Leptin and hunger levels in young healthy adults after one night of sleep loss

Short‐term sleep curtailment associated with activation of the stress system in healthy, young adults has been shown to be associated with decreased leptin levels, impaired insulin sensitivity, and increased hunger and appetite. To assess the effects of one night of sleep loss in a less stressful environment on hunger, leptin, adiponectin, cortisol and blood pressure/heart rate, and whether a 2‐h mid‐afternoon nap reverses the changes associated with sleep loss, 21 young healthy individuals (10 men, 11 women) participated in a 7‐day sleep deprivation experiment (four consecutive nights followed by one night of sleep loss and two recovery nights). Half of the subjects were randomly assigned to take a mid‐afternoon nap (14:00–16:00 hours) the day following the night of total sleep loss. Serial 24‐h blood sampling and hunger scales were completed on the fourth (predeprivation) and sixth day (postdeprivation). Leptin levels were significantly increased after one night of total sleep loss, whereas adiponectin, cortisol levels, blood pressure/heart rate, and hunger were not affected. Daytime napping did not influence the effects of sleep loss on leptin, adiponectin, or hunger. Acute sleep loss, in a less stressful environment, influences leptin levels in an opposite manner from that of short‐term sleep curtailment associated with activation of the stress system. It appears that sleep loss associated with activation of the stress system but not sleep loss per se may lead to increased hunger and appetite and hormonal changes, which ultimately may lead to increased consumption of ‘comfort’ food and obesity.     

Automatic CPAP based on impedance-comparison of constant CPAP with an individual pressure range

Summary Introduction   Self-adjusting positive airways pressure treatment based on the impedance of the airways (APAP_FOT) has proven effective in obstructive sleep apnoea syndrome. To avoid patient discomfort during periods of high treatment pressure we lowered the upper pressure limit with APAP_FOT and investigated whether this provided equally as effective treatment as constant CPAP. Methods   37 patients (33 males, 57.9 ± 9.9 years, BMI 32.5 ± 3.8 kg/m²) underwent after diagnostic polysomnography and manual nCPAP titration two treatment nights in randomized order, one with constant nCPAP (mode 1), one with APAP_FOT (mode 2). Under APAP_FOT treatment pressure varied between 4 hPa (set lower limit for all patients) and 13.3 ± 1.4 hPa (individually variable upper pressure limit). Results   AHI was reduced from 32.8 ± 18.1/h to 4.6 ± 4.9/h (mode 1, p < 0.01) and to 5.0 ± 4.1/h (mode 2, p < 0.01). Rapid eye movement sleep (REM) and respiratory arousals improved significantly with both modes. With APAP_FOT, the mean pressure was 5.7 ± 1.7 hPa as compared to 8.3 ± 1.4 hPa with constant nCPAP (p < 0.01). Conclusions   APAP_FOT with a reduced upper pressure is as effective as constant nCPAP for OSAS. With APAP_FOT the mean pressure is substantially reduced.     

Sweet taste perception not altered after acute sleep deprivation in healthy young men

Background

We hypothesized that acutely sleep-deprived participants would rate ascending concentrations of sucrose as more intense and pleasant, than they would do after one night of normal sleep. Such a finding would offer a potential mechanism through which acute sleep loss could promote overeating in humans.

Method

A total of 16 healthy normal-weight men participated in 2 conditions: sleep (permitted between 22:30 and 06:30 h) and total sleep deprivation (TSD) respectively. On the morning after regular sleep and TSD, circulating concentrations of ghrelin and glucose were measured. In addition, participants hunger level was assessed by means of visual analogue scales, both before and after a caloric preload. Finally, following the preload, participants rated both intensity and pleasantness of six orally presented yogurt probes with varying sucrose concentrations (2–29?%).

Results

Feelings of hunger were significantly more intense under both fasted and sated conditions when subjects were sleep-deprived. In contrast, the change in hunger induced by the preload was similar between the sleep and TSD conditions. Plasma concentrations of ghrelin were significantly higher under conditions of TSD, whereas plasma glucose did not differ between the conditions. No effects were found either on sweet taste intensity or on pleasantness after TSD.

Conclusion

One night of TSD increases morning plasma concentrations of the hunger-promoting hormone ghrelin in healthy young men. In contrast, sweet taste perception was not affected by nocturnal wakefulness. This suggests that an altered sweet taste perception is an unlikely mechanism by which TSD enhances food intake.     

Time course of continuous positive airway pressure effects on central sleep apnoea in patients with chronic heart failure

Continuous positive airway pressure (CPAP) causes a variable immediate reduction in the frequency of central apnoeas and hypopnoeas in patients with congestive heart failure (CHF) and central sleep apnoea (CSA), but has beneficial mid-term effects on factors known to destabilize the ventilatory control system. We, therefore, tested whether CPAP therapy leads, in addition to its short-term effects on CSA, to a significant further alleviation of CSA after 12 weeks of treatment on the same CPAP level in such patients. CPAP therapy was initiated in 10 CHF patients with CSA. During the first night on CPAP, the pressure was stepwise increased to a target pressure of 8–12 cmH₂O or the highest level the patients tolerated (<12 cmH₂O). Throughout the second night (baseline CPAP), the achieved CPAP of the first night was applied. After 12 weeks of CPAP treatment, we performed a follow-up polysomnography (12 weeks CPAP) on the same CPAP level (8.6 ± 1.1 cmH₂0). We found a significant reduction of the apnoea-hypopnoea index (AHI) between the diagnostic polysomnography and baseline CPAP night (41.8 ± 19.2 versus 22.2 ± 12.6 events per hour; P  = 0.005). The AHI further significantly decreased between the baseline CPAP night and the 12 weeks CPAP night on the same CPAP level (22.2 ± 12.6 versus 12.8 ± 11.0 events per hour; P  = 0.028). We conclude that, in addition to its immediate effects, CPAP therapy leads to a time-dependent alleviation of CSA in some CHF patients, indicating that in such patients neither clinical nor scientific decisions should be based on a short-term trial of CPAP.     

Low leptin concentration may identify heart failure patients with central sleep apnea

Low leptin concentration has been shown to be associated with central sleep apnea in heart failure patients. We hypothesized that low leptin concentration predicts central sleep apnea. Consecutive ambulatory New York Heart Association (NYHA ) classes I–IV heart failure patients were studied prospectively, including measurement of serum leptin, echocardiography and polysomnography. Sleep apnea was defined by type (central/mixed/obstructive) and by apnea–hypopnea index ≥5 by polysomnography. Subjects were divided into four groups by polysomnography: (1) central sleep apnea, (2) mixed apnea, (3) no apnea and (4) obstructive sleep apnea. Fifty‐six subjects were included. Eighteen subjects were diagnosed with central sleep apnea, 15 with mixed apnea, 12 with obstructive apnea and 11 with no sleep apnea. Leptin concentration was significantly lower in central sleep apnea compared to obstructive apnea (8 ± 10.7 ng mL^?1 versus 19.7 ± 14.7 ng mL^?1, P  ? 0.01) or no sleep apnea (8 ± 10.7 ng mL^?1 versus 17.1 ± 8.4 ng mL^?1, P  ? 0.01). Logistic regression showed leptin to be associated independently with central sleep apnea [odds ratio (OR ): 0.19; 95% confidence interval (CI ): 0.06–0.62; area under the curve (AUC ): 0.80, P  < 0.01]. For the detection of central sleep apnea, a cut‐off value for leptin concentration 5 ng mL^?1 yielded a sensitivity of 50% and specificity of 89%. In conclusion, a low leptin concentration may have utility for the screening of heart failure patients for central sleep apnea.     

Intermittent Hypoxia Increases Insulin Resistance in Genetically Obese Mice

Obstructive sleep apnoea, a syndrome that leads to recurrent intermittent hypoxia, is associated with insulin resistance in obese individuals, but the mechanisms underlying this association remain unknown. We utilized a mouse model to examine the effects of intermittent hypoxia on insulin resistance in lean C57BL/6J mice and leptin-deficient obese (C57BL/6J− Lep ^ob) mice. In lean mice, exposure to intermittent hypoxia for 5 days (short term) resulted in a decrease in fasting blood glucose levels (from 173 ± 11 mg dl⁻¹ on day 0 to 138 ± 10 mg dl⁻¹ on day 5, P < 0.01), improvement in glucose tolerance without a change in serum insulin levels and an increase in serum leptin levels in comparison with control (2.6 ± 0.3 vs. 1.7 ± 0.2 ng ml⁻¹, P < 0.05). Microarray mRNA analysis of adipose tissue revealed that leptin was the only upregulated gene affecting glucose uptake. In obese mice, short-term intermittent hypoxia led to a decrease in blood glucose levels accompanied by a 607 ± 136 % (   P < 0.01  ) increase in serum insulin levels. This increase in insulin secretion after 5 days of intermittent hypoxia was completely abolished by prior leptin infusion. Obese mice exposed to intermittent hypoxia for 12 weeks (long term) developed a time-dependent increase in fasting serum insulin levels (from 3.6 ± 1.1 ng ml⁻¹ at baseline to 9.8 ± 1.8 ng ml⁻¹ at week 12, P < 0.001) and worsening glucose tolerance, consistent with an increase in insulin resistance. We conclude that the increase in insulin resistance in response to intermittent hypoxia is dependent on the disruption of leptin pathways.     

Retrograde effects of triazolam and zolpidem on sleep-dependent motor learning in humans

Drugs that act as allosteric activators at the benzodiazepine site of the gamma-aminobutyric acid (GABA_A) receptor complex are used commonly to treat insomnia but relatively little is known of how such use affects learning and memory. Although anterograde effects on memory acquisition have been shown, possible retrograde effects on consolidation are more relevant when such agents are administered at bedtime. We tested the effects of two GABA_A allosteric activators on sleep-dependent motor skill memory consolidation in 12 healthy male subjects. Subjects slept in a sleep laboratory for four consecutive nights (one accommodation night followed by three experimental nights). Placebo, triazolam 0.375 mg, and zolpidem 10 mg were given to each subject in counterbalanced order on the experimental nights. Polysomnographic (PSG) sleep measurement and sleep-dependent motor learning were assessed at each condition. Triazolam was associated with longer total sleep time and increased Stage 2 sleep. Both zolpidem and triazolam were associated with increased latency to rapid eye movement (REM) sleep. Overnight motor learning correlated with total sleep time in the placebo condition but not in the triazolam or zolpidem conditions. A statistically significant impairment in motor performance occurred overnight in the triazolam condition only. Triazolam, given in sufficient doses to prolong sleep in healthy people, affected overnight motor learning adversely. Zolpidem, in a dose sufficient to prolong REM onset latency but without other effects on PSG-measured sleep, degraded the relationship between total sleep time and overnight motor learning. These data indicate that non-selective or α1-preferring benzodiazepine site allosteric activators can interfere with sleep-dependent memory consolidation.     

Sleep restriction increases blood neutrophils, total cholesterol and low density lipoprotein cholesterol in postmenopausal women: A preliminary study

OBJECTIVES: This study examines the effects of sleep restricted to 4h for three consecutive nights on blood parameters known to be associated with cardiovascular risk in healthy postmenopausal women. MATERIAL AND METHODS: Ten healthy postmenopausal women aged 55-65 years treated with hormonal replacement therapy (HT) were included in the study. After one baseline night, three nights of sleep restricted to 4h were performed and were followed by one recovery night of 8h. Blood samplings were performed after the baseline night and after the third night of sleep restriction. RESULTS: A significant increase in white blood cells (WBC), monocytes, neutrophils, total cholesterol, and low density lipoprotein cholesterol (LDL-c) was observed after the third night of sleep restriction. CONCLUSION: Sleep restriction to 4h of sleep for three consecutive nights affected two factors associated with cardiovascular risk in healthy postmenopausal women treated with HT.     

Impact of acute sleep restriction on cortisol and leptin levels in young women

Sleep restriction alters hormone patterns and appetite in men, but less is known about effects on women. We assessed effects of overnight sleep restriction on cortisol and leptin levels and on appetite in young women. Participants' baseline sleep duration and eating habits were monitored for a week before the study. Salivary cortisol and leptin were sampled from fifteen healthy women (aged 18-25) during two consecutive days: first after a 10 h overnight sleep opportunity (Baseline day) and then after a night including only 3 h sleep (Post sleep-restriction day). Participants also completed appetite questionnaires on both days. Sleep restriction significantly reduced morning cortisol levels (p = 0.02), elevated morning leptin levels (p = 0.04), elevated afternoon/evening cortisol area under the curve values (p = 0.008), and slowed the decline in cortisol concentration during the day (p = 0.04). Hunger and craving scores did not differ significantly between days. A single night of restricted sleep affected cortisol rhythms and morning leptin levels in young women.     

Partial sleep restriction modulates secretory activity of thyrotropic axis in healthy men

Sleep and endocrine function are known to be closely related, but studies on the effect of moderate sleep loss on endocrine axes are still sparse. We examined the influence of partial sleep restriction for 2 days on the secretory activity of the thyrotropic axis. Fifteen healthy, normal‐weight men were tested in a balanced, cross‐over study. Serum concentrations of thyrotrophin (TSH), free triiodothyronine (fT3) and free thyroxine (fT4) were monitored at 1‐h intervals during a 15‐h daytime period (08:00–23:00 h) following two nights of restricted sleep (bedtime 02:45–07:00 h) and two nights of regular sleep (bedtime 22:45–07:00 h), respectively. Serum concentrations of fT3 (P < 0.026) and fT4 (P = 0.089) were higher after sleep restriction than regular sleep, with a subsequent blunting of TSH concentrations in the evening hours of the sleep restriction condition (P = 0.008). These results indicate profound alterations in the secretory activity of the thyrotropic axis after 2 days of sleep restriction to ~4 h, suggesting that acute partial sleep loss impacts endocrine homeostasis, with potential consequences for health and wellbeing.     

Memory encoding is impaired after multiple nights of partial sleep restriction

Sleep is important for normative cognitive functioning. A single night of total sleep deprivation can reduce the capacity to encode new memories. However, it is unclear how sleep restriction during several consecutive nights affects memory encoding. To explore this, we employed a parallel‐group design with 59 adolescents randomized into sleep‐restricted (SR) and control groups. Both groups were afforded 9 h time in bed (TIB) for 2 baseline nights, followed by 5 consecutive nights of 5 h TIB for the SR group (n = 29) and 9 h TIB for the control group (n = 30). Participants then performed a picture‐encoding task. Encoding ability was measured with a recognition test after 3 nights of 9 h TIB recovery sleep for both groups, allowing the assessment of encoding ability without the confounding effects of fatigue at retrieval. Memory was significantly worse in the sleep‐restricted group (P = 0.001), and this impairment was not correlated with decline in vigilance. We conclude that memory‐encoding deteriorates after several nights of partial sleep restriction, and this typical pattern of sleep negatively affects adolescents’ ability to learn declarative information.     

Effects of two nights sleep deprivation and two nights recovery sleep on response inhibition

This study examined the effects of two nights of total sleep deprivation (TSD) and two nights of recovery sleep on response inhibition. Thirty-eight young, healthy adults performed a Go-NoGo task at 14 : 00 after: (1) a normal night of sleep; (2) each of two consecutive nights of TSD; and (3) each of two consecutive nights of recovery sleep; they also performed the task at 05 : 00 during the first night of sleep deprivation. We hypothesized that TSD would lead to an impaired ability to withhold a response that would be reversed with recovery sleep. Subjects did experience a significant increase in false positive responses throughout all of TSD, errors of omission (i.e. missed 'go' targets) were not significant until after the second night of TSD. Both components (withholding a response and automatic responding) of the task returned to baseline levels after one night of recovery sleep. These data suggest that individuals experience difficulty in withholding an inappropriate response during TSD, even when they are able to attend to the incoming stimuli and respond accurately to appropriate stimuli.     

Sleep-related sweating in obstructive sleep apnoea: association with sleep stages and blood pressure

The aim of this study was to investigate sleep-related sweating as a symptom of obstructive sleep apnoea (OSA). Fifteen otherwise healthy male non-smoking patients with untreated moderate-to-severe OSA underwent polysomnography, including measurements of skin and core body temperature and electrodermal activity (EDA) as an objective indicator of sweating. Evening and morning blood pressure was measured as well as catecholamines in nocturnal urine. All measurements were repeated after 3 months on successful continuous positive airway pressure (CPAP) treatment. The untreated OSA subjects had a mean (±SD) apnoea–hypopnoea index of 45.3 ± 3.9 and a mean EDA index during sleep of 131.9 ± 22.4 events per hour. Patients with higher EDA indices had higher systolic blood pressure in the evening and morning ( P  = 0.001 and 0.006) and lower rapid eye movement (REM) sleep percentage ( P  = 0.003). The EDA index decreased significantly to 78.5 ± 17.7 in the patients on CPAP treatment ( P  = 0.04). The decrease correlated with lower evening systolic and diastolic blood pressure ( P  = 0.05 and 0.006) and an increase in REM% ( P  = 0.02). No relationship was observed between EDA and skin or core body temperature, or to catecholamine levels in urine. OSA patients who experience sleep-related sweating may have increased blood pressure and decreased REM sleep compared with other OSA patients. CPAP treatment appears to lower blood pressure and increase REM sleep to a higher extent in these patients compared with other OSA patients.     

Overnight emotional adaptation to negative stimuli is altered by REM sleep deprivation and is correlated with intervening dream emotions

Rapid eye movement (REM) sleep and dreaming may be implicated in cross-night adaptation to emotionally negative events. To evaluate the impact of REM sleep deprivation (REMD) and the presence of dream emotions on a possible emotional adaptation (EA) function, 35 healthy subjects randomly assigned to REMD ( n  = 17; mean age 26.4 ± 4.3 years) and control ( n  = 18; mean age 23.7 ± 4.4 years) groups underwent a partial REMD and control nights in the laboratory, respectively. In the evening preceding and morning following REMD, subjects rated neutral and negative pictures on scales of valence and arousal and EA scores were calculated. Subjects also rated dream emotions using the same scales and a 10-item emotions list. REMD was relatively successful in decreasing REM% on the experimental night, although a mean split procedure was applied to better differentiate subjects high and low in REM%. High and low groups differed – but in a direction contrary to expectations. Subjects high in REMD% showed greater adaptation to negative pictures on arousal ratings than did those low in REMD% ( P  < 0.05), even after statistically controlling sleep efficiency and awakening times. Subjects above the median on EA_valence had less intense overall dream negativity ( P  < 0.005) and dream sadness ( P  < 0.004) than subjects below the median. A correlation between the emotional intensities of the morning dream and the morning picture ratings supports a possible emotional carry-over effect. REM sleep may enhance morning reactivity to negative emotional stimuli. Further, REM sleep and dreaming may be implicated in different dimensions of cross-night adaptation to negative emotions.     

Total sleep deprivation decreases saliva ghrelin levels in adolescents

Ghrelin, a regulator of food intake and energy expenditure, has been shown to be associated with insufficient sleep. The goal of the present study was to investigate the effect of a single night of total sleep deprivation on fasting saliva ghrelin and on nocturnal variation of saliva ghrelin concentration. A further aim of the study was to investigate the influence of body mass index on changes in saliva ghrelin levels. Altogether 35 adolescents (18 boys; age: 13.8 ± 1.14 years) were studied on two subsequent days (sleep and total sleep deprivation). Saliva samples were collected during the two experimental nights at 21:00 hours, 01:00 hours and 06:00 hours. Total-ghrelin concentration showed a continuous increase from the evening until 06:00 hours. This increase was blunted significantly (p = 0.003) by total sleep deprivation. Total-ghrelin level was significantly lower (p = 0.02) during total sleep deprivation at 06:00 hours (median 403.6 pg ml⁻¹; 95% confidence interval: 343.1–468.9 pg ml⁻¹) as compared with values during the sleep condition (median 471.2 pg ml⁻¹; 95% confidence interval: 205.4–1578.7 pg ml⁻¹). Acyl-ghrelin levels did not present any change at the three time points, and were not affected by total sleep deprivation. Stratifying the study population according to body mass index (normal weight and overweight/obese groups), the blunting effect of total sleep deprivation was more pronounced in the obese/overweight group (sleep: median 428.2 pg ml⁻¹; 95% confidence interval: 331.3–606.9 pg ml⁻¹ versus total sleep deprivation: median 333.1 pg ml⁻¹; 95% confidence interval: 261.5–412.9 pg ml⁻¹; p = 0.0479). Saliva total-ghrelin concentrations gradually increased during the night, and total sleep deprivation significantly blunted this increase. This blunting effect was mainly observed in subjects with overweight/obesity. The physiological and clinical implications of the present observation are to be clarified by further studies.     

The sensitivity of a PDA-based psychomotor vigilance task to sleep restriction in 10-year-old girls

The impact of sleep restriction on sustained attention in children has not been well quantified. To address this shortcoming, this study tested the sensitivity of a 5-min personal digital assistant-psychomotor vigilance task (PDA-PVT) to sleep restriction in 14 female children [mean (SD) age = 10.6 ± 0.3 years]. The children underwent PDA-PVT trials at regular intervals both before and after a sleep restriction (5 h time-in-bed) and a control (10 h time-in-bed) condition. Sleep restriction was associated with longer mean response times and increased number of lapses. These results are consistent with findings in the adult literature suggesting an association between inadequate sleep and impaired functioning. In conclusion, the 5-min PDA-PVT is sensitive to sleep restriction in pre-adolescent female children supporting the utility of the PDA-PVT for examining the impact of sleep deprivation on daytime functioning in children.     

Effects of sleep restriction on adiponectin levels in healthy men and women

Objective

Population studies have consistently found that shorter sleep durations are associated with obesity and cardiovascular disease, particularly among women. Adiponectin is an adipocyte-derived, anti-inflammatory hormone that is related to cardiovascular disease risk. We hypothesized that sleep restriction would reduce adiponectin levels in healthy young adults.

Methods

74 healthy adults (57% men, 63% African American, mean age 29.9 years) completed 2 nights of baseline sleep at 10 h time in bed (TIB) per night followed by 5 nights of sleep restricted to 4 h TIB per night. An additional 8 participants were randomized to a control group that received 10 h TIB per night throughout the study. Plasma adiponectin levels were measured following the second night of baseline sleep and the fifth night of sleep restriction or control sleep.

Results

Sleep restriction resulted in a decrease in plasma adiponectin levels among Caucasian women (Z = −2.19, p = 0.028), but an increase among African American women (Z = −2.73, p = 0.006). No significant effects of sleep restriction on adiponectin levels were found among men. A 2 × 2 between-group analysis of covariance on adiponectin change scores controlling for BMI confirmed significant interactions between sleep restriction and race/ethnicity [F(1,66) = 13.73, p < 0.001], as well as among sleep restriction, race/ethnicity and sex [F(1,66) = 4.27, p = 0.043)].

Conclusions

Inflammatory responses to sleep loss appear to be moderated by sex and race/ethnicity; observed decreases in adiponectin following sleep restriction may be one avenue by which reduced sleep duration promotes cardiovascular risk in Caucasian women.     

The impact of nasal obstruction on obstructive sleep apnea syndrome

Summary Objective   Nasal obstruction is a predictive factor for snoring and may contribute to the development of obstructive sleep apnea syndrome (OSAS) by causing a higher negative intrapharyngeal pressure during inspiration. This may lead to obstructive apneas and hypopneas in predisposed people. The aim of this study was to further enrole the impact of nasal obstruction on OSAS. Patients and Methods   We investigated two groups of OSAS patients, matched pairs concerning gender, age, and BMI: OSAS patients with nasal obstruction (N, n = 28): total nasal airflow < 500 ml/s* (*referred to 150 pa pressure of difference; anterior rhinomanometry) or unilateral nasal resistance > 1 pa/ml/s*; and 28 OSAS patients without nasal obstruction (control-group C ; total nasal airflow > 700 ml/l/s*). All patients had routine examination including a standardized questionnaire, examination by an otorhinolaryngologist, anterior rhinomanometry, skin prick-testing with 18 common allergens, lung function testing, and full polysomnography. Results   We found the following significant differences: 1) In N more patients (n = 17) complained about nocturnal dyspnea than in C (n = 7; p < 0,05, (Chi²-test); 2) N had a higher apnea index (20,4 ± 19,0/h) than C (9,6 ± 10,0/h; p < 0,05, student's t -test). There were, however, no significant differences concerning lung function, skin prick test, otorhinolaryngologistical results, sleep architecture, number of hypopneas, nocturnal S_aO₂, heart rate, and level of CPAP pressure. Conclusion   Hence, beside pathophysiologically interesting effects increased nasal resistance has no clinically relevant importance in patients with OSAS.     

Periodic leg movements in patients with obstructive sleep apnea syndrome during nCPAP therapy

Summary Excessive daytime sleepiness and concentration deficits are complained by patients with obstructive sleep apnea syndrome (OSAS) as well as by patients with periodic leg movements (PLM). PLM observed during nCPAP (nasal continuous airways pressure) therapy may therefore cause persistent complaints of diurnal symptoms despite sufficient treatment. 65 OSAS-patients (58 men, 7 women, aged 55.6 ± 8.0 years) were investigated before starting and after the first two nights of nCPAP therapy. Apnea/Hypopnea index decreased in all patients (28.8 ± 18.4/h to 11.5 ± 13.0/h, p ≤ 0.01). 26 patients had an initial PLM index > 5/­h which decreased during treatment (14.6 ± 6.4/h to 10.7 ± 7.8/h) with significant increase of sleep stages 3 and 4. In 22 patients with PLM index < 5/h index increased during therapy (2.7 ± 1.2 to 5.6 ± 7.7/h, p ≤ 0.01). 17 patients developed PLM for the first time during nCPAP-therapy (10.9 ± 3.2 PLM/h). Optimizing of nCPAP therapy did not change PLM frequency. Though the pathogenesis and daytime consequences of PLM in OSAS are not fully proved yet our study may entail different therapeutic approaches. In patients with a decrease of PLM during CPAP-therapy movements seemed at least partially induced by OSAS and CPAP may be the sufficient treatment. In the majority of our cases PLM was demasked during nCPAP therapy thus indicating an independent coexistence of periodic limb movement disorder and OSAS. These patients may profit from a treatment similar to the one in restless legs syndrome when daytime symptoms persist during CPAP therapy.     

Effect of sleep disruption on sleep, performance, and mood

Eleven young adult subjects were briefly awakened after each minute of electroencephalographic-defined sleep for 2 consecutive nights after undisturbed laboratory adaptation and baseline nights. Two undisturbed recovery nights followed disruption nights. On disruption nights, subjects were awakened with an audiometer and signaled the awakening by subjective rating of sleep state or button push response. The disruption procedure resulted in severely fragmented sleep with only very small amounts of slow-wave and REM sleep. Total sleep time was reduced by approximately 1 h on each night. Arousal threshold increased 56 dB across the disruption nights. Following disruption, subjects performed more poorly and rated themselves sleepier than on baseline. The level of decline was similar to that seen after periods of total sleep loss of 40-64 h. Recovery sleep was also similar to that seen after total sleep loss. It was concluded that periodic disruption of sleep, perhaps by destroying sleep continuity, quickly results in impaired function. These data may help explain function loss in severe sleep apneics.