 2) the respiratory EMGgg “afterdischarge” after a brief hypoxic stimulus, and 3) the relationship between the EMGgg and pharyngeal airway pressure. Inspired minute ventilation (V˙i), epiglottic pressure (P epi ), and EMGgg and diaphragm EMG (EMGdi) activity were measured in 24 subjects (12 men, 12 women in the luteal menstrual phase) and were compared between genders while lying supine awake. Every 7–8 min over 2 h, subjects were exposed to 45-s periods of isocapnic hypoxia (9% O 2 in N 2 ) that were abruptly terminated with one breath of 100% O 2 . The relationship between P epi and EMGgg activity was also compared between genders. The results of 117 trials with satisfactory end-tidal Pco 2 control and no sighs or swallows are reported. There was no gender difference in the resting level of peak inspiratory EMGgg [3.7 ± 0.8 (women) vs. 3.2 ± 0.6% maximal activity (men)]. Repeated-measures ANOVA showed no gender or gender-by-time interaction effect between men and women inV˙i or EMGgg or EMGdi activity during or after the hypoxic stimulus. The relationship between P epi and EMGgg was not different between men (slope −0.63 ± 0.20) and women (slope −0.69 ± 0.33). These results do not support the hypothesis that the higher prevalence of OSA in men is related to an underlying gender difference in respiratory neural control of upper airway dilator muscles.
Publisher: Wiley
Date: 10-2019
DOI: 10.1111/JSR.73_12912
Publisher: Springer Science and Business Media LLC
Date: 10-2008
Publisher: Informa UK Limited
Date: 10-2022
DOI: 10.2147/NSS.S379252
Publisher: Elsevier BV
Date: 07-2023
Publisher: BMJ
Date: 22-10-2009
Abstract: Patients with obstructive sleep apnoea (OSA) have reduced event rates during slow wave sleep (SWS) compared with stage 2 sleep. To explore this phenomenon, ventilatory and arousal timing responses to partial and complete airflow obstruction during SWS versus stage 2 sleep were examined. Ten patients, mean+/-SD apnoea-hypopnoea index (AHI) 49.7+/-16.5 events/h with reduced OSA frequency during SWS (SWS AHI 18.9+/-14.0 events/h) slept with an epiglottic pressure catheter and nasal mask neumotachograph. Patients underwent rapid continuous positive airway pressure (CPAP) dialdowns to three subtherapeutic levels and brief airway occlusions in random order. Post-dialdown, there were marked reductions in peak flow and minute ventilation, and progressive increases in inspiratory effort (p<0.001), but with limited ventilatory recovery and no differences between sleep stages. CPAP versus peak flow relationships on the third and second to last breath pre-arousal were not different between sleep stages. Arousals occurred later and post-dialdown arousal probability was lower during SWS compared with stage 2 sleep, Cox hazard ratio (95% CI) 0.65 (0.48 to 0.88), p=0.006. During SWS occlusions, time to arousal (mean+/-SEM) was prolonged (23.0+/-2.6 vs 17.1+/-1.7 s, p=0.02). Inspiratory effort developed more rapidly (-1.0+/-0.2 vs -0.6+/-0.1 cm H(2)O/s, p=0.019) and was more negative (-28.7+/-2.7 vs -20.3+/-1.6 cm H(2)O, p<0.001) on the breath preceding arousal. Except for a heightened ventilatory drive response during airway occlusion, airway function and ventilatory compensation to ventilatory challenge appear to be similar, but with consistently and substantially delayed arousal responses, in SWS versus stage 2 sleep.
Publisher: American Thoracic Society
Date: 07-2022
Publisher: Elsevier BV
Date: 10-2019
Publisher: RWTH Aachen University
Date: 2019
Publisher: Wiley
Date: 25-08-2004
DOI: 10.1113/JPHYSIOL.2004.066084
Abstract: Sleep hypoventilation is common in hypercapnic chronic obstructive pulmonary disease (COPD) and may contribute to daytime hypercapnia. The contributions of respiratory drive and respiratory mechanics to alterations in minute ventilation ( V̇ I ) during sleep in this group have not been assessed. We assessed V̇ I , breathing pattern, upper airway and total lung resistance (UAR, R L ), intraoesohageal diaphragmatic EMG (EMG oes ), intrinsic positive end‐expiratory pressure (PEEP i ), dynamic compliance ( C dyn ), pressure–time product of oesophageal pressure (PTP oes ), tension–time index of the diaphragm (TTI di ), end‐expiratory lung volume (EELV) and respiratory drive (assessed as the slope of P oes versus time in the isovolumetric interval before PEEP i is overcome). Measurements were made in wakefulness and non‐rapid eye movement (NREM) sleep, on 76%N 2 /24%O 2 and on 76%He/24%O 2 (heliox). Satisfactory data for analysis were obtained in 10 patients five had measurements on heliox. V̇ I fell from (mean ( s.e.m. )) 8.84(0.46) to 6.64(0.91 l min −1 , P = 0.011) between wakefulness and stage II sleep, due to a fall in tidal volume. No changes were seen in PEEP i , C dyn , EELV, PTP oes , TTI di , EMG oes or respiratory drive. UAR increased (3.11(0.8) to 10.24(2.96) cmH 2 O l −1 s ( P = 0.013) but R L was unchanged. UAR was reduced on heliox (5.20(1.67) to 3.45(1.35) cmH 2 O l −1 s, P = 0.049) but V̇ I during sleep did not increase. PTP oes (350.2(51.0) to 259.4(46.3) cmH 2 O s min −1 , P = 0.016), TTI di (0.13(0.02) to 0.10(0.02) P = 0.04), and respiratory drive (20.48(4.69) to 15.02(4.57) cmH 2 O s −1 , P = 0.01) were all reduced. This suggests respiratory drive alters to maintain a preset V̇ I in sleep, irrespective of load, at least while the fatigue threshold of respiratory muscles is not exceeded.
Publisher: Springer Science and Business Media LLC
Date: 10-2015
DOI: 10.1111/SBR.12132
Publisher: American Medical Association (AMA)
Date: 06-2013
DOI: 10.1001/JAMADERMATOL.2013.2466
Abstract: Nodular melanoma (NM) is a rapidly progressing potentially lethal skin tumor for which early diagnosis is critical. To determine the dermoscopy features of NM. Eighty-three cases of NM, 134 of invasive non-NM, 115 of nodular benign melanocytic tumors, and 135 of nodular nonmelanocytic tumors were scored for dermoscopy features using modified and previously described methods. Lesions were separated into amelanotic/hypomelanotic or pigmented to assess outcomes. Predominantly hospital-based clinics from 5 continents. Sensitivity, specificity, and odds ratios for features/models for the diagnosis of melanoma. Nodular melanoma occurred more frequently as amelanotic/hypomelanotic (37.3%) than did invasive non-NM (7.5%). Pigmented NM had a more frequent (compared with invasive non-NM in descending order of odds ratio) symmetrical pigmentation pattern (5.8% vs 0.8%), large-diameter vessels, areas of homogeneous blue pigmentation, symmetrical shape, predominant peripheral vessels, blue-white veil, pink color, black color, and milky red ink areas. Pigmented NM less frequently displayed an atypical broadened network, pigment network or pseudonetwork, multiple blue-gray dots, scarlike depigmentation, irregularly distributed and sized brown dots and globules, tan color, irregularly shaped depigmentation, and irregularly distributed and sized dots and globules of any color. The most important positive correlating features of pigmented NM vs nodular nonmelanoma were peripheral black dots/globules, multiple brown dots, irregular black dots/globules, blue-white veil, homogeneous blue pigmentation, 5 to 6 colors, and black color. A model to classify a lesion as melanocytic gave a high sensitivity (>98.0%) for both nodular pigmented and nonnodular pigmented melanoma but a lower sensitivity for amelanotic/hypomelanotic NM (84%). A method for diagnosing amelanotic/hypomelanotic malignant lesions (including basal cell carcinoma) gave a 93% sensitivity and 70% specificity for NM. When a progressively growing, symmetrically patterned melanocytic nodule is identified, NM needs to be excluded.
Publisher: American Academy of Sleep Medicine (AASM)
Date: 15-09-2016
DOI: 10.5664/JCSM.6118
Publisher: American Thoracic Society
Date: 04-2022
Publisher: Oxford University Press (OUP)
Date: 20-04-2019
DOI: 10.1093/SLEEP/ZSZ092
Abstract: Quantitative electroencephalography (EEG) measures of sleep may identify vulnerability to obstructive sleep apnea (OSA) sequelae, however, small clinical studies of sleep microarchitecture in OSA show inconsistent alterations. We examined relationships between quantitative EEG measures during rapid eye movement (REM) and non-REM (NREM) sleep and OSA severity among a large population-based s le of men while accounting for insomnia. All-night EEG (F4-M1) recordings from full in-home polysomnography (Embletta X100) in 664 men with no prior OSA diagnosis (age ≥ 40) were processed following exclusion of artifacts. Power spectral analysis included non-REM and REM sleep computed absolute EEG power for delta, theta, alpha, sigma, and beta frequency ranges, total power (0.5–32 Hz) and EEG slowing ratio. Apnea–hypopnea index (AHI) ≥10/h was present in 51.2% (severe OSA [AHI ≥ 30/h] 11.6%). In mixed effects regressions, AHI was positively associated with EEG slowing ratio and EEG power across all frequency bands in REM sleep (all p 0.05) and with beta power during NREM sleep (p = 0.06). Similar associations were observed with oxygen desaturation index (3%). Percentage total sleep time with oxygen saturation % was only significantly associated with increased delta, theta, and alpha EEG power in REM sleep. No associations with subjective sleepiness were observed. In a large s le of community-dwelling men, OSA was significantly associated with increased EEG power and EEG slowing predominantly in REM sleep, independent of insomnia. Further study is required to assess if REM EEG slowing related to nocturnal hypoxemia is more sensitive than standard PSG indices or sleepiness in predicting cognitive decline.
Publisher: American Physiological Society
Date: 08-2021
DOI: 10.1152/JAPPLPHYSIOL.00896.2020
Abstract: Esophageal and epiglottic pressure deflection measurements are widely used as gold-standard measures of ventilatory effort during sleep without consideration of differential obstruction effects between measurement sites. This study is the first to quantify the effect of airway occlusion on esophageal versus epiglottic pressure recordings during sleep. The findings of substantial acute effects of occlusion itself on esophageal and particularly epiglottic pressure deflections are important to consider in the planning, analysis, and interpretation of studies that rely on pressure deflections for inferences regarding inspiratory effort.
Publisher: European Respiratory Society (ERS)
Date: 08-2004
Publisher: MDPI AG
Date: 09-02-2022
DOI: 10.3390/APP12041787
Abstract: People with insomnia frequently underestimate the duration of their sleep compared to objective polysomnography-measured sleep duration. Cognitive behavioural therapy for insomnia (CBT-I) is the most effective treatment for insomnia and also reduces the degree of sleep underestimation. Obstructive sleep apnoea (OSA) is a highly prevalent sleep disorder characterised by frequent narrowing (hypopnoea) and closure (apnoea) of the upper airway during sleep. Comorbid insomnia and sleep apnoea (COMISA) is a prevalent and debilitating disorder. No study has investigated subjectively (sleep diary) versus objectively (polysomnography) measured sleep discrepancies (SOSD) in in iduals with COMISA before or following CBT-I. This randomised waitlist-controlled trial investigated SOSD in 145 participants with COMISA before and 6-weeks after CBT-I (n = 72) versus control (n = 73). All participants were studied prior to continuous positive airway pressure treatment for sleep apnoea. At baseline, participants underestimated their total sleep time (mean ± SD −51.9 ± 94.1 min) and sleep efficiency (−9.6 ± 18.3%), and overestimated sleep onset latency (34.5 ± 86.1 min all p = 0.001). Mixed models indicated a main effect of time on reduction of SOSD in both groups, but no between-group difference in the reduction of any SOSD parameters. These findings may indicate that untreated OSA contributes to a discrepancy between perceived and objective sleep parameters in people with COMISA that is not amenable to CBT-I alone (ACTRN12613001178730).
Publisher: American Thoracic Society
Date: 06-2004
Publisher: Elsevier BV
Date: 09-2012
DOI: 10.1016/J.SLEEP.2012.06.010
Abstract: Patients with primary Sjögren's syndrome (pSS) have higher fatigue levels and also suffer from excessive day time sleepiness. The underlying mechanisms for this are not fully understood. Knowing that these patients have higher salivary surface tension, we postulated that sleep disordered breathing (SDB) would be more common and would be a contributor to these symptoms amongst pSS patients. We investigated the prevalence of SDB in pSS patients and its relationship to their symptoms of fatigue and excessive daytime sleepiness. This was an observational study of 28 pSS patients (mean±SEM age, 58.7±1.9) and 18 healthy subjects (mean±SEM age, 55.8±3.4) matched for age, sex, and BMI. All the participants underwent an overnight polysomnography. The two groups were compared for fatigue, sleepiness, anxiety, and depression scores, and for the frequency of obstructive apneas and hypopneas during sleep. Correlation analyses were used to explore relationships between sleep study variables and excess sleepiness and fatigue. Fatigue, sleepiness, anxiety and depression symptoms, and sleep onset latency were significantly greater in pSS patients than controls. pSS patients had twice the frequency of obstructive apneas and hypopneas compared with control subjects (median[IQR],18.6/h [10.4-40.1] vs. 9.9/h [6.5-23.4] p=0.032) and OSA defined as an apnea-hypopnea index >15 events/h of sleep was more prevalent amongst pSS patients than controls (64% vs. 28% p=0.033). While no significant correlations were found between parameters of sleep disordered breathing and sleepiness scores or fatigue scores in the pSS group, CPAP treatment in a small subset of the pSS who were more severely affected by OSA suggested significant symptomatic benefit. OSA appears to be increased in pSS and may be a useful therapeutic target to improve the quality of life of these patients.
Publisher: Elsevier BV
Date: 03-2023
Publisher: Oxford University Press (OUP)
Date: 04-2018
Publisher: Informa UK Limited
Date: 10-10-2019
DOI: 10.1080/07420528.2019.1676256
Abstract: Altering meal timing could improve cognition, alertness, and thus safety during the nightshift. This study investigated the differential impact of consuming a meal, snack, or not eating during the nightshift on cognitive performance (ANZCTR12615001107516). 39 healthy participants (59% male, age mean±SD: 24.5 ± 5.0y) completed a 7-day laboratory study and underwent four simulated nightshifts. Participants were randomly allocated to: Meal at Night (MN
Publisher: Wiley
Date: 28-08-2008
Publisher: Wiley
Date: 06-06-2007
Publisher: Wiley
Date: 19-10-2023
DOI: 10.1111/JSR.14078
Publisher: Oxford University Press (OUP)
Date: 29-12-2022
Abstract: This study was designed to test the utility of cardiovascular responses as markers of potentially different environmental noise disruption effects of wind farm compared to traffic noise exposure during sleep. Twenty participants underwent polysomnography. In random order, and at six sound pressure levels from 33 dBA to 48 dBA in 3 dB increments, three types of wind farm and two types of road traffic noise recordings of 20-s duration were played during established N2 or deeper sleep, each separated by 20 s without noise. Each noise sequence also included a no-noise control. Electrocardiogram and finger pulse oximeter recorded pulse wave litude changes from the pre-noise onset baseline following each noise exposure and were assessed algorithmically to quantify the magnitude of heart rate and finger vasoconstriction responses to noise exposure. Higher sound pressure levels were more likely to induce drops in pulse wave litude. Sound pressure levels as low as 39 dBA evoked a pulse wave litude response (Odds ratio [95% confidence interval] 1.52 [1.15, 2.02]). Wind farm noise with litude modulation was less likely to evoke a pulse wave litude response than the other noise types, but warrants cautious interpretation given low numbers of replications within each noise type. These preliminary data support that drops in pulse wave litude are a particularly sensitive marker of noise-induced cardiovascular responses during. Larger trials are clearly warranted to further assess relationships between recurrent cardiovascular activation responses to environmental noise and potential long-term health effects.
Publisher: American Thoracic Society
Date: 04-2009
DOI: 10.1164/AJRCCM-CONFERENCE.2009.179.1_MEETINGABSTRACTS.A5319
Publisher: Elsevier BV
Date: 12-2017
Publisher: American Physiological Society
Date: 2000
DOI: 10.1152/JAPPL.2000.88.1.3
Abstract: The gradual decay in ventilation after removal of a respiratory stimulus has been proposed to protect against cyclic breathing disorders such as obstructive sleep apnea (OSA). The male predominance of OSA, and the increased incidence of OSA in women after menopause, indicates that the respiratory-stimulating effect of progesterone may provide protection against OSA by altering the rate of poststimulus ventilatory decline (PSVD). It was therefore hypothesized that PSVD is longer in premenopausal women than in men and is longer in the luteal menstrual phase compared with the follicular phase. PSVD was measured in 12 men and in 11 women at both their luteal and follicular phases, after cessation of isocapnic hypoxia and normoxic hypercapnia. PSVD was compared between genders and between women in the luteal and follicular phases by repeated-measures ANOVA. There were no significant differences in PSVD between any of the groups after either respiratory stimulus. This suggests that the higher occurrence of OSA in men does not reflect an underlying gender difference in PSVD and implies the increased prevalence of OSA in women after menopause is not representative of an effect of progesterone on PSVD.
Publisher: Wiley
Date: 27-07-2004
Publisher: Portland Press Ltd.
Date: 23-02-2018
DOI: 10.1042/BCJ20170655
Abstract: While mitochondrial mutants of the respiratory machinery are rare and often lethal, cytoplasmic male sterility (CMS), a mitochondrially inherited trait that results in pollen abortion, is frequently encountered in wild populations. It generates a breeding system called gynodioecy. In Beta vulgaris ssp. maritima, a gynodioecious species, we found CMS-G to be widespread across the distribution range of the species. Despite the sequencing of the mitochondrial genome of CMS-G, the mitochondrial sterilizing factor causing CMS-G is still unknown. By characterizing biochemically CMS-G, we found that the expression of several mitochondrial proteins is altered in CMS-G plants. In particular, Cox1, a core subunit of the cytochrome c oxidase (complex IV), is larger but can still assemble into complex IV. However, the CMS-G-specific complex IV was only detected as a stabilized dimer. We did not observe any alteration of the affinity of complex IV for cytochrome c however, in CMS-G, complex IV capacity is reduced. Our results show that CMS-G is maintained in many natural populations despite being associated with an atypical complex IV. We suggest that the modified complex IV could incur the associated cost predicted by theoretical models to maintain gynodioecy in wild populations.
Publisher: American Academy of Sleep Medicine (AASM)
Date: 15-06-2014
DOI: 10.5664/JCSM.3792
Publisher: Springer Science and Business Media LLC
Date: 23-06-2022
Publisher: American Academy of Sleep Medicine (AASM)
Date: 15-08-2014
DOI: 10.5664/JCSM.3950
Publisher: Scandinavian Journal of Work, Environment and Health
Date: 15-11-2021
DOI: 10.5271/SJWEH.3934
Publisher: Oxford University Press (OUP)
Date: 2011
Publisher: European Respiratory Society (ERS)
Date: 02-12-2021
DOI: 10.1183/13993003.01958-2021
Abstract: Increased mortality has been reported in people with insomnia and in those with obstructive sleep apnoea (OSA). However, these conditions commonly co-occur and the combined effect of comorbid insomnia and sleep apnoea (COMISA) on mortality risk is unknown. This study used Sleep Heart Health Study (SHHS) data to assess associations between COMISA and all-cause mortality risk. Insomnia was defined as difficulties falling asleep, maintaining sleep and/or early morning awakenings from sleep ≥16 times per month, and daytime impairments. OSA was defined as an apnoea–hypopnoea index ≥15 events·h −1 . COMISA was defined if both conditions were present. Multivariable adjusted Cox proportional hazards models were used to determine the association between COMISA and all-cause mortality (n=1210) over 15 years of follow-up. 5236 participants were included. 2708 (52%) did not have insomnia/OSA (reference group), 170 (3%) had insomnia-alone, 2221 (42%) had OSA-alone and 137 (3%) had COMISA. COMISA participants had a higher prevalence of hypertension (OR 2.00, 95% CI 1.39–2.90) and cardiovascular disease (CVD) (OR 1.70, 95% CI 1.11–2.61) compared with the reference group. Insomnia-alone and OSA-alone were associated with higher risk of hypertension but not CVD compared with the reference group. Compared with the reference group, COMISA was associated with a 47% (hazard ratio 1.47, 95% CI 1.06–2.07) increased risk of mortality. The association between COMISA and mortality was consistent across multiple definitions of OSA and insomnia. COMISA was associated with higher rates of hypertension and CVD at baseline, and an increased risk of all-cause mortality compared with no insomnia/OSA.
Publisher: American Academy of Sleep Medicine (AASM)
Date: 06-2022
DOI: 10.5664/JCSM.9934
Publisher: Oxford University Press (OUP)
Date: 14-04-2022
Abstract: Carefully controlled studies of wind turbine noise (WTN) and sleep are lacking, despite anecdotal complaints from some residents in wind farm areas and known detrimental effects of other noises on sleep. This laboratory-based study investigated the impact of overnight WTN exposure on objective and self-reported sleep outcomes. Sixty-eight participants (38 females) aged (mean ± SD) 49.2 ± 19.5 were recruited from four groups N = 14, living <10 km from a wind farm and reporting WTN related sleep disruption N = 18, living .05). These results do not support that WTN at 25 dB(A) impacts sleep outcomes in participants with or without prior WTN exposure or self-reported habitual noise-related sleep disruption. These findings do not rule out effects at higher noise exposure levels or potential effects of WTN on more sensitive markers of sleep disruption. ACTRN12619000501145, UTN U1111-1229-6126. Establishing the physiological and sleep disruption characteristics of noise disturbances in sleep. www.anzctr.org.au/. This study was prospectively registered on the Australian and New Zealand Clinical Trial Registry.
Publisher: S. Karger AG
Date: 2021
DOI: 10.1159/000513887
Abstract: b i Introduction: /i /b Sleep-disordered breathing (SDB) in patients with motor neurone disease (MND) is normally attributed to hypoventilation due to muscle weakness. However, we have observed different patterns of SDB among MND patients referred for non-invasive ventilation, which do not appear to be explained by respiratory muscle weakness alone. b i Aim: /i /b The aim of this study was to examine the characteristics of SDB in MND. b i Methods: /i /b This is a retrospective analysis of sleep studies (using polysomnography [PSG]), pulmonary function tests, and arterial blood gases in MND patients referred to a tertiary sleep medicine service for clinical review. Sleep apnoeas were characterised as obstructive or central, and to further characterise the nature of SDB, hypopnoeas were classified as obstructive versus central. b i Results: /i /b Among 13 MND patients who had a diagnostic PSG, the mean ± SD age was 68.9 ± 9.8 years, BMI 23.0 ± 4.3 kg/m sup /sup , forced vital capacity 55.7 ± 20.9% predicted, and partial pressure of CO sub /sub (arterial blood) 52.7 ± 12.1 mm Hg. A total of 38% of patients (5/13) showed evidence of sleep hypoventilation. The total apnoea/hypopnoea index (AHI) was (median [interquartile range]) 44.4(36.2–56.4)/h, with 92% (12/13) showing an AHI & #x3e /h, predominantly due to obstructive events, although 8% (1/13) also showed frequent central apnoea/hypopnoeas. b i Conclusions: /i /b Patients with MND exhibit a wide variety of SDB. The prevalence of obstructive sleep apnoea (OSA) is surprising considering the normal BMI in most patients. A dystonic tongue and increased upper-airway collapsibility might predispose these patients to OSA. The wide variety of SDB demonstrated might have implications for ventilator settings and patients’ outcomes.
Publisher: MDPI AG
Date: 15-06-2019
DOI: 10.3390/NU11061352
Abstract: Shiftworkers report eating during the night when the body is primed to sleep. This study investigated the impact of altering food timing on subjective responses. Healthy participants (n = 44, 26 male, age Mean ± SD = 25.0 ± 2.9 years, BMI = 23.82 ± 2.59kg/m2) participated in a 7-day simulated shiftwork protocol. Participants were randomly allocated to one of three eating conditions. At 00:30, participants consumed a meal comprising 30% of 24 h energy intake (Meal condition n = 14, 8 males), a snack comprising 10% of 24 h energy intake (Snack condition n = 14 8 males) or did not eat during the night (No Eating condition n = 16, 10 males). Total 24 h in idual energy intake and macronutrient content was constant across conditions. During the night, participants reported hunger, gut reaction, and sleepiness levels at 21:00, 23:30, 2:30, and 5:00. Mixed model analyses revealed that the snack condition reported significantly more hunger than the meal group (p 0.001) with the no eating at night group reporting the greatest hunger (p 0.001). There was no difference in desire to eat between meal and snack groups. Participants reported less sleepiness after the snack compared to after the meal (p 0.001) or when not eating during the night (p 0.001). Gastric upset did not differ between conditions. A snack during the nightshift could alleviate hunger during the nightshift without causing fullness or increased sleepiness.
Publisher: Cold Spring Harbor Laboratory
Date: 05-03-2023
DOI: 10.1101/2023.03.02.23286654
Abstract: Snoring may be a risk factor for cardiovascular disease and stroke. However, most prior studies have relied on subjective snoring evaluation from self-reports, or relatively short time-scale objective measures in small s les. This study assessed the prevalence of objectively quantified snoring measured over multiple months, and its association with blood pressure and hypertension. 12,287 participants were monitored nightly in-home for approximately six months using an under-the-mattress sleep sensor to estimate the average percentage of sleep time spent snoring per night and the apnea-hypopnea index (AHI). Blood pressure cuff measurements from multiple daytime assessments were averaged to define uncontrolled hypertension based on mean systolic blood pressure ≥140 mmHg and/or a mean diastolic blood pressure ≥90 mmHg. Associations between snoring and uncontrolled hypertension were examined using logistic regressions controlled for age, body mass index (BMI), sex, and AHI. Participants were predominantly middle-aged (mean±SD 50±12 y) and male (88%). There were 2,467 cases (20%) with uncontrolled hypertension. Approximately 29, 14 and 7% of the study population snored for an average of , 20, and 30% per night, respectively. A higher proportion of time spent snoring (75th vs. 5th 12% vs. 0·04%) was associated with an ∼1·9-fold increase (OR [95%CI] 1·87 [1·63, 2·15]) in uncontrolled hypertension independent of sleep apnea. The effect size of the association between snoring and uncontrolled hypertension was higher in younger adults and those who were not obese (BMI kg/m 2 ). Multi-night recordings in a large consumer s le indicate that snoring is common, and that snoring duration is positively associated with hypertension. These findings highlight the potential clinical utility of simple, objective, and non-invasive methods to detect snoring. This was an unfunded, investigator-initiated study led by the Adelaide Institute for Sleep Health sleep research team. DJE is supported by a National Health and Medical Research Council (NHMRC) of Australia Leadership Fellowship (1196261). We searched PubMed, Google, and Google Scholar for research articles published in English up to June 1, 2022, using common search terms including “wearable”, “nearable”, “sleep apnea”, and “snoring”. Articles were also retrieved through searching the citations of known literature. Snoring is a major feature of sleep disordered breathing, including hypopnea events which reflect partial airway obstruction typically with snoring. A meta-regression of 63 studies reported a highly variable snoring prevalence of between 2-83% in men and between 1-71% in women. These studies relied on self-reported snoring assessments, which may not be sufficiently reliable to evaluate prevalence and potential snoring impacts on cardiovascular health outcomes. A few small scale clinical and epidemiological studies with objective snoring assessments on a single night suggest associations between snoring and adverse cardiovascular health outcomes. However, a recent meta-analysis indicates that assessment of sleep apnea severity is highly variable night to night. Like sleep apnea severity, single time-point estimation of snoring parameters may not reliably reflect potentially problematic features of snoring and cumulative exposure risks over time. We investigated the prevalence of snoring and its association with uncontrolled hypertension on the largest dataset to date ( ,000 participants), including multi-night assessment of snoring over ∼6 months (∼2 million nights in total). Approximately 15% of the study population snored for an average of 20% per night, and a higher proportion of time spent snoring was associated with an 87% increase in uncontrolled hypertension independent of sleep apnea severity. These findings provide important insight into the consequences of snoring on hypertension risk and highlight the potential need to consider snoring as part of clinical care and management of sleep problems. These findings demonstrate the potential clinical utility of simple, objective, and non-invasive methods to detect and evaluate snoring.
Publisher: Wiley
Date: 19-05-2009
DOI: 10.1111/J.1365-2869.2008.00720.X
Abstract: Sudden cardiac death appears to be more prevalent during the normal sleeping hours in obstructive sleep apnoea (OSA) patients compared with the general population as well as to cardiovascular disease patients. The reasons for this remain unclear, but there are three likely main contributors to nocturnal death in OSA patients cardiac arrhythmias, stroke/ruptured cerebral aneurism and myocardial infarction. Particularly marked cardiovascular system activation with arousal may play a role in initiating sudden adverse cardiovascular events in OSA. The purpose of this study was to investigate cardiac RR, QT and PR interval changes in the electrocardiogram (ECG) associated with spontaneous and respiratory-related arousals in OSA patients. A detailed observational study of ECG records obtained during conventional diagnostic sleep study with no further interventions was carried out in 20 patients (12 males, age 42.8 +/- 2.1 years, body mass index 35.1 +/- 1.9 kg m(-2), and respiratory disturbance index 51.8 +/- 6.4 events/hour). RR and QT intervals showed significant shortening during arousals. RR interval shortening was found to be greater during respiratory arousals when compared to spontaneous arousals. PR interval showed a trend toward a greater prolongation during respiratory arousal. QT interval shortening was weakly correlated with arterial oxygen saturation levels preceding arousal. In conclusion, these data suggest that despite greater cardiac acceleration following respiratory versus spontaneous arousals from sleep, QT shortening and PR prolongation responses are similar independent of arousal type. These data support that arousals produce quite marked and differential cardiac conduction system activation in OSA and that the degree and pattern of activation may be partly influenced by the presence and severity of preceding respiratory events.
Publisher: Informa UK Limited
Date: 30-08-2016
DOI: 10.1080/17461391.2016.1221470
Abstract: To improve well-being and performance indicators in a group of Australian Football League (AFL) players via a six-week sleep optimisation programme. Prospective intervention study following observations suggestive of reduced sleep and excessive daytime sleepiness in an AFL group. Athletes from the Adelaide Football Club were invited to participate if they had played AFL senior-level football for 1-5 years, or if they had excessive daytime sleepiness (Epworth Sleepiness Scale [ESS] >10), measured via ESS. An initial education session explained normal sleep needs, and how to achieve increased sleep duration and quality. Participants (n = 25) received ongoing feedback on their sleep, and a mid-programme education and feedback session. Sleep duration, quality and related outcomes were measured during week one and at the conclusion of the six-week intervention period using sleep diaries, actigraphy, ESS, Pittsburgh Sleep Quality Index, Profile of Mood States, Training Distress Scale, Perceived Stress Scale and the Psychomotor Vigilance Task. Sleep diaries demonstrated an increase in total sleep time of approximately 20 min (498.8 ± 53.8 to 518.7 ± 34.3 p < .05) and a 2% increase in sleep efficiency (p < 0.05). There was a corresponding increase in vigour (p < 0.001) and decrease in fatigue (p < 0.05). Improvements in measures of sleep efficiency, fatigue and vigour indicate that a sleep optimisation programme may improve athletes' well-being. More research is required into the effects of sleep optimisation on athletic performance.
Publisher: Elsevier BV
Date: 12-2020
Publisher: Oxford University Press (OUP)
Date: 11-2011
DOI: 10.5665/SLEEP.1380
Publisher: American Physiological Society
Date: 11-2018
DOI: 10.1152/JAPPLPHYSIOL.00175.2018
Abstract: Reduced ventilatory control stability (elevated loop gain) is a key nonanatomical, pathological trait contributing to obstructive sleep apnea (OSA), yet the mechanisms responsible remain unclear. We sought to identify the key factors contributing to elevated loop gain in OSA (controller vs. plant contributions) and to examine whether abnormalities in these factors persist after OSA treatment. In 15 males (8 OSA, 7 height, weight- and age -matched controls), we measured loop gain, controller gain, and plant gain using a pseudorandom binary CO 2 stimulation method during wakefulness. Factors potentially influencing plant gain were also assessed (supine lung volume via helium dilution and spirometry). Measures were repeated 2 and 6 wk after initiating continuous positive airway pressure treatment. Loop gain (LG) was higher in OSA versus controls (LG at 1 cycle/min 0.28 ± 0.04 vs. 0.16 ± 0.04, P = 0.046, respectively), and the controller exhibited a greater peak response to CO 2 and faster roll-off in OSA. OSA patients also exhibited reduced forced expiratory volume in the first second and forced vital capacity compared with controls (92.2 ± 1.7 vs. 102.9 ± 3.5% predicted, P = 0.021 93.4 ± 3.1 vs. 106.6 ± 3.6% predicted, P = 0.015, respectively). There was no effect of treatment on any variable. These findings confirm loop gain is higher in untreated OSA patients than in matched controls however, this was not affected by treatment. NEW & NOTEWORTHY Elevated loop gain contributes to obstructive sleep apnea (OSA) pathophysiology. However, whether loop gain is inherently elevated in OSA or induced by OSA itself, whether it is elevated due to increased chemoreflex sensitivity or obesity-dependent reduced lung volume, and whether it is treatment reversible, are all currently uncertain. This study found loop gain was elevated in OSA versus age-, sex-, height-, and weight-matched controls. However, this was not altered by 6-wk continuous positive airway pressure treatment.
Publisher: Oxford University Press (OUP)
Date: 08-04-2020
Abstract: Quantification of upper airway collapsibility in obstructive sleep apnea (OSA) could help inform targeted therapy decisions. However, current techniques are clinically impractical. The primary aim of this study was to assess if a simple, novel technique could be implemented as part of a continuous positive airway pressure (CPAP) titration study to assess pharyngeal collapsibility. A total of 35 participants (15 female) with OSA (mean ± SD apnea–hypopnea index = 35 ± 19 events/h) were studied. Participants first completed a simple clinical intervention during a routine CPAP titration, where CPAP was transiently turned off from the therapeutic pressure for ≤5 breaths/efforts on ≥5 occasions during stable non-rapid eye movement (non-REM) sleep for quantitative assessment of airflow responses (%peak inspiratory flow [PIF] from preceding 5 breaths). Participants then underwent an overnight physiology study to determine the pharyngeal critical closing pressure (Pcrit) and repeat transient drops to zero CPAP to assess airflow response reproducibility. Mean PIF of breaths 3–5 during zero CPAP on the simple clinical intervention versus the physiology night were similar (34 ± 29% vs. 28 ± 30% on therapeutic CPAP, p = 0.2 range 0%–90% vs. 0%–95%). Pcrit was −1.0 ± 2.5 cmH2O (range −6 to 5 cmH2O). Mean PIF during zero CPAP on the simple clinical intervention and the physiology night correlated with Pcrit (r = −0.7 and −0.9, respectively, p & 0.0001). Receiver operating characteristic curve analysis indicated significant diagnostic utility for the simple intervention to predict Pcrit & −2 and & 0 cmH2O (AUC = 0.81 and 0.92), respectively. A simple CPAP intervention can successfully discriminate between patients with and without mild to moderately collapsible pharyngeal airways. This scalable approach may help select in iduals most likely to respond to non-CPAP therapies.
Publisher: Oxford University Press (OUP)
Date: 03-2008
Publisher: Oxford University Press (OUP)
Date: 22-08-2023
Abstract: The Sleep Apnea Multi-level Surgery (SAMS) randomised clinical trial showed surgery improved outcomes at 6 months compared to ongoing medical management in patients with moderate or severe obstructive sleep apnea (OSA) who failed continuous positive airway pressure therapy. This study reports the long-term outcomes of the multi-level surgery as a case series. Surgical participants were reassessed & years post-operatively with the same outcomes reported in the main SAMS trial. Primary outcomes were apnea-hypopnea index (AHI) and Epworth Sleepiness Scale (ESS), with secondary outcomes including other polysomnography measures, symptoms, quality of life, and adverse events. Long-term effectiveness (baseline to long-term follow-up) and interval changes (six-month to long-term follow-up) were assessed using mixed effects regression models. Control participants were also reassessed for rate of subsequent surgery and outcomes. 36/48 (75%) of surgical participants were re-evaluated (mean [SD]) 3.5 [1.0] years following surgery, with 29 undergoing polysomnography. AHI was 41/hour [23] at pre-operative baseline and 21/hour [18] at follow-up, representing persistent improvement of -24/hour [95% CI -32, -17 p& .001]. ESS was 12.3 [3.5] at baseline and 5.5 [3.9] at follow-up, representing persistent improvement of -6.8 [95% CI -8.3, -5.4 p& .001]. Secondary outcomes were improved long-term, and adverse events were minor. Interval change analysis suggests stability of outcomes. 36/43 (84%) of the control participants were re-evaluated, with 25 (69%) reporting subsequent surgery, with symptom and quality of life improvements. Multi-level upper airway surgery improves OSA burden with long-term maintenance of treatment effect in adults with moderate or severe OSA in whom conventional therapy failed.
Publisher: American Academy of Sleep Medicine (AASM)
Date: 15-01-2018
DOI: 10.5664/JCSM.6892
Publisher: Daedalus Enterprises
Date: 04-2011
Abstract: When polysomnography is indicated in a patient with a presumed sleep disorder, continuous monitoring of arterial carbon dioxide tension (P(aCO(2))) is desirable, especially if nocturnal hypoventilation is suspected. Transcutaneous CO(2) monitors (P(tcCO(2))) provide a noninvasive correlate of P(aCO(2)), but their accuracy and stability over extended monitoring have been considered inadequate for the diagnosis of hypoventilation. We examined the stability and accuracy of P(tcCO(2)) measurements and the performance of a previously described linear interpolation technique designed to correct for calibration drift. We compared the P(tcCO(2)) values from 2 TINA TCM-3 monitors to P(aCO(2)) values from arterial blood s les obtained at the beginning, every 15 min of the first hour, and then hourly over 8 hours of monitoring in 6 hemodynamically stable, male, intensive care patients (mean age 46 ± 17 y). Time had a significant (P = .002) linear effect on the P(tcCO(2))-P(aCO(2)) difference, suggesting calibration drift over the monitoring period. We found no differences between monitor type or interaction between time and monitor type. For the 2 monitors the uncorrected bias was 3.6 mm Hg and the limits of agreement were -5.1 to 12.3 mm Hg. Our linear interpolation algorithm improved the bias and limits of agreement to 0.4 and -5.5 to 6.4 mm Hg, respectively. Following stabilization and correction for both offset and drift, P(tcCO(2)) tracks P(aCO(2)) with minimal residual bias over 8 hours of monitoring. Should future research confirm these findings, then interpolated P(tcCO(2)) may have an increased role in detecting sleep hypoventilation and assessing the efficacy of treatment.
Publisher: Oxford University Press (OUP)
Date: 04-2018
Publisher: Wiley
Date: 30-09-2011
Publisher: American Physiological Society
Date: 07-2007
DOI: 10.1152/JAPPLPHYSIOL.01618.2005
Abstract: Inspiratory load compensation is impaired in patients with obstructive sleep apnea (OSA), a condition characterized by hypoxia during sleep. We sought to compare the effects of sustained hypoxia on ventilation during inspiratory resistive loading in OSA patients and matched controls. Ten OSA patients and 10 controls received 30 min of isocapnic hypoxia (arterial oxygen saturation 80%) and normoxia in random order. Following the gas period, subjects were administered six incremental 2-min inspiratory resistive loads while breathing room air. Ventilation was measured throughout the loading period. In both patients and controls, there was a significant increase in inspiratory time with increasing load ( P = 0.006 and 0.003, respectively), accompanied by a significant fall in peak inspiratory flow ( P = 0.006 and P 0.001, respectively). The result was a significant fall in minute ventilation in both groups with increasing load ( P = 0.003 and P 0.001, respectively). There was no difference between the two groups for these parameters. The only difference between the two groups was a transient increase in tidal volume in controls ( P = 0.02) but not in OSA patients ( P = 0.57) during loading. Following hypoxia, there was a significant increase in minute ventilation during loading in both groups ( P 0.001). These results suggest that ventilation during incremental resistive loading is preserved in OSA patients and that it appears relatively impervious to the effects of hypoxia.
Publisher: American Thoracic Society
Date: 03-2022
Publisher: Oxford University Press (OUP)
Date: 29-11-2021
Abstract: Sleep spindles show morphological changes in obstructive sleep apnea (OSA). However, previous small studies have limited generalizability, leaving associations between OSA severity measures and spindle metrics uncertain. This study examined cross-sectional associations between OSA severity measures and spindle metrics among a large population-based s le of men. Community-dwelling men with no previous OSA diagnosis underwent home-based polysomnography. All-night EEG (F4-M1) recordings were processed for artifacts and spindle events identified using previously validated algorithms. Spindle metrics of interest included frequency (Hz), litude (µV2), overall density (11–16 Hz), slow density (11–13 Hz), and fast density (13–16 Hz) (number/minute). Multivariable linear regression models controlling for demographic, biomedical, and behavioral confounders were used to examine cross-sectional associations between OSA severity measures and spindle metrics. In adjusted analyses, higher apnea-hypopnea index (AHI/h, as a continuous variable) and percentage total sleep time with oxygen saturation & % (TST90) were associated with decreased slow spindle density (AHI, B = −0.003, p = 0.032 TST90, B = −0.004, p = 0.047) but increased frequency (AHI, B = 0.002, p = 0.009 TST90, B = 0.002, p = 0.043). Higher TST90 was also associated with greater spindle litude (N2 sleep, B = 0.04, p = 0.011 N3 sleep, B = 0.11, p & 0.001). Furthermore, higher arousal index was associated with greater spindle litude during N2 sleep (B = 0.31, p & 0.001) but decreased overall density (B = −1.27, p = 0.030) and fast density (B = −4.36, p = 0.028) during N3 sleep. Among this large population-based s le of men, OSA severity measures were independently associated with spindle abnormalities. Further population studies are needed to determine associations between spindle metrics and functional outcomes.
Publisher: Wiley
Date: 24-08-2017
DOI: 10.1111/MEC.14291
Abstract: Social interactions are rarely random. In some instances, animals exhibit homophily or heterophily, the tendency to interact with similar or dissimilar conspecifics, respectively. Genetic homophily and heterophily influence the evolutionary dynamics of populations, because they potentially affect sexual and social selection. Here, we investigate the link between social interactions and allele frequencies in foraging flocks of great tits (Parus major) over three consecutive years. We constructed co-occurrence networks which explicitly described the splitting and merging of 85,602 flocks through time (fission-fusion dynamics), at 60 feeding sites. Of the 1,711 birds in those flocks, we genotyped 962 in iduals at 4,701 autosomal single nucleotide polymorphisms (SNPs). By combining genomewide genotyping with repeated field observations of the same in iduals, we were able to investigate links between social structure and allele frequencies at a much finer scale than was previously possible. We explicitly accounted for potential spatial effects underlying genetic structure at the population level. We modelled social structure and spatial configuration of great tit fission-fusion dynamics with eigenvector maps. Variance partitioning revealed that allele frequencies were strongly affected by group fidelity (explaining 27%-45% of variance) as in iduals tended to maintain associations with the same conspecifics. These conspecifics were genetically more dissimilar than expected, shown by genomewide heterophily for pure social (i.e., space-independent) grouping preferences. Genomewide homophily was linked to spatial configuration, indicating spatial segregation of genotypes. We did not find evidence for homophily or heterophily for putative socially relevant candidate genes or any other SNP markers. Together, these results demonstrate the importance of distinguishing social and spatial processes in determining population structure.
Publisher: Acoustical Society of America (ASA)
Date: 08-2021
DOI: 10.1121/10.0005849
Abstract: This paper presents results from a one-year study of indoor annoyance and self-reported sleep times for two participants located near different wind farms. Continuous measurements of outdoor and indoor noise and meteorological conditions were taken at each location for the duration of the study. In at least 50% of the annoyance recordings, participants described noise as “swish” or “swoosh.” Furthermore, the majority of the annoyance recordings occurred at nighttime and in the early morning. The third quartile of A-weighted indoor sound pressure level [SPL(A)], between 27 and 31 dBA, was associated with an 88% increased probability of annoyance compared to the lowest reference quartile, which was between 12 and 22 dBA [odds ratio and 95% confidence intervals, 7.72 (2.61,22.8), p & 0.001]. The outdoor SPL(A) was also predictive of annoyance but only between 40 and 45 dBA. The outdoor prevalence of litude modulation (AM), defined as the percentage of time that AM was detectable by an algorithm for each annoyance period, was also associated with annoyance. Self-reported sleep efficiency (time spent asleep relative to time in bed available for sleep) was significantly associated with nighttime annoyance (β = −0.66, p = 0.02) but only explained a small fraction of the variance (R2 = 5%).
Publisher: American Physiological Society
Date: 1993
DOI: 10.1152/JAPPL.1993.74.1.435
Abstract: Arterial blood lactate was elevated by supine leg exercise (20 min at approximately 65% maximal oxygen uptake) in five untrained male subjects, and the contribution to blood lactate removal from passive uptake vs. metabolic disposal was compared in resting and lightly exercising (15% maximal voluntary contraction static handgrip) forearm skeletal muscle. An integrated form of the Fick equation was used to predict venous lactate levels resulting solely from passive equilibration of lactate between incoming arterial blood and the forearm muscles. In the resting forearm, predicted and measured venous lactate levels were closely correlated during the exercise period (r = 0.995, P 0.001), indicating that lactate removal could be accounted for in terms of passive uptake alone. In the lightly exercising forearm, measured venous lactate levels were higher than both the arterial and predicted venous levels, indicating net lactate production. It was concluded that most of the blood lactate generated by moderate-intensity supine leg exercise is taken up passively and not metabolized by resting skeletal muscle and that the rate of lactate disposal is unlikely to be enhanced in lightly exercising muscle.
Publisher: Oxford University Press (OUP)
Date: 25-05-2022
DOI: 10.1093/SLEEP/ZSAC079.202
Abstract: Sleep irregularity has been associated with worse cardio-metabolic health compared to regular sleep, but prior studies have been limited in s le size and have assessed sleep irregularity by actigraphy or questionnaires over a relatively short duration (~ 14 days). The current study investigated associations between sleep regularity and hypertension in a large, global s le over multiple months. Data from 12,300 participants (aged 18-90 years) who used an under-mattress sleep device and a portable blood pressure monitor between July 2020 and March 2021 were included in this study. Sleep duration regularity was assessed as the standard deviation via device-assessed total sleep time. Sleep timing regularity was assessed as the standard deviation in sleep onset time and in sleep midpoint. Logistic regressions controlling for age, sex, BMI, and mean total sleep time were conducted to investigate potential associations between sleep regularity and hypertension. Participants were typically middle-aged (Mean ± SD 50 ± 12 years) and predominantly male (12% females). Each participant had ~180 nights of recordings and ~70 blood pressure entries. There were 2,499 cases of hypertension defined as SBP& and/or DBP & mmHg (20% of the s le). Across total sleep time quartiles, high sleep duration irregularity was consistently associated with a 9 to 15% increase in hypertension risk. A 38-minute increase in sleep midpoint irregularity was associated with an 11% (1.11 [1.03, 1.20]) increase in hypertension risk, independent of mean total sleep time and mean sleep midpoint. Similarly, a ~31-minute increase in sleep onset time irregularity was associated with a 29% increased risk of hypertension (1.29 [1.18, 1.42]). These novel findings provide insight into the potential important impact of sleep irregularity on cardiovascular health. Further assessment of day-to-day fluctuations in sleep duration and timing for potential effects on next-day blood pressure and other cardiovascular health outcomes are warranted. This was an unfunded investigator-initiated study. De-identified data were provided by Withings for unrestricted investigator-led analysis. PE serves as a consultant for Withings.
Publisher: American Physiological Society
Date: 12-2002
DOI: 10.1152/JAPPLPHYSIOL.00135.2002
Abstract: Obstructive sleep apnea (OSA) is more common in men than in women for reasons that are unclear. The stability of the respiratory controller has been proposed to be important in OSA pathogenesis and may be involved in the gender difference in prevalence. Repetitive hypoxia elicits a progressive rise in ventilation in animals [long-term facilitation (LTF)]. There is uncertainty whether LTF occurs in humans, but if present it may stabilize respiration and possibly also the upper airway. This study was conducted to determine 1) whether LTF exists during wakefulness in healthy human subjects and, if so, whether it is more pronounced in women than men and 2) whether inspiratory pump and upper airway dilator muscle activities are affected differently by repetitive hypoxia. Twelve healthy young men and ten women in the luteal menstrual phase were fitted with a nasal mask and intramuscular genioglossal EMG (EMGgg) recording electrodes. After 5 min of rest, subjects were exposed to ten 2-min isocapnic hypoxic periods (∼9% O 2 in N 2 , arterial O 2 saturation ∼80%) separated by 2 min of room air. Inspired minute ventilation (V˙i) and peak inspiratory EMGgg activity were averaged over 30-s intervals, and respiratory data were compared between genders during and after repetitive hypoxia by using ANOVA for repeated measures. V˙i during recovery from repetitive hypoxia was not different from the resting level and not different between genders. There was no facilitation of EMGgg activity during or after repetitive hypoxia. EMGgg activity was reduced below baseline during recovery from repetitive hypoxia in women. In conclusion, we have found no evidence of LTF of ventilation or upper airway dilator muscle activity in healthy subjects during wakefulness.
Publisher: Oxford University Press (OUP)
Date: 29-01-2019
Abstract: Wind turbine noise (WTN) exposure could potentially interfere with the initiation of sleep. However, effects on objectively assessed sleep latency are largely unknown. This study sought to assess the impact of WTN on polysomnographically measured and sleep diary-determined sleep latency compared to control background noise alone in healthy good sleepers without habitual prior WTN exposure. Twenty-three WTN naïve urban residents (mean ± SD age: 21.7 ± 2.1 years, range 18–29, 13 females) attended the sleep laboratory for two polysomnography studies, one week apart. Participants were blind to noise conditions and only informed that they may or may not hear noise during each night. During the sleep onset period, participants were exposed to counterbalanced nights of WTN at 33 dB(A), the upper end of expected indoor values or background noise alone as the control condition (23 dB(A)). Linear mixed model analysis revealed no differences in log10 normalized objective or subjective sleep latency between the WTN versus control nights (median [interquartile range] objective 16.5 [11.0 to 18.5] vs. 16.5 [10.5 to 29.0] min, p = .401 subjective 20.0 [15.0 to 25.0] vs. 15.0 [10.0 to 30.0] min, p = .907). Although undetected small effects cannot be ruled out, these results do not support that WTN extends sleep latency in young urban-dwelling in iduals without prior WTN exposure.
Publisher: Springer Science and Business Media LLC
Date: 10-2009
Publisher: Oxford University Press (OUP)
Date: 13-12-2021
Abstract: Extended wakefulness (EW) and obstructive sleep apnea (OSA) impair working memory (WM), but their combined effects are unclear. This study examined the impact of EW on WM function in OSA patients and identified clinical predictors of WM impairment. Following polysomnography (PSG), 56 OSA patients (mean ± SD, age 49.5 ± 8.9, apnea hypopnea index 38.1 ± 25.0) completed WM 2-back performance tasks 10 times over 24 h of wakefulness to assess average accuracy and completion times measured after 6–12 h awake (baseline) compared to 18–24 h awake (EW). Hierarchical cluster analysis classified participants with poorer versus better WM performance at baseline and during EW. Clinical predictors of performance were examined via regression and receiver operator characteristic (ROC) analyses. WM performance decreased following EW and showed consistent correlations with age, Epworth Sleepiness Score (ESS), total sleep time, and hypoxemia (O2 nadir and mean O2 desaturation) at baseline and with EW (all p & .01). O2 nadir and age were significant independent predictors of performance at baseline (adjusted R2 = 0.30, p & .01), while O2 nadir and ESS were predictors of WM following EW (adjusted R2 = 0.38, p & .001). ROC analysis demonstrated high sensitivity and specificity of models to predict poorer versus better performing participants at baseline (83% and 69%) and during EW (84% and 74%). O2 nadir, age, and sleepiness show prognostic value for predicting WM impairment in both rested and sleep-deprived OSA patients and may guide clinicians in identifying patients most at risk of impaired WM under both rested and heightened sleep pressure conditions. Clinical Trial Registration: This manuscript presents data collected as part of a larger trial—ANZCTR: Novel brain biomarkers of performance impairment in sleep apnea—www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=363830, No. ACTRN12613001171707.
Publisher: Elsevier BV
Date: 2023
DOI: 10.1016/J.SLEEP.2022.10.030
Abstract: Self-reported sleep difficulties are the primary concern associated with diagnosis and treatment of chronic insomnia. This said, in-home sleep monitoring technology in combination with self-reported sleep outcomes may usefully assist with the management of insomnia. The rapid acceleration in consumer sleep technology capabilities together with their growing use by consumers means that the implementation of clinically useful techniques to more precisely diagnose and better treat insomnia are now possible. This review describes emerging techniques which may facilitate better identification and management of insomnia through objective sleep monitoring. Diagnostic techniques covered include insomnia phenotyping, better detection of comorbid sleep disorders, and identification of patients potentially at greatest risk of adverse outcomes. Treatment techniques reviewed include the administration of therapies (e.g., Intensive Sleep Retraining, digital treatment programs), methods to assess and improve treatment adherence, and sleep feedback to address concerns about sleep and sleep loss. Gaps in sleep device capabilities are also discussed, such as the practical assessment of circadian rhythms. Proof-of-concept studies remain needed to test these sleep monitoring-supported techniques in insomnia patient populations, with the goal to progress towards more precise diagnoses and efficacious treatments for in iduals with insomnia.
Publisher: Oxford University Press (OUP)
Date: 05-2006
Abstract: The depressive effects of hypoxia on the central nervous system are well known. The purpose of this study was to determine the influence of mild overnight hypoxia on the ability of healthy in iduals to arouse from non-rapid-eye-movement (NREM) sleep to auditory tones. Randomized cross-over. Participants slept in a sound-insulated room with the physiologic recordings and experimental interventions controlled from a separate room. Eleven healthy men aged 18 to 24 years. On separate nights, participants were exposed to mild overnight hypoxia (SaO2 approximately 90%) or medical air in single-blind fashion. During established sleep, subjects were administered 1 of 10 auditory tones (500 Hz, 54-90 dB, 5 seconds duration) via earphones, or a sham tone (recording period with no tone). The probability and intensity of arousal responses in the 30 seconds following tones or shams were compared between gas conditions and between stage 2 and slow-wave sleep. Arousal probability and intensity increased with tone intensity and were significantly lower during slow-wave compared with stage 2 sleep but were not different between hypoxia and normoxia nights. These data suggest that mild overnight hypoxia does not impair the neural mechanisms involved in arousal from sleep to auditory stimuli.
Publisher: BMJ
Date: 12-02-2009
Abstract: Sleep hypoventilation has been proposed as a cause of progressive hypercapnic respiratory failure and death in patients with severe chronic obstructive pulmonary disease (COPD). A study was undertaken to determine the effects of nocturnal non-invasive bi-level pressure support ventilation (NIV) on survival, lung function and quality of life in patients with severe hypercapnic COPD. A multicentre, open-label, randomised controlled trial of NIV plus long-term oxygen therapy (LTOT) versus LTOT alone was performed in four Australian University Hospital sleep/respiratory medicine departments in patients with severe stable smoking-related COPD (forced expiratory volume in 1 s (FEV1.0) <1.5 litres or <50% predicted and ratio of FEV1.0 to forced vital capacity (FVC) 46 mm Hg and on LTOT for at least 3 months) and age 20/h) or morbid obesity (body mass index >40) were excluded. Outcome measures were survival, spirometry, arterial blood gases, polysomnography, general and disease-specific quality of life and mood. 144 patients were randomised (72 to NIV + LTOT and 72 to LTOT alone). NIV improved sleep quality and sleep-related hypercapnia acutely, and patients complied well with therapy (mean (SD) nightly use 4.5 (3.2) h). Compared with LTOT alone, NIV (mean follow-up 2.21 years, range 0.01-5.59) showed an improvement in survival with the adjusted but not the unadjusted Cox model (adjusted hazard ratio (HR) 0.63, 95% CI 0.40 to 0.99, p = 0.045 unadjusted HR 0.82, 95% CI 0.53 to 1.25, p = NS). FEV1.0 and PaCO2 measured at 6 and 12 months were not different between groups. Patients assigned to NIV + LTOT had reduced general and mental health and vigour. Nocturnal NIV in stable oxygen-dependent patients with hypercapnic COPD may improve survival, but this appears to be at the cost of worsening quality of life. ACTRN12605000205639.
Publisher: American Academy of Sleep Medicine (AASM)
Date: 06-2022
DOI: 10.5664/JCSM.9950
Publisher: Wiley
Date: 04-1999
Publisher: Springer Science and Business Media LLC
Date: 15-02-2018
Publisher: RWTH Aachen University
Date: 2019
Publisher: Informa UK Limited
Date: 06-2023
DOI: 10.2147/NSS.S423397
Publisher: Elsevier BV
Date: 06-2014
DOI: 10.1016/J.SEIZURE.2014.03.007
Abstract: Seizure related unconscious face-down positioning could contribute to sudden unexpected death in epilepsy via asphyxia. Low airflow resistance lattice foam pillows have been advocated for this group. However, data to support this approach remain lacking, and low airflow resistance per se may not negate asphyxia risk from expired gas rebreathing. This study was designed to compare the airflow resistance and CO2 rebreathing properties of lattice vs conventional pillows. Airflow resistance and inspired CO2 levels during replicate 10 min periods of simulated adult ventilation and CO2 rebreathing were compared between cotton, latex and two lattice pillows designed for use in epilepsy (one commercially available, one prototype). Kaplan-Meier and Cox regression analyses were used to examine the hazard of exceeding 10% inspired CO2 within 10-min of rebreathing. Inspiratory resistance was significantly lower in the commercially available and prototype lattice compared to cotton and latex pillows (mean±SD 3.2±0.8, 2.6±0.4, 26.1±3.5, 4.6±0.4 cm H2O l(-1)s respectively at 0.2l s(-1)). During simulated rebreathing, inspired CO2 exceeded 10% within 2 min with cotton and latex pillows, compared to an upper asymptote around 8-9% at 10 min with lattice pillows. The hazard of exceeding 10% inspired CO2 was therefore markedly reduced with lattice compared to cotton and latex pillows (hazard ratio vs cotton pillow commercial 0.04 [0.01-0.18], prototype 0.08 [0.02-0.26], latex 0.79 [0.33-1.87]). Conventional pillows can rapidly accumulate potentially life-threatening CO2 levels during simulated rebreathing. Lattice pillows appear to reduce asphyxia risk but accumulated CO2 may still reach levels threatening to health and survival.
Publisher: Elsevier BV
Date: 10-2023
Publisher: Wiley
Date: 07-04-2013
DOI: 10.1111/EJN.12203
Abstract: Obstructive sleep apnoea (OSA) is a respiratory condition occurring during sleep characterised by repeated collapse of the upper airway. Patients with OSA show altered brain structure and function that may manifest as impaired neuroplasticity. We assessed this hypothesis in 13 patients with moderate-to-severe OSA and 11 healthy control subjects. Transcranial magnetic stimulation was used to induce and measure neuroplastic changes in the motor cortex by assessing changes in motor-evoked potentials (MEPs) in a hand muscle. Baseline measurements of cortical excitability included active (AMT) and resting motor thresholds (RMT), and the maximal stimulator output producing a 1-mV MEP. Intracortical inhibition (ICI) was investigated with short- and long-interval ICI paradigms (SICI and LICI, respectively), and neuroplastic changes were induced using continuous theta burst stimulation (cTBS). At baseline, differences were found between groups for RMT (9.5% maximal stimulator output higher in OSA) and 1-mV MEPs (10.3% maximal stimulator output higher in OSA), but not AMT. No differences were found between groups for SICI or LICI. The response to cTBS was different between groups, with control subjects showing an expected reduction in MEP litude after cTBS, whereas the MEPs in patients with OSA did not change. The lack of response to cTBS suggests impaired long-term depression-like neuroplasticity in patients with OSA, which may be a consequence of sleep fragmentation or chronic blood gas disturbance in sleep. This reduced neuroplastic capacity may have implications for the learning, retention or consolidation of motor skills in patients with OSA.
Publisher: Springer Science and Business Media LLC
Date: 30-03-2023
DOI: 10.1038/S41746-023-00801-2
Abstract: Obstructive sleep apnea (OSA) severity can vary markedly from night-to-night. However, the impact of night-to-night variability in OSA severity on key cardiovascular outcomes such as hypertension is unknown. Thus, the primary aim of this study is to determine the effects of night-to-night variability in OSA severity on hypertension likelihood. This study uses in-home monitoring of 15,526 adults with ~180 nights per participant with an under-mattress sleep sensor device, plus ~30 repeat blood pressure measures. OSA severity is defined from the mean estimated apnea–hypopnoea index (AHI) over the ~6-month recording period for each participant. Night-to-night variability in severity is determined from the standard deviation of the estimated AHI across recording nights. Uncontrolled hypertension is defined as mean systolic blood pressure ≥140 mmHg and/or mean diastolic blood pressure ≥90 mmHg. Regression analyses are performed adjusted for age, sex, and body mass index. A total of 12,287 participants (12% female) are included in the analyses. Participants in the highest night-to-night variability quartile within each OSA severity category, have a 50–70% increase in uncontrolled hypertension likelihood versus the lowest variability quartile, independent of OSA severity. This study demonstrates that high night-to-night variability in OSA severity is a predictor of uncontrolled hypertension, independent of OSA severity. These findings have important implications for the identification of which OSA patients are most at risk of cardiovascular harm.
Publisher: Elsevier BV
Date: 08-2015
DOI: 10.1016/J.SMRV.2014.10.003
Abstract: Intermittent hypoxia and unstable breathing are key features of obstructive sleep apnoea (OSA), the most common pathological problem of breathing in sleep. Unstable ventilatory control is characterised by high loop gain (LG), and likely contributes to cyclical airway obstruction by promoting airway collapse during periods of low ventilatory drive. Potential new strategies to treat OSA include manipulations designed to lower LG. However, the contribution of inherent versus induced LG abnormalities in OSA remains unclear. Hence, a better understanding of the mechanisms causing high LG in OSA is needed to guide the design of LG based treatments. OSA patients exhibit abnormal chemoreflex control which contributes to increased LG. These abnormalities have been shown to normalise after continuous positive airway pressure treatment, suggesting induced rather than inherent trait abnormalities. Experimental intermittent hypoxia, mimicking OSA, increases hypoxic chemosensitivity and induces long term facilitation a sustained increase in ventilatory neural output which outlasts the original stimulus. These neuroplastic changes induce the same abnormalities in chemoreflex control as seen in OSA patients. This review outlines the evidence to support that a key component of high LG in OSA is induced by intermittent hypoxia, and is reversed by simply preventing this inducing stimulus.
Publisher: Elsevier BV
Date: 02-2013
Publisher: European Respiratory Society (ERS)
Date: 06-2003
DOI: 10.1183/09031936.03.00066802
Abstract: Sleep hypoventilation (SH) may be important in the development of hypercapnic respiratory failure in chronic obstructive pulmonary disease (COPD). The prevalence of SH, associated factors, and overnight changes in waking arterial blood gases (ABG), were assessed in 54 stable hypercapnic COPD patients without concomitant sleep apnoea or morbid obesity. Lung function assessment, anthropomorphic measurements, and polysomnography with ABG measurement before and after sleep were conducted in all patients. Transcutaneous carbon dioxide tension (Pt,CO2) was measured in sleep, using simultaneous arterial carbon dioxide tension (Pa,CO2) for in vivo calibration and to correct for drift in the sensor. Of the patients, 43% spent > or = 20% of sleep time with Pt,CO2 > 1.33 kPa (10 mmHg) above waking baseline. Severity of SH was best predicted by a combination of baseline Pa,CO2, body mass index and per cent rapid-eye movement (REM) sleep. REM-related hypoventilation correlated significantly with severity of inspiratory flow limitation in REM, and with apnoea/hypopnoea index. Pa,CO2 increased mean+/-SD 0.70+/-0.65 kPa (5.29+/-4.92 mmHg) from night to morning, and this change was highly significant. The change in Pa,CO2 was strongly correlated with severity of SH. Sleep hypoventilation is common in hypercapnic chronic obstructive pulmonary disease, and related to baseline arterial carbon dioxide tension, body mass index and indices of upper airway obstruction. Sleep hypoventilation is associated with significant increases in arterial carbon dioxide tension night-to-morning, and may contribute to long-term elevations in arterial carbon dioxide tension.
Publisher: Oxford University Press (OUP)
Date: 12-01-2020
Abstract: While cognitive and behavioral therapy for insomnia (CBTi) is an effective treatment in patients with comorbid moderate and severe obstructive sleep apnea (OSA), there is concern that the bedtime restriction component of CBTi might dangerously exacerbate daytime sleepiness in such patients. We examined randomized controlled trial data to investigate the effect of OSA severity, and pretreatment daytime sleepiness on week-to-week changes in daytime sleepiness and sleep parameters during CBTi and no-treatment control. One hundred and forty-five patients with untreated physician-diagnosed OSA (apnea–hypopnea index ≥15) and psychologist-diagnosed insomnia (ICSD-3) were randomized to a 4-week CBTi program (n = 72) or no-treatment control (n = 73). The Epworth sleepiness scale (ESS) and sleep diaries were completed during pretreatment, weekly CBTi sessions, and posttreatment. Effects of OSA severity, pretreatment daytime sleepiness, and intervention group on weekly changes in daytime sleepiness and sleep parameters were investigated. The CBTi group reported a 15% increase in ESS scores following the first week of bedtime restriction (M change = 1.3 points, 95% CI = 0.1–2.5, p = 0.031, Cohen’s d = 0.27) which immediately returned to pretreatment levels for all subsequent weeks, while sleep parameters gradually improved throughout CBTi. There were no differences in changes in daytime sleepiness during treatment between CBTi and control groups or OSA-severity groups. Higher pretreatment ESS scores were associated with a greater ESS reduction during CBTi. CBTi appears to be a safe and effective treatment in the presence of comorbid moderate and severe OSA. Nevertheless, patients living with comorbid insomnia and sleep apnea and treated with CBTi should be monitored closely for increased daytime sleepiness during the initial weeks of bedtime restriction therapy. Treating comorbid insomnia with obstructive sleep apnoea (COMISA) study: A new treatment strategy for patients with combined insomnia and sleep apnoea, www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id = 365184 Australian New Zealand Clinical Trials Registry: ACTRN12613001178730. Universal Trial Number: U1111-1149-4230.
Publisher: Elsevier BV
Date: 09-2021
Publisher: Wiley
Date: 30-09-2011
Publisher: Wiley
Date: 13-11-2022
DOI: 10.1111/JSR.13517
Abstract: Wind turbine noise is dominated by low frequencies for which effects on sleep relative to more common environmental noise sources such as road traffic noise remain unknown. This study examined the effect of wind turbine noise compared with road traffic noise on sleep using quantitative electroencephalogram power spectral analysis. Twenty-three participants were exposed to 3-min s les of wind turbine noise and road traffic noise at three sound pressure levels (33, 38 and 43 dBA) in randomised order during established sleep. Acute (0-30 s) and more sustained (30-180 s) effects of noise presentations during N2 and N3 sleep were examined using spectral analysis of changes in electroencephalogram power frequency ranges across time in 5-s intervals. Both noise types produced time- and sound pressure level-dependent increases in electroencephalogram power, but with significant noise type by sound pressure level interactions in beta, alpha, theta and delta frequency bands (all p < 0.05). Wind turbine noise showed significantly lower delta, theta and beta activity immediately following noise onset compared with road traffic noise (all p < 0.05). However, alpha activity was higher for wind turbine noise played at lower sound pressure levels (33 dBA [p = 0.001] and 38 dBA [p = 0.003]) compared with traffic noise during N2 sleep. These findings support that spectral analyses show subtle effects of noise on sleep and that electroencephalogram changes following wind turbine noise and road traffic noise onset differ depending on sound pressure levels however, these effects were mostly transient and had little impact on conventionally scored sleep. Further studies are needed to establish if electroencephalogram changes associated with modest environmental noise exposures have significant impacts on sleep quality and next-day functioning.
Publisher: Informa UK Limited
Date: 05-2023
DOI: 10.2147/NSS.S401655
Publisher: IEEE
Date: 09-2007
Publisher: Oxford University Press (OUP)
Date: 12-03-2021
Abstract: The primary aim of this study was to examine dose–response relationships between sound pressure levels (SPLs) and K-complex occurrence probability for wind farm and road traffic noise. A secondary aim was to compare K-complex dose–responses to manually scored electroencephalography arousals and awakenings. Twenty-five participants underwent polysomnography recordings and noise exposure during sleep in a laboratory. Wind farm and road traffic noise recordings of 20-sec duration were played in random order at 6 SPLs between 33 and 48 dBA during established N2 or deeper sleep. Noise periods were separated with periods of 23 dBA background noise. K-complexes were scored using a validated algorithm. K-complex occurrence probability was compared between noise types controlling for noise SPL, subjective noise sensitivity, and measured hearing acuity. Noise-induced K-complexes were observed in N2 sleep at SPLs as low as 33 dBA (Odds ratio, 33 dBA vs 23 dBA, mean (95% confidence interval) 1.75 (1.16, 2.66)) and increased with SPL. EEG arousals and awakenings were only associated with noise above 39 dBA in N2 sleep. K-complexes were 2 times more likely to occur in response to noise than EEG arousals or awakenings. Subjective noise sensitivity and hearing acuity were associated with the K-complex occurrence, but not arousal or awakening. Noise type did not detectably influence K-complexes, EEG arousals, or awakening responses. These findings support that K-complexes are a sensitive marker of sensory processing of environmental noise during sleep and that increased hearing acuity and decreased self-reported noise sensitivity increase K-complex probability.
Publisher: Oxford University Press (OUP)
Date: 2015
DOI: 10.5665/SLEEP.4324
Publisher: Elsevier BV
Date: 03-2023
Publisher: American Physiological Society
Date: 10-2010
DOI: 10.1152/JAPPLPHYSIOL.01397.2009
Abstract: Obese obstructive sleep apnea (OSA) patients potentially defend end-expiratory lung volume (EELV) during wakefulness via increased expiratory diaphragmatic activity (eEMG dia ). A reduction in eEMG dia and EELV at sleep onset could, therefore, increase upper airway collapsibility via reduced tracheal traction. The aim of this study was to establish if eEMG dia is greater in obese OSA patients vs. healthy-weight controls during wakefulness, and to compare eEMG dia and EELV changes at sleep onset between groups as a function of stable breathing, hypopnea vs. apnea events developing within the first few breaths after sleep onset. Eight obese men with OSA and eight healthy-weight men without OSA were studied in the supine position while instrumented with an intraesophageal catheter to measure eEMG dia and magnetometer coils to assess changes in EELV. While eEMG dia expressed as %maximal activity was not significantly different between groups during wakefulness, OSA patients experienced a greater fall in eEMG dia following sleep onset (group × breath, P 0.001) and a greater decrease when respiratory events accompanied sleep onsets (category × breath, P 0.001). The decrease in EELV by the third postsleep onset breath was small (OSA, 61.4 ± 8.0 ml, P 0.001 controls, 34.0 ± 4.2 ml, P 0.001), with the decrease significantly greater in OSA patients over time (group × breath, P = 0.007). There was a greater decrease with more severe events (category × breath, P 0.001), with EELV decreasing by 89.6 ± 14.2 ml ( P 0.001) at the onset of apneas in the OSA group. These data support that diaphragm tone and EELV frequently decrease following sleep onset, with greater falls at transitions accompanied by respiratory events. In addition to decrements in upper airway dilator muscle activity, decreasing lung volume potentially contributes to an increased propensity for upper airway collapse in OSA patients at sleep onset.
Publisher: Elsevier BV
Date: 05-2021
Publisher: Oxford University Press (OUP)
Date: 10-2002
Abstract: Changes in cardiovascular measures such as heart rate (HR) and pulse transit time (PTT) have been advocated as sensitive markers of autonomic arousal from sleep. In animal studies, alerting stimuli produce particularly marked skin vascular responses. We hypothesized that changes in skin vascular conductance would provide more sensitive markers of autonomic arousal during sleep compared to central cardiovascular response measures such as HR and PTT. Cardiovascular responses to auditory-induced arousals were recorded during overnight sleep studies. Sleep disorders unit in a 270-bed teaching hospital. Eleven young healthy male subjects. Throughout ovemight sleep studies, auditory tones (5-second duration, 54-90 decibels, 22-56 per subject) were presented during non-rapid-eye-movement sleep. Beat-by-beat HR, PTT, laser-Doppler fingertip skin blood flow (SBF) and finger and ear photoplethysmogram pulse wave litudes (PWA) were measured in the 20 seconds preceding and 30 seconds following each tone and compared to control measurements obtained during 50-second periods of recording with no stimulus (no tone, 6-22 per subject). Electroencephalographic (EEG) arousals were scored according to standard criteria (American Sleep Disorders Association) into no discemible, 3- to 10-second duration, or 10- to 15-second duration arousals. Poststimulus cardiovascular measurements were expressed as a percentage of the prestimulus mean and response magnitudes quantified from peak responses and the area under the poststimulus response curve. The ability of each cardiovascular response measure to discriminate EEG arousals (EEG changes lasting more than 3 seconds) was assessed from the area under the receiver operating characteristic (ROC) curve. There were no significant changes in any cardiovascular parameter during control recordings. In contrast to all other parameters, finger PWA and SBF decreased following tones that produced no discernible EEG arousal (P < 0.05). A significant HR rise and decreases in all cardiovascular measures occurred with greater than 3-second arousals, with longer duration arousals generally exhibiting larger responses. Conventional EEG arousals (greater than 3 seconds) were relatively poorly detected from HR responses (ROC area HR rise 0.80 +/- 0.04) compared to changes in SBF (0.85 +/- 0.02), PTT (0.85 +/- 0.03) and finger PWA (0.90 +/- 0.01). Decreases in skin vascular conductance (finger PWA and SBF) provide sensitive markers of autonomic arousal during sleep. They are at least as sensitive as PTT for detecting conventionally scored EEG arousals and may be more sensitive in detecting "subcortical" arousals.
Publisher: Oxford University Press (OUP)
Date: 04-04-2019
DOI: 10.1093/SLEEP/ZSZ056
Abstract: Obstructive sleep apnea (OSA) is a serious and costly public health problem. The main medical treatment, continuous positive airway pressure, is efficacious when used, but poorly tolerated in up to 50% of patients. Upper airway reconstructive surgery is available when medical treatments fail but randomized trial evidence supporting its use is limited. This protocol details a randomized controlled trial designed to assess the clinical effectiveness, safety, and cost-effectiveness of a multilevel upper airway surgical procedure for OSA. A prospective, parallel-group, open label, randomized, controlled, multicenter clinical trial in adults with moderate or severe OSA who have failed or refused medical therapies. Six clinical sites in Australia randomly allocated participants in a 1:1 ratio to receive either an upper airway surgical procedure consisting of a modified uvulopalatopharyngoplasty and minimally invasive tongue volume reduction, or to continue with ongoing medical management, and followed them for 6 months. Primary outcomes: difference between groups in baseline-adjusted 6 month OSA severity (apnea–hypopnea index) and subjective sleepiness (Epworth Sleepiness Scale). Secondary outcomes: other OSA symptoms (e.g. snoring and objective sleepiness), other polysomnography parameters (e.g. arousal index and 4% oxygen desaturation index), quality of life, 24 hr ambulatory blood pressure, adverse events, and adherence to ongoing medical therapies (medical group). The Sleep Apnea Multilevel Surgery (SAMS) trial is of global public health importance for testing the effectiveness and safety of a multilevel surgical procedure for patients with OSA who have failed medical treatment. Multilevel airway surgery in patients with moderate-severe Obstructive Sleep Apnea (OSA) who have failed medical management to assess change in OSA events and daytime sleepiness. www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=366019& isReview=true Australian New Zealand Clinical Trials Registry ACTRN12614000338662, prospectively registered on 31 March 2014.
Publisher: Frontiers Media SA
Date: 07-10-2021
DOI: 10.3389/FNINS.2021.751730
Abstract: Current approaches to quantify and diagnose sleep disorders and circadian rhythm disruption are imprecise, laborious, and often do not relate well to key clinical and health outcomes. Newer emerging approaches that aim to overcome the practical and technical constraints of current sleep metrics have considerable potential to better explain sleep disorder pathophysiology and thus to more precisely align diagnostic, treatment and management approaches to underlying pathology. These include more fine-grained and continuous EEG signal feature detection and novel oxygenation metrics to better encapsulate hypoxia duration, frequency, and magnitude readily possible via more advanced data acquisition and scoring algorithm approaches. Recent technological advances may also soon facilitate simple assessment of circadian rhythm physiology at home to enable sleep disorder diagnostics even for “non-circadian rhythm” sleep disorders, such as chronic insomnia and sleep apnea, which in many cases also include a circadian disruption component. Bringing these novel approaches into the clinic and the home settings should be a priority for the field. Modern sleep tracking technology can also further facilitate the transition of sleep diagnostics from the laboratory to the home, where environmental factors such as noise and light could usefully inform clinical decision-making. The “endpoint” of these new and emerging assessments will be better targeted therapies that directly address underlying sleep disorder pathophysiology via an in idualized, precision medicine approach. This review outlines the current state-of-the-art in sleep and circadian monitoring and diagnostics and covers several new and emerging approaches to better define sleep disruption and its consequences.
Publisher: Elsevier BV
Date: 12-2023
Publisher: Springer Science and Business Media LLC
Date: 13-09-2013
DOI: 10.1111/SBR.12028
Publisher: American Academy of Sleep Medicine (AASM)
Date: 15-10-2009
DOI: 10.5664/JCSM.27597
Publisher: Wiley
Date: 12-11-2021
DOI: 10.1111/JSR.13228
Abstract: Little is known about the potential impacts of wind turbine noise (WTN) on sleep. Previous research is limited to cross‐sectional studies reporting anecdotal impacts on sleep using inconsistent sleep metrics. This meta‐analysis sought to comprehensively review studies evaluating the impact of WTN using widely accepted and validated objective and subjective sleep assessments. Search terms included: “wind farm noise”, “wind turbine noise”, “wind turbine sound”, “wind turbine noise exposure” AND “sleep”. Only original articles published in English published after the year 2000 and reporting sleep outcomes in the presence of WTN using polysomnography, actigraphy or psychometrically validated sleep questionnaires were included. Uniform outcomes of the retrieved studies were meta‐analysed to examine WTN effects on objective and subjective sleep outcomes. Nine studies were eligible for review and five studies were meta‐analysed. Meta‐analyses (Hedges’ g 95% confidence interval [CI]) revealed no significant differences in objective sleep onset latency (0.03, 95% CI −0.34 to 0.41), total sleep time (−0.05, 95% CI −0.77 to 0.67), sleep efficiency (−0.25, 95% CI −0.71 to 0.22) or wake after sleep onset (1.25, 95% CI −2.00 to 4.50) in the presence versus absence of WTN (all p .05). Subjective sleep estimates were not meta‐analysed because measurement outcomes were not sufficiently uniform for comparisons between studies. This systematic review and meta‐analysis suggests that WTN does not significantly impact key indicators of objective sleep. Cautious interpretation remains warranted given variable measurement methodologies, WTN interventions, limited s le sizes, and cross‐sectional study designs, where cause‐and‐effect relationships are uncertain. Well‐controlled experimental studies using ecologically valid WTN, objective and psychometrically validated sleep assessments are needed to provide conclusive evidence regarding WTN impacts on sleep.
Publisher: American Thoracic Society
Date: 15-12-2003
Publisher: Acoustical Society of America (ASA)
Date: 05-2022
DOI: 10.1121/10.0010494
Abstract: This study proposes an approach for the characterisation and assessment of wind farm noise (WFN), which is based on extraction of acoustic features between 125 and 7500 Hz from a pretrained deep learning model (referred to as deep acoustic features). Using data measured at a variety of locations, this study shows that deep acoustic features can be linked to meaningful characteristics of the noise. This study finds that deep acoustic features can reveal an improved spatial and temporal representation of WFN compared to what is revealed using traditional spectral analysis and overall noise descriptors. These results showed that this approach is promising, and thus it could provide the basis for an improved framework for WFN assessment in the future.
Publisher: Elsevier BV
Date: 10-2018
DOI: 10.1016/J.SMRV.2018.01.003
Abstract: Obstructive sleep apnea (OSA) is a common disorder associated with multiple adverse health consequences and its prevalence is increasing in parallel with rising obesity trends. Early support for ethnic differences in OSA prevalence and severity has been derived from studies of relatively homogenous ethnic groups. However, between-study comparisons are problematic given differing methodologies. Recent large inter-ethnic studies examining different ethnic populations using standardized protocols support the notion that Chinese have an increased OSA prevalence and severity compared to those of European descent. Although the evidence is less clear, some data suggest that Hispanic/Mexican Americans also show higher rates of OSA, while OSA prevalence in African Americans is not dissimilar to that of populations of European ancestry. Of the anatomical traits underlying differences in OSA prevalence and severity between ethnic groups (i.e., obesity, fat distribution, and craniofacial structure) obesity appears to be the most important. The effect of ethnicity on non-anatomical factors (i.e., upper airway muscle responsiveness, arousal threshold, and loop gain) responsible for OSA severity and potentially prevalence is currently unknown and needs further research.
Publisher: Oxford University Press (OUP)
Date: 2013
DOI: 10.5665/SLEEP.2314
Publisher: Elsevier BV
Date: 12-2022
Publisher: Springer Science and Business Media LLC
Date: 18-09-2012
Publisher: SPIE
Date: 27-02-2019
DOI: 10.1117/12.2506567
Publisher: American Physiological Society
Date: 05-2008
DOI: 10.1152/JAPPLPHYSIOL.01056.2007
Abstract: Hypoxia can depress ventilation, respiratory load sensation, and the cough reflex, and potentially other protective respiratory reflexes such as respiratory muscle responses to increased respiratory load. In sleep-disordered breathing, increased respiratory load and hypoxia frequently coexist. This study aimed to examine the effects of hypoxia on the reflex responses of 1) the genioglossus (the largest upper airway dilator muscle) and 2) the scalene muscle (an obligatory inspiratory muscle) to negative-pressure pulse stimuli during wakefulness and sleep. We hypothesized that hypoxia would impair these reflex responses. Fourteen healthy men, 19–42 yr old, were studied on two separate occasions, ∼1 wk apart. Bipolar fine-wire electrodes were inserted orally into the genioglossus muscle, and surface electrodes were placed overlying the left scalene muscle to record EMG activity. In random order, participants were exposed to mild overnight hypoxia (arterial oxygen saturation ∼85%) or medical air. Respiratory muscle reflex responses were elicited via negative-pressure pulse stimuli (approximately −10 cmH 2 O at the mask, 250-ms duration) delivered in early inspiration during wakefulness and sleep. Negative-pressure pulse stimuli resulted in a short-latency activation followed by a suppression of the genioglossus EMG that did not alter with hypoxia. Conversely, the predominant response of the scalene EMG to negative-pressure pulse stimuli was suppression followed by activation with more pronounced suppression during hypoxia compared with normoxia (mean ± SE suppression duration 64 ± 6 vs. 38 ± 6 ms, P = 0.006). These results indicate differential sensitivity to the depressive effects of hypoxia in the reflex responsiveness to sudden respiratory loads to breathing between these two respiratory muscles.
Publisher: Oxford University Press (OUP)
Date: 10-2010
Publisher: American Medical Association (AMA)
Date: 22-09-2020
Publisher: Oxford University Press (OUP)
Date: 12-2001
Abstract: There is uncertainty concerning the relative contribution of arousal, chemoreceptor stimulation, and their potentially interactive effects, to the acute cardiovascular changes observed during sleep in patients with sleep-disordered breathing. The purpose of this study was to compare cardiovascular responses (heart rate, skin blood flow, and pulse transit time, a non-invasive measure of arterial wall stiffness) to auditory induced arousal from stage 2 sleep under conditions of normoxia and overnight mild hypoxia. Randomised crossover. Sleep Disorders Unit in a 270-bed teaching hospital. Eleven healthy male subjects. Subjects slept wearing a facemask and breathed room air (one night SaO2 approximately 98%) or an hypoxic gas mixture (two nights SaO2 approximately 92%). Once in stage 2 sleep, subjects were administered one of 10 auditory tones (500 Hz, range 54-90 dB, 5-sec duration) via earphones or a sham tone (recording with no tone). Cardiovascular responses were examined beat-by-beat for 20 seconds before and 30 seconds after auditory tones associated with arousals (3-10 second EEG changes) and after sham tones. Sleep efficiency and the percentage of sleep spent in each stage were not different between hypoxia and normoxia nights. Baseline heart rate was elevated on hypoxia nights compared with normoxia nights (59.5+/-1.7 vs. 54.4+/-1.6 b x min(-1), p=0.007). Heart rate, pulse transit time, and skin blood flow showed significant changes after arousal consistent with rapid parasympathetic withdrawal and sympathetic nervous system activation. No changes were observed after sham tones. There were no differences in time course or magnitude of cardiovascular responses between hypoxia and normoxia nights. We conclude that while mild hypoxia stimulates autonomic activity it does not augment the cardiovascular response to arousal from stage 2 sleep in normal subjects.
Publisher: American Thoracic Society
Date: 15-10-2005
Publisher: American Physiological Society
Date: 09-2017
DOI: 10.1152/JAPPLPHYSIOL.01005.2016
Abstract: Intermittent hypoxia-induced ventilatory neuroplasticity is likely important in obstructive sleep apnea pathophysiology. Although concomitant CO 2 levels and arousal state critically influence neuroplastic effects of intermittent hypoxia, no studies have investigated intermittent hypercapnic hypoxia effects during sleep in humans. Thus the purpose of this study was to investigate if intermittent hypercapnic hypoxia during sleep induces neuroplasticity (ventilatory long-term facilitation and increased chemoreflex responsiveness) in humans. Twelve healthy males were exposed to intermittent hypercapnic hypoxia (24 × 30 s episodes of 3% CO 2 and 3.0 ± 0.2% O 2 ) and intermittent medical air during sleep after 2 wk washout period in a randomized crossover study design. Minute ventilation, end-tidal CO 2 , O 2 saturation, breath timing, upper airway resistance, and genioglossal and diaphragm electromyograms were examined during 10 min of stable stage 2 sleep preceding gas exposure, during gas and intervening room air periods, and throughout 1 h of room air recovery. There were no significant differences between conditions across time to indicate long-term facilitation of ventilation, genioglossal or diaphragm electromyogram activity, and no change in ventilatory response from the first to last gas exposure to suggest any change in chemoreflex responsiveness. These findings contrast with previous intermittent hypoxia studies without intermittent hypercapnia and suggest that the more relevant gas disturbance stimulus of concomitant intermittent hypercapnia frequently occurring in sleep apnea influences acute neuroplastic effects of intermittent hypoxia. These findings highlight the need for further studies of intermittent hypercapnic hypoxia during sleep to clarify the role of ventilatory neuroplasticity in the pathophysiology of sleep apnea. NEW & NOTEWORTHY Both arousal state and concomitant CO 2 levels are known modulators of the effects of intermittent hypoxia on ventilatory neuroplasticity. This is the first study to investigate the effects of combined intermittent hypercapnic hypoxia during sleep in humans. The lack of neuroplastic effects suggests a need for further studies more closely replicating obstructive sleep apnea to determine the pathophysiological relevance of intermittent hypoxia-induced ventilatory neuroplasticity.
Publisher: Elsevier BV
Date: 05-2023
Publisher: Wiley
Date: 07-06-2017
DOI: 10.1111/RESP.13064
Abstract: Obstructive sleep apnoea (OSA) and insomnia coexist in clinical populations but prevalence in the community and risk factors remain largely unknown. We examined the prevalence and profile of previously undiagnosed co-morbid OSA and insomnia symptoms (COMISA) in community-dwelling men. Men (n = 700, aged 58.5 ± 11.0 (mean ± SD) years) without a prior diagnosis of OSA completed full at-home unattended polysomnography, the Pittsburgh Sleep Quality Index and 36-item short form (SF-36) survey (2007-2012). Insomnia symptoms included difficulty initiating/maintaining sleep in the presence of daytime fatigue (DIMS-F). Depressive symptoms were assessed using the Beck Depression Inventory-1A, Centre for Epidemiological Studies Depression Scale and Patient Health Questionnaire-9 (PHQ-9) (2007-2010). Univariate (χ COMISA prevalence was 6.7%. Depression prevalence (COMISA, 42.6% DIMS-F, 21.6% OSA, 8.4%, χ 14.0 ± 4.9, P < 0.01 and OSA: 11.4 ± 3.0, P = 0.01) were highest in men with COMISA. In COMISA, respiratory and arousal indices were similar to those observed in OSA whilst reductions in subjective sleep and day dysfunction scores were similar to DIMS-F. After adjustment, predicted mean depression scores were all higher in DIMS-F and COMISA using linear regression (e.g. PHQ-9 β (95% CI): DIMS-F: 2.3 (1.2, 3.5) COMISA: 4.1 (3.0, 5.1)). Men with COMISA have a greater prevalence, and severity, of depression than men with only one disorder.
Publisher: Springer Science and Business Media LLC
Date: 09-2001
Publisher: Springer Science and Business Media LLC
Date: 10-1993
DOI: 10.1007/BF00357636
Publisher: European Respiratory Society (ERS)
Date: 04-2020
DOI: 10.1183/23120541.00161-2020
Abstract: Insomnia and obstructive sleep apnoea (OSA) frequently co-occur and may be causally related through sleep fragmentation and/or hyperarousal mechanisms. Previous studies suggest that OSA treatment can improve insomnia severity. However, the effect of insomnia treatment on OSA severity has not been investigated. We performed a randomised controlled trial to investigate the effect of cognitive behavioural therapy for insomnia (CBTi) on OSA severity, controlling for potential sleep-stage and posture effects. 145 patients with comorbid insomnia (International Classification of Sleep Disorders, 3rd Edn) and untreated OSA (apnoea–hypopnoea index (AHI) ≥15 events·h −1 sleep) were randomised to a four-session CBTi programme or to a no-treatment control. Overnight sleep studies were completed pre- and post-treatment to measure AHI, arousal index and sleep architecture, to investigate the effect of intervention group, time, sleep stage (N1–3 or REM) and posture (supine or nonsupine) on OSA severity. The CBTi group showed a 7.5 event·h −1 greater AHI difference (mean (95% CI) decrease 5.5 (1.3–9.7) events·h −1 , Cohen's d =0.2, from 36.4 events·h −1 pre-treatment) across sleep-stages and postures, compared to control (mean increase 2.0 (−2.0–6.1) events·h −1 , d =0.01, from 37.5 events·h −1 at pre-treatment interaction p=0.012). Compared to control, the CBTi group also had a greater reduction in total number (mean difference 5.6 (0.6–10.6) greater overall reduction p=0.029) and duration of nocturnal awakenings (mean difference 21.1 (2.0–40.3) min greater reduction p=0.031) but showed no difference in the arousal index, or sleep architecture. CBTi consolidates sleep periods and promotes a 15% decrease in OSA severity in patients with comorbid insomnia and OSA. This suggests that insomnia disorder may exacerbate OSA and provides further support for treating insomnia in the presence of comorbid OSA.
Publisher: Frontiers Media SA
Date: 04-05-2021
DOI: 10.3389/FPSYG.2021.676763
Abstract: Co-morbid insomnia and sleep apnea (COMISA) is a common and debilitating condition that is more difficult to treat compared to insomnia or sleep apnea-alone. Emerging evidence suggests that cognitive behavioral therapy for insomnia (CBTi) is effective in patients with COMISA, however, those with more severe sleep apnea and evidence of greater objective sleep disturbance may be less responsive to CBTi. Polysomnographic sleep study data has been used to predict treatment response to CBTi in patients with insomnia-alone, but not in patients with COMISA. We used randomized controlled trial data to investigate polysomnographic predictors of insomnia improvement following CBTi, versus control in participants with COMISA. One hundred and forty five participants with insomnia (ICSD-3) and sleep apnea [apnea-hypopnea index (AHI) ≥ 15] were randomized to CBTi ( n = 72) or no-treatment control ( n = 73). Mixed models were used to investigate the effect of pre-treatment AHI, sleep duration, and other traditional (AASM sleep macrostructure), and novel [quantitative electroencephalography (qEEG)] polysomnographic predictors of between-group changes in Insomnia Severity Index (ISI) scores from pre-treatment to post-treatment. Compared to control, CBTi was associated with greater ISI improvement among participants with higher AHI (interaction p = 0.011), less wake after sleep onset (interaction p = 0.045), and less N3 sleep (interaction p = 0.005). No quantitative electroencephalographic, or other traditional polysomnographic variables predicted between-group ISI change (all p & 0.09). Among participants with COMISA, higher OSA severity predicted a greater treatment-response to CBTi, versus control. People with COMISA should be treated with CBTi, which is effective even in the presence of severe OSA and objective sleep disturbance.
Start Date: 2018
End Date: 2020
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2017
End Date: 2019
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2016
End Date: 2020
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2014
End Date: 2018
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2008
End Date: 2011
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2017
End Date: 2019
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2015
End Date: 2018
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2012
End Date: 2015
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2013
End Date: 2016
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2012
End Date: 2018
Funder: Australian Research Council
View Funded ActivityStart Date: 2005
End Date: 2007
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2001
End Date: 2003
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2019
End Date: 2007
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2005
End Date: 2007
Funder: National Health and Medical Research Council
View Funded ActivityStart Date: 2012
End Date: 2016
Funder: Australian Research Council
View Funded ActivityStart Date: 10-2012
End Date: 10-2018
Amount: $821,831.00
Funder: Australian Research Council
View Funded Activity