The influence of alcohol on genioglossus single motor units in men and women during wakefulness.

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

Who benefits from adolescent sleep interventions? Moderators of treatment efficacy in a randomized controlled trial of a cognitive-behavioral and mindfulness-based group sleep intervention for at-risk adolescents.

BACKGROUND: The aim of this study was to test moderators of therapeutic improvement in an adolescent cognitive-behavioral and mindfulness-based group sleep intervention. Specifically, we examined whether the effects of the program on postintervention sleep outcomes were dependent on participant gender and/or measures of sleep duration, anxiety, depression, and self-efficacy prior to the interventions. METHOD: Secondary analysis of a randomized controlled trial conducted with 123 adolescent participants (female = 59.34%; mean age = 14.48 years, range 12.04-16.31 years) who had elevated levels of sleep problems and anxiety symptoms. Participants were randomized into either a group sleep improvement intervention (n = 63) or group active control 'study skills' intervention (n = 60). The sleep intervention ('Sleep SENSE') was cognitive behavioral in approach, incorporating sleep education, sleep hygiene, stimulus control, and cognitive restructuring, but also had added anxiety-reducing, mindfulness, and motivational interviewing elements. Components of the active control intervention ('Study SENSE') included personal organization, persuasive writing, critical reading, referencing, memorization, and note taking. Participants completed the Pittsburgh Sleep Quality Index (PSQI), Spence Children's Anxiety Scale (SCAS), Center for Epidemiologic Studies Depression Scale (CES-D), and General Self-Efficacy Scale (GSE) and wore an actigraph and completed a sleep diary for five school nights prior to the interventions. Sleep assessments were repeated at postintervention. The trial is registered with the Australian New Zealand Clinical Trials Registry (ACTRN12612001177842; http://www.anzctr.org.au/TrialSearch.aspx?searchTxt=ACTRN12612001177842&isBasic=True). RESULTS: The results showed that compared with the active control intervention, the effect of the sleep intervention on self-reported sleep quality (PSQI global score) at postintervention was statistically significant among adolescents with relatively moderate to high SCAS, CES-D, and GSE prior to the intervention, but not among adolescents with relatively low SCAS, CES-D, and GSE prior to the intervention. The results were consistent across genders. However, the effects of the sleep intervention on actigraphy-measured sleep onset latency and sleep diary-measured sleep efficiency at postintervention were not dependent on actigraphy-measured total sleep time, SCAS, CES-D, or GSE prior to the intervention. CONCLUSIONS: This study provides evidence that some sleep benefits of adolescent cognitive-behavioral sleep interventions are greatest among those with higher levels of anxiety and depressive symptoms, suggesting that this may be an especially propitious group to whom intervention efforts could be targeted. Furthermore, adolescents with lower levels of self-efficacy may need further targeted support (e.g. additional motivational interviewing) to help them reach treatment goals.

Sleep Duration and Sleep Quality: Associations With Depressive Symptoms Across Adolescence.

This study explored whether short sleep duration and sleep quality mediate the relationship between age and depressive symptoms. For comparison, we also explored whether depressive symptoms mediate the relationship between age and short sleep duration and sleep quality. The sample comprised 741 adolescents (63.5% female, mean age 15.78 years, range 11.92-19.67 years) in grades 7-12 from 11 secondary schools in metropolitan Melbourne, Australia. Students completed the Pittsburgh Sleep Quality Index (PSQI) and Center for Epidemiologic Studies Depression Scale (CES-D). Path analyses suggested that short sleep duration significantly mediated the relationship between age and depressive symptoms. Poor sleep quality also significantly mediated this relationship when sleep quality was defined by subjective judgement, but not sleep disturbance, sleep efficiency, or sleep onset latency. Depressive symptoms significantly mediated the relationship between age and short sleep duration and sleep quality (subjective judgement, sleep disturbance, sleep efficiency, and sleep onset latency). These findings suggest that the population-wide increase in depressive symptoms across adolescence is partially mediated by sleep-related developmental changes. They also highlight the importance of examining specific sleep problems when investigating the relationship between sleep and mood in this age group.

Highs and lows: Naturalistic changes in mood and everyday hassles over school and vacation periods in adolescents.

This study investigated changes in adolescents' mood and everyday hassles across school-terms and vacation periods. 146 (52.7% female) community-dwelling adolescents aged 16.2 ± 1.0 years (M±SD) completed self-report measures on depression, anxiety, and everyday hassles at four time points: during a school vacation, and the start, middle, and end of school-terms. Latent growth modeling showed that the end of a school-term was associated with significantly higher symptoms of depression, anxiety, and hassles; these measures were lower during the vacation. Hassles were strongly associated with more negative mood at all times. Our findings suggest significant fluctuations in adolescent mood and everyday hassles across school-vacation cycles. These findings call for careful consideration and reporting of timing in mood and stress assessment in adolescent research, as school-vacation cycles may have strong influence on both. Naturalistic changes in mood over school-vacation cycles reported are also clinically informative for designing and delivering adolescent wellbeing programs.

Early warning systems and rapid response to the deteriorating patient in hospital: A realist evaluation.

AIM: To test the Rapid Response Systems programme theory against actual practice components of the Rapid Response Systems implemented to identify those contexts and mechanisms which have an impact on the successful achievement of desired outcomes in practice. BACKGROUND: Rapid Response Systems allow deteriorating patients to be recognized using Early Warning Systems, referred early via escalation protocols and managed at the bedside by competent staff. DESIGN: Realist evaluation. METHODS: The research design was an embedded multiple case study approach of four wards in two hospitals in Northern Ireland which followed the principles of Realist Evaluation. We used various mixed methods including individual and focus group interviews, observation of nursing practice between June-November 2010 and document analysis of Early Warning Systems audit data between May-October 2010 and hospital acute care training records over 4.5 years from 2003-2008. Data were analysed using NiVivo8 and SPPS. RESULTS: A cross-case analysis highlighted similar patterns of factors which enabled or constrained successful recognition, referral and response to deteriorating patients in practice. Key enabling factors were the use of clinical judgement by experienced nurses and the empowerment of nurses as a result of organizational change associated with implementation of Early Warning System protocols. Key constraining factors were low staffing and inappropriate skill mix levels, rigid implementation of protocols and culturally embedded suboptimal communication processes. CONCLUSION: Successful implementation of Rapid Response Systems was dependent on adopting organizational and cultural changes that facilitated staff empowerment, flexible implementation of protocols and ongoing experiential learning.

Autobiographical memory impairment in obstructive sleep apnea patients with and without depressive symptoms.

Obstructive sleep apnea is associated with memory impairments, and higher rates of depressive symptoms and major depressive disorder compared with community estimates. Autobiographical memory overgenerality, a behaviour characterized by difficulty recalling specific memories from one's own life, is recognized as a marker of depression. Previous studies have demonstrated the predictive quality of specific autobiographical memory recall on the course of depression in patients with obstructive sleep apnea. However, it remains unclear whether impaired autobiographical memory is simply a feature of depression, or whether it is also impaired in patients with obstructive sleep apnea without depression. This study aimed to investigate whether autobiographical memory impairments can be observed in patients with obstructive sleep apnea, independent of the severity of depressive symptoms. Twenty-one patients with obstructive sleep apnea symptomatic for depressive symptoms (mean age = 43.43 years, SD = 9.97), 17 patients with obstructive sleep apnea asymptomatic for depressive symptoms (mean age = 40.65 years, SD = 9.39), and 20 healthy controls without sleep-disordered breathing (mean age = 32.80 years, SD = 6.69) completed an Autobiographical Memory Test. Patients with obstructive sleep apnea symptomatic for depressive symptoms recalled significantly fewer specific memories when compared with healthy controls (P = 0.010). No difference in the recall of specific autobiographical memory was observed between symptomatic and asymptomatic patients with obstructive sleep apnea. With regard to valence, symptomatic patients with obstructive sleep apnea recalled significantly fewer negative specific memories when compared with controls (P = 0.010). Impairment in specific autobiographical memory recall can be observed in patients with obstructive sleep apnea, regardless of the severity of depressive symptoms; however, this effect may not be as prominent in younger patients with obstructive sleep apnea.

Nocturnal indicators of increased cardiovascular risk in depressed adolescent girls.

Depression is an independent risk factor for cardiovascular disease in adults, and recent literature suggests preclinical signs of cardiovascular risk are also present in depressed adolescents. No study has examined the effect of clinical depression on cardiovascular factors during sleep. This study examined the relationship between clinical depression and nocturnal indicators of cardiovascular risk in depressed adolescent girls from the general community (13-18 years old; 11 clinically depressed, eight healthy control). Continuous beat-to-beat finger arterial blood pressure and heart rate were monitored via Portapres and electrocardiogram, respectively. Cardiovascular data were averaged over each hour for the first 6 h of sleep, as well as in 2-min epochs of stable sleep that were then averaged within sleep stages. Data were also averaged across 2-min epochs of pre-sleep wakefulness and the first 5 min of continuous non-rapid eye movement sleep to investigate the blood pressure dipping response over the sleep-onset period. Compared with controls, depressed adolescents displayed a similar but significantly elevated blood pressure profile across sleep. Depressed adolescents had significantly higher systolic and diastolic blood pressure and mean arterial pressures across the entire night (P < 0.01), as well as during all sleep stages (P < 0.001). Depressed adolescents also had higher blood pressure across the sleep-onset period, but the groups did not differ in the rate of decline across the period. Higher blood pressure during sleep in depressed adolescent females suggests that depression has a significant association with cardiovascular functioning during sleep in adolescent females, which may increase risk for future cardiovascular pathology.

Common drive to the upper airway muscle genioglossus during inspiratory loading.

Common drive is thought to constitute a central mechanism by which the efficiency of a motor neuron pool is increased. This study tested the hypothesis that common drive to the upper airway muscle genioglossus (GG) would increase with increased respiratory drive in response to an inspiratory load. Respiration, GG electromyographic (EMG) activity, single-motor unit activity, and coherence in the 0-5 Hz range between pairs of GG motor units were assessed for the 30 s before an inspiratory load, the first and second 30 s of the load, and the 30 s after the load. Twelve of twenty young, healthy male subjects provided usable data, yielding 77 pairs of motor units: 2 Inspiratory Phasic, 39 Inspiratory Tonic, 15 Expiratory Tonic, and 21 Tonic. Respiratory and GG inspiratory activity significantly increased during the loads and returned to preload levels during the postload periods (all showed significant quadratic functions over load trials, P < 0.05). As hypothesized, common drive increased during the load in inspiratory modulated motor units to a greater extent than in expiratory/tonic motor units (significant load × discharge pattern interaction, P < 0.05). Furthermore, this effect persisted during the postload period. In conclusion, common drive to inspiratory modulated motor units was elevated in response to increased respiratory drive. The postload elevation in common drive was suggestive of a poststimulus activation effect.

Crossed motor innervation of the base of human tongue.

Muscle fibers of the genioglossus (GG) form the bulk of the muscle mass at the base of the tongue. The motor control of the tongue is critical for vocalization, feeding, and breathing. Our goal was to assess the patterns of motor innervation of GG single motor units (SMUs) in humans. Simultaneous monopolar recordings were obtained from four sites in the base of the tongue bilaterally at two antero-posterior levels from 16 resting, awake, healthy adult males, who wore a face mask with airway pressure and airflow sensors. We analyzed 69 data segments in which at least one lead contained large action potentials generated by an SMU. Such potentials served as triggers for spike-triggered averaging (STA) of signals recorded from the other three sites. Spontaneous activity of the SMUs was classified as inspiratory modulated, expiratory modulated, or tonic. Consistent with the antero-posterior orientation of GG fibers, 44 STAs (77%) recorded ipsilateral to the trigger yielded sharp action potentials with a median amplitude of 52 µV [interquartile range (IQR): 25-190] that were time shifted relative to the trigger by about 1 ms. Notably, 48% of recordings on the side opposite to the trigger also yielded sharp action potentials. Of those, 17 (29%) had a median amplitude of 63 µV (IQR: 39-96), and most were generated by tonic SMUs. Thus a considerable proportion of GG muscle fibers receive a crossed motor innervation. Crossed innervation may help ensure symmetry and stability of tongue position and movements under normal conditions and following injury or degenerative changes affecting the tongue.

The acute effects of alcohol on sleep electroencephalogram power spectra in late adolescence.

BACKGROUND: Alcohol's effect on sleep electroencephalogram (EEG) power spectra during late adolescence is of interest given that this age group shows both dramatic increases in alcohol consumption and major sleep-related developmental changes in quantitative EEG measures. This study examined the effect of alcohol on sleep EEG power spectra in 18- to 21-year-old college students. METHODS: Participants were 24 (12 female) healthy 18- to 21-year-old social drinkers. Participants underwent 2 conditions: presleep alcohol and placebo, followed by standard polysomnography with comprehensive EEG recordings. RESULTS: After alcohol, mean breath alcohol concentration at lights-out was 0.084%. Interaction effects indicated simultaneous increases in frontal non-rapid eye movement sleep (NREM) delta (p = 0.031) and alpha (p = 0.005) power in the first sleep cycles following alcohol consumption which was most prominent at frontal scalp sites (p < 0.001). A decrease in sigma power (p = 0.001) was also observed after alcohol. CONCLUSIONS: As hypothesized, alcohol increased slow wave sleep-related NREM delta power. However, there was a simultaneous increase in frontal alpha power. Results suggest that alcohol may exert an arousal influence which may compete with the sleep maintenance influence of increased delta activity. The phenomenon is similar to, or the same as, alpha-delta sleep which has been associated with the presence of disruptive stimuli during sleep. This may have negative implications for the impact of presleep alcohol consumption on sleep and consequent daytime functioning.

Actigraphy-assessed sleep during school and vacation periods: a naturalistic study of restricted and extended sleep opportunities in adolescents.

School-related sleep restriction in adolescents has been identified by studies comparing weekday and weekend sleep. This study compared weekday and vacation sleep to assess restricted and extended sleep opportunities. One-hundred and forty-six adolescents (47.3% male) aged 16.2 ± 1.0 years (M ± SD) from the general community wore an actigraph continuously for 4 weeks: the last week of a school term (Time-E), the following 2-week vacation, and the first week of the next term. Self-reported sleep was assessed for each of the three time intervals, and chronotype was assessed using the Morningness-Eveningness Questionnaire at Time-E. Daily actigraphy bedtime, rise-time, time-in-bed, total sleep time, sleep onset latency, sleep efficiency, and % wake after sleep onset were analysed using latent growth curve modelling. The removal of school-related sleep restriction was associated with an abrupt delay in sleep timing and increase in sleep duration. Subsequently, bedtime and rise-time showed further linear delays throughout the vacation, while changes in time-in-bed were non-significant. Sleep onset latency increased linearly, peaking in the middle of the second vacation week. Across the first vacation week, total sleep time and sleep efficiency linearly decreased, while % wake after sleep onset increased. These changes stabilized during the second vacation week. Older age and eveningness were associated with later bedtime and rise-time, whilst females had longer time-in-bed, total sleep time and sleep onset latency. Compared with school days, sleep during the vacation was characterized by later timing, longer duration, lower quality and greater variability. Recovery from school-related sleep restriction appeared to be completed within the 2 weeks of naturalistic extended sleep.

Poor autonomic nervous system functioning during sleep in recently detoxified alcohol-dependent men and women.

BACKGROUND: Alcoholism is considered an important risk factor for cardiovascular (CV) disease. Autonomic nervous system (ANS) function is a major indicator of CV health. Sleep is a suitable model to investigate ANS activity free from wake-related confounders. We investigated nighttime ANS functioning, and the relation between ANS activity and severity of alcohol dependence in chronic alcoholism. METHODS: Fourteen recently abstaining alcoholics (age: 42.0 ± 9.0 years, 7 women) and 16 age- and sex-matched controls (age: 45.2 ± 9.1 years, 8 women) underwent a night of standard clinical polysomnography, including electrocardiographic recording. Time- and frequency-domain spectral analysis of heart rate variability (HRV) was performed across hours of the night and during artifact-free epochs of stable sleep and wakefulness (presleep wakefulness, rapid-eye-movement [REM], and non-REM sleep). RESULTS: Alcoholics had a poorer subjective and objective sleep quality compared to controls. Across the night, alcoholic men and women had elevated heart rate, reduced total HRV, that is, lower standard deviation of normal-to-normal interbeat intervals, and reduced high frequency (HF) activity (assessed by the HF power and by the square root of the mean squared of successive heart period differences). This ANS pattern was most apparent at the beginning of the night. None of the ANS measures was associated with lifetime alcohol consumption or duration of alcohol dependence. CONCLUSIONS: Our results show that ANS functioning is disrupted during the night, even in undisturbed sleep periods, indicating poor CV functioning in recently detoxified alcohol-dependent men and women.

Mood and objective and subjective measures of sleep during late pregnancy and the postpartum period.

This study examined the association between measures of objective sleep (OS) and subjective sleep (SS) to postpartum mood in healthy women from the third trimester of pregnancy to 10 to 12 weeks postpartum. Twenty-nine pregnant women completed self-report measures of mood and SS, and wore actigraphs for 7 continuous days during the third trimester (Time 1), within 15 days (Time 2), and 10 to 12 weeks postpartum (Time 3). The subjective perception of marked daytime dysfunction was associated with low mood during Time 1 and Time 3. Poor nighttime SS was related to low mood only at Time 2, whereas poor nighttime OS influenced stress during the same assessment time. These data indicate a stronger association between postpartum mood and the subjective perception of sleep than with OS quality and duration in healthy, non-depressed women, and highlight the awareness of poor daytime functioning as a significant contributor to new mothers' emotional wellbeing.

Mechanisms underlying the prolonged activation of the genioglossus following arousal from sleep.

STUDY OBJECTIVES: Transient arousal from sleep has been shown to elicit a prolonged increase in genioglossus muscle activity that persists following the return to sleep and which may protect against subsequent airway collapse. We hypothesized that this increased genioglossal activity following return to sleep after an arousal is due to persistent firing of inspiratory-modulated motor units (MUs) that are recruited during the arousal. METHODS: Thirty-four healthy participants were studied overnight while wearing a nasal mask with pneumotachograph to measure ventilation and with 4 intramuscular genioglossus EMG electrodes. During stable N2 and N3 sleep, auditory tones were played to induce brief (3-15s) AASM arousals. Ventilation and genioglossus MUs were quantified before the tone, during the arousal and for 10 breaths after the return to sleep. RESULTS: A total of 1089 auditory tones were played and gave rise to 239 MUs recorded across arousal and the return to sleep in 20 participants (aged 23 ±â€…4.2 years and BMI 22.5 ±â€…2.2 kg/m2). Ventilation was elevated above baseline during arousal and the first post-arousal breath (p < .001). Genioglossal activity was elevated for five breaths following the return to sleep, due to increased firing rate and recruitment of inspiratory modulated MUs, as well as a small increase in tonic MU firing frequency. CONCLUSIONS: The sustained increase in genioglossal activity that occurs on return to sleep after arousal is primarily a result of persistent activity of inspiratory-modulated MUs, with a slight contribution from tonic units. Harnessing genioglossal activation following arousal may potentially be useful for preventing obstructive respiratory events.

Acute phase protein and cytokine levels in serum and saliva: a comparison of detectable levels and correlations in a depressed and healthy adolescent sample.

Recent research has examined associations between inflammation and mental health, and has increasingly focused on utilising younger samples to characterise the temporal relationship between inflammatory responses and the emergence of other symptoms. These studies have typically used blood to measure inflammation, although rates of detection for many inflammatory markers appear to be low. Saliva is a safe and low-cost alternative, and adult research has shown that levels of some salivary markers correlate well with those in serum. However, no research has examined this association in young people. This study examined 16 inflammatory markers in serum and saliva in 17 depressed adolescents and 18 healthy controls, aged 13-18 years. In general, detection rates were higher in saliva compared to in serum. When non-detectable levels were excluded, serum levels of C-reactive protein (CRP) correlated with salivary CRP (r=0.424, p=0.015), and this correlation appeared to only exist for those individuals with high levels of serum CRP (r=0.599, p=0.014). However, when non-detectable levels were included as zero, salivary levels of CRP, interleukin (IL)-2, IL-12p70, and interferon (IFN)-γ correlated with their serum counterparts. No significant clinical group differences in any acute phase proteins or cytokines were present. This study suggests that saliva can be used to measure inflammation in studies with adolescent participants, especially CRP, as it appears to correlate with systemic inflammation for those individuals who are expected to have high levels of inflammation. Implications for future directions in research on salivary inflammatory markers are discussed.

The acute effects of alcohol on sleep architecture in late adolescence.

BACKGROUND: Alcohol consumption is prevalent in late adolescence; however, little is known about its effect on sleep in this group. In mature adults, alcohol decreases sleep onset latency (SOL) and sleep efficiency (SE) and increases wake after sleep onset (WASO). It also increases slow wave sleep (SWS) and decreases rapid eye movement (REM) sleep in the first half of the night, with the inverse occurring in the second half. Alcohol's effect on sleep during late adolescence is of interest given that this age group shows both dramatic increases in alcohol consumption and significant developmental changes in the central nervous system. This study examined the effect of alcohol on sleep architecture in women and men aged 18 to 21 years and whether previously reported sleep architecture effects may have been as an artificial result of changes to sleep cycle length. METHODS: Twenty-four (12 women) healthy 18- to 21-year-old light social drinkers (19.1 ± 1.0 years) underwent 2 conditions: presleep alcohol (target breath alcohol concentration [BAC] 0.10%) and placebo-administered under controlled conditions, followed by standard polysomnography. RESULTS: In the alcohol condition, mean BAC at lights out was 0.084 ± 0.016%. Time in bed, total sleep time, and SOL (all p > 0.05) did not differ between conditions. However, there was less REM (p = 0.011) and more stage-2 sleep (p = 0.035) in the alcohol condition. Further, alcohol increased SWS (p = 0.02) and decreased REM sleep (p < 0.001) in the first half of the night and disrupted sleep in the second half, with increased WASO (interaction: p = 0.034), and decreased SE (p = 0.04) and SWS (p = 0.01) and no REM sleep rebound in the second half of the night (p = 0.262). Additionally, alcohol had no effect on sleep cycle length (p = 0.598). CONCLUSIONS: The results were broadly consistent with the adult literature with the novel extension that half night sleep architecture effects could not be attributed to changes in sleep cycle length. However, alcohol did not reduce SOL, or result in a REM rebound following reduced REM in the first half of the night. The results suggest that the effects of alcohol on sleep are modified by sleep's prevailing developmental stage.

Neurogenic changes in the upper airway of patients with obstructive sleep apnea.

RATIONALE: Controversy persists regarding the presence and importance of hypoglossal nerve dysfunction in obstructive sleep apnea (OSA). OBJECTIVES: We assessed quantitative parameters related to motor unit potential (MUP) morphology derived from electromyographic (EMG) signals in patients with OSA versus control subjects and hypothesized that signs of neurogenic remodeling would be present in the patients with OSA. METHODS: Participants underwent diagnostic sleep studies to obtain apnea-hypopnea indices. Muscle activity was detected with 50-mm concentric needle electrodes. The concentric needle was positioned at more than 10 independent sites per subject, after the local anatomy of the upper airway musculature was examined by ultrasonography. All activity was quantified with subjects awake, during supine eupneic breathing while wearing a nasal mask connected to a pneumotachograph. Genioglossus EMG signals were analyzed offline by automated software (DQEMG), which extracted motor unit potential trains (MUPTs) contributed by individual motor units from the composite EMG signals. Quantitative measurements of MUP templates, including duration, peak-to-peak amplitude, area, area-to-amplitude ratio, and size index, were compared between the untreated patients with OSA and healthy control subjects. MEASUREMENTS AND MAIN RESULTS: A total of 1,655 MUPTs from patients with OSA (n = 17; AHI, 55 ± 6/h) and control subjects (n = 14; AHI, 4 ± 1/h) were extracted from the genioglossus muscle EMG signals. MUP peak-to-peak amplitudes in the patients with OSA were not different compared with the control subjects (397.5 ± 9.0 vs. 382.5 ± 10.0 µV). However, the MUPs of the patients with OSA were longer in duration (11.5 ± 0.1 vs. 10.3 ± 0.1 ms; P < 0.001) and had a larger size index (4.09 ± 0.02 vs. 3.92 ± 0.02; P < 0.001) compared with control subjects. CONCLUSIONS: These results confirm and quantify the extent and existence of structural neural remodeling in OSA.

Sleep and cardiovascular regulation.

Normal sleep has a profound effect on the cardiovascular system, reducing cardiovascular activity throughout non-rapid eye movement sleep; changes that are modified and augmented by circadian system influence. There is also evidence that sleep-initiated changes in autonomic balance may in turn modify the development of sleep within a night, particularly the development of slow wave sleep. It is assumed that the cardiovascular changes that accompany sleep reflect a functional aspect of sleep, although the precise functional role has not been agreed upon. Nevertheless, there is good evidence that the cardiovascular changes that occur during normal sleep are beneficial for the cardiovascular system. Arousals from sleep, which are common even in normal sleep, are associated with a surge in activity in cardiorespiratory systems, with marked effects on the sleep-related pattern of cardiovascular activity when they occur frequently. Despite the importance of this aspect of sleep, controversy remains as to both the nature of the activation response and the circumstances under which it is elicited. The concept that sleep-related changes in cardiovascular activity are beneficial leads to the corollary that sleep disturbance would result in adverse cardiovascular consequences. While there is strong empirical evidence for such a relationship, it remains unclear whether this is a direct effect or, as has been suggested recently, the effect of disturbed sleep is mediated via stress-related modification of neuroendocrine systems.