980 resultados para sleep time
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Nearly 22 million Americans operate as shift workers, and shift work has been linked to the development of cardiovascular disease (CVD). This study is aimed at identifying pivotal risk factors of CVD by assessing 24 hour ambulatory blood pressure, state anxiety levels and sleep patterns in 12 hour fixed shift workers. We hypothesized that night shift work would negatively affect blood pressure regulation, anxiety levels and sleep patterns. A total of 28 subjects (ages 22-60) were divided into two groups: 12 hour fixed night shift workers (n=15) and 12 hour fixed day shift workers (n=13). 24 hour ambulatory blood pressure measurements (Space Labs 90207) were taken twice: once during a regular work day and once on a non-work day. State anxiety levels were assessed on both test days using the Speilberger’s State Trait Anxiety Inventory. Total sleep time (TST) was determined using self recorded sleep diary. Night shift workers demonstrated increases in 24 hour systolic (122 ± 2 to 126 ± 2 mmHg, P=0.012); diastolic (75 ± 1 to 79 ± 2 mmHg, P=0.001); and mean arterial pressures (90 ± 2 to 94 ± 2mmHg, P<0.001) during work days compared to off days. In contrast, 24 hour blood pressures were similar during work and off days in day shift workers. Night shift workers reported less TST on work days versus off days (345 ± 16 vs. 552 ± 30 min; P<0.001), whereas day shift workers reported similar TST during work and off days (475 ± 16 minutes to 437 ± 20 minutes; P=0.231). State anxiety scores did not differ between the groups or testing days (time*group interaction P=0.248), suggesting increased 24 hour blood pressure during night shift work is related to decreased TST, not short term anxiety. Our findings suggest that fixed night shift work causes disruption of the normal sleep-wake cycle negatively affecting acute blood pressure regulation, which may increase the long-term risk for CVD.
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Objective Obstructive sleep apnea (OSA) and hypertension (HYP) frequently coexist and have additive harmful effects on the cardiovascular system. There is also growing evidence that short sleep duration may contribute independently to poor cardiovascular outcome. The aim of this study was to evaluate the potential influence of antihypertensive medication on sleep parameters objectively measured by standard polysomnography in hypertensive patients with OSA. Methods We evaluated consecutive patients with a recent diagnosis of OSA by full polysomnography (apnea hypopnea index >= 5 events/h) and HYP. Smokers, patients with diabetes mellitus, heart failure, or using hypnotics and benzodiazepines were excluded. Results We evaluated 186 hypertensive patients with OSA, 64% men. All patients were on at least one antihypertensive medication, including angiotensin-converting enzyme inhibitors (37%), beta-blockers (35%), angiotensin receptor blockers (32%), diuretics (29%) and calcium channel blockers (21%). Backward multiple regression analysis showed that age (P <= 0.001) and the use of calcium channel blockers (P=0.037) were the only factors inversely associated with lower total sleep time. Sleep efficiency was inversely associated only with age (P <= 0.001), whereas the use of calcium channel blockers had a nonsignificant trend (P=0.092). Use of calcium channel blockers was associated with significant reduction in total sleep time (-41 min, P=0.005) and 8% lower sleep efficiency (P=0.004). No other antihypertensive medication, including diuretics and beta-blockers, was associated with sleep impairment. Conclusion Calcium channel blockers may impact negatively on sleep duration in hypertensive patients with OSA. The mechanisms and significance of this novel finding warrants further investigation. J Hypertens 29: 1236-1241 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
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Objectives: Previous studies using subjective assessments have reported associations between sleep quantity and quality and cardiometabolic disorders, but little is known regarding the associ-ations with objective sleep characteristics. The purpose of this study was to evaluate the association between objective sleep measure sand metabolic syndrome (MS), hypertension, diabetes and obesity. Methods: 2162 subjects (51.2% women, mean age 58,11.1) from the general population were evaluated for hypertension,diabetes, overweight/obesity and MS, and underwent a full polysom-nography (PSG). PSG measured variables included: Total sleep time(TST), percentage and time spent in slow wave sleep (SWS) and in rapid eye movement (REM) sleep, sleep efficiency and arousal index(ArI) Results: In univariate analyses, MS was associated with decreased TST, SWS, REM sleep, sleep efficiency and increased ArI. After adjustment for age, gender, smoking, alcohol, physical activity, drugsthat affect sleep and depression, the ArI remained significantly higher, but the difference disappeared in subjects without significant sleep disordered breathing (SDB). Differences in sleep structure were also found according to the presence or absence of hypertension, diabetes and overweight/obesity in univariate analysis. However, these differences were attenuated after multivariate adjustment and after excluding subjects with significant SDB. Conclusions: In this population-based sample we found significant associations between sleep structure and MS, hypertension, diabetes and obesity. However, these associations were cancelled after multivariate adjustment. We conclude that normal variations in sleep contribute little if any to MS and associated disorders.
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Light influences sleep and alertness either indirectly through a well-characterized circadian pathway or directly through yet poorly understood mechanisms. Melanopsin (Opn4) is a retinal photopigment crucial for conveying nonvisual light information to the brain. Through extensive characterization of sleep and the electrocorticogram (ECoG) in melanopsin-deficient (Opn4(-/-)) mice under various light-dark (LD) schedules, we assessed the role of melanopsin in mediating the effects of light on sleep and ECoG activity. In control mice, a light pulse given during the habitual dark period readily induced sleep, whereas a dark pulse given during the habitual light period induced waking with pronounced theta (7-10 Hz) and gamma (40-70 Hz) activity, the ECoG correlates of alertness. In contrast, light failed to induce sleep in Opn4(-/-) mice, and the dark-pulse-induced increase in theta and gamma activity was delayed. A 24-h recording under a LD 1-hratio1-h schedule revealed that the failure to respond to light in Opn4(-/-) mice was restricted to the subjective dark period. Light induced c-Fos immunoreactivity in the suprachiasmatic nuclei (SCN) and in sleep-active ventrolateral preoptic (VLPO) neurons was importantly reduced in Opn4(-/-) mice, implicating both sleep-regulatory structures in the melanopsin-mediated effects of light. In addition to these acute light effects, Opn4(-/-) mice slept 1 h less during the 12-h light period of a LD 12ratio12 schedule owing to a lengthening of waking bouts. Despite this reduction in sleep time, ECoG delta power, a marker of sleep need, was decreased in Opn4(-/-) mice for most of the (subjective) dark period. Delta power reached after a 6-h sleep deprivation was similarly reduced in Opn4(-/-) mice. In mice, melanopsin's contribution to the direct effects of light on sleep is limited to the dark or active period, suggesting that at this circadian phase, melanopsin compensates for circadian variations in the photo sensitivity of other light-encoding pathways such as rod and cones. Our study, furthermore, demonstrates that lack of melanopsin alters sleep homeostasis. These findings call for a reevaluation of the role of light on mammalian physiology and behavior.
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Aging produces major changes in sleep structure and intensity which might be linked to cognitive impairment in the elderly. In this study, the genetic contribution to age-related changes in sleep was assessed in three inbred mouse strains of various ages. Baseline sleep and the response to 6 hours sleep deprivation (SD) achieved by gentle handling were quantified in young, middle-aged, and older male mice using electroencephalography. Total sleep time initially increased with age but then decreased in the oldest group mainly due to changes in sleep duration during the active phase. The effect of age on electroencephalographic (EEG) delta power depends on genotype and sleep pressure level with SD increasing the age-related differences. The strong effect of age upon the spectral profile of the different behavioral states was modulated by genetic background. Overall, our results suggest that sleep pressure can modulate the effect of age, that most sleep variables do not monotonically change with age in contrast to previous reports in humans and other species, and that genetic factors have a major impact on the aging processes affecting sleep.
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OBJECTIVETo compare the total sleep time of premature infant in the presence or absence of reducing sensory and environmental stimuli in the neonatal unit.METHODLongitudinal study in a Neonatal Intermediate Care Unit of a public hospital in Sao Paulo. The sample consisted of 13 premature infants. We used polysomnograph and unstructured observation for data collection. We analyzed 240 and 1200 minutes corresponding to the periods of the presence and absence of environmental management, respectively. Data were compared in proportion to the total sleep time in the two moments proposed by the study.RESULTSThe total sleep time in periods without environmental management was on average 696.4 (± 112.1) minutes and with management 168.5 (± 27.9) minutes, proportionally premature infant slept an average of 70.2% during periods with no intervention and 58.0% without management (p=0.002).CONCLUSIONReducing stimulation and handling of premature infant environment periods was effective to provide greater total sleep time.
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STUDY OBJECTIVES: To evaluate the association between objective sleep measures and metabolic syndrome (MS), hypertension, diabetes, and obesity. DESIGN: Cross-sectional study. SETTING: General population sample. PARTICIPANTS: There were 2,162 patients (51.2% women, mean age 58.4 ± 11.1). INTERVENTIONS: Patients were evaluated for hypertension, diabetes, overweight/obesity, and MS, and underwent a full polysomnography (PSG). MEASUREMENTS AND RESULTS: PSG measured variables included: total sleep time (TST), percentage and time spent in slow wave sleep (SWS) and in rapid eye movement (REM) sleep, sleep efficiency and arousal index (ArI). In univariate analyses, MS was associated with decreased TST, SWS, REM sleep, and sleep efficiency, and increased ArI. After adjustment for age, sex, smoking, alcohol, physical activity, drugs that affect sleep and depression, the ArI remained significantly higher, but the difference disappeared in patients without significant sleep disordered breathing (SDB). Differences in sleep structure were also found according to the presence or absence of hypertension, diabetes, and overweight/obesity in univariate analysis. However, these differences were attenuated after multivariate adjustment and after excluding subjects with significant SDB. CONCLUSIONS: In this population-based sample we found significant associations between sleep structure and MS, hypertension, diabetes, and obesity. However, these associations were cancelled after multivariate adjustment. We conclude that normal variations in sleep contribute little if any to MS and associated disorders.
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STUDY OBJECTIVES: Sodium oxybate (SO) is a GABA(B) agonist used to treat the sleep disorder narcolepsy. SO was shown to increase slow wave sleep (SWS) and EEG delta power (0.75-4.5 Hz), both indexes of NREM sleep (NREMS) intensity and depth, suggesting that SO enhances recuperative function of NREM. We investigated whether SO induces physiological deep sleep. DESIGN: SO was administered before an afternoon nap or before the subsequent experimental night in 13 healthy volunteers. The effects of SO were compared to baclofen (BAC), another GABA(B) receptor agonist, to assess the role of GABA(B) receptors in the SO response. MEASUREMENTS AND RESULTS: As expected, a nap significantly decreased sleep need and intensity the subsequent night. Both drugs reversed this nap effect on the subsequent night by decreasing sleep latency and increasing total sleep time, SWS during the first NREMS episode, and EEG delta and theta (0.75-7.25 Hz) power during NREMS. The SO-induced increase in EEG delta and theta power was, however, not specific to NREMS and was also observed during REM sleep (REMS) and wakefulness. Moreover, the high levels of delta power during a nap following SO administration did not affect delta power the following night. SO and BAC taken before the nap did not improve subsequent psychomotor performance and subjective alertness, or memory consolidation. Finally, SO and BAC strongly promoted the appearance of sleep onset REM periods. CONCLUSIONS: The SO-induced EEG slow waves seem not to be functionally similar to physiological slow waves. Our findings also suggest a role for GABA(B) receptors in REMS generation. CITATION: Vienne J; Lecciso G; Constantinescu I; Schwartz S; Franken P; Heinzer R; Tafti M. Differential effects of sodium oxybate and baclofen on EEG, sleep, neurobehavioral performance, and memory. SLEEP 2012;35(8):1071-1084.
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STUDY OBJECTIVES: Traditionally, sleep studies in mammals are performed using electroencephalogram/electromyogram (EEG/EMG) recordings to determine sleep-wake state. In laboratory animals, this requires surgery and recovery time and causes discomfort to the animal. In this study, we evaluated the performance of an alternative, noninvasive approach utilizing piezoelectric films to determine sleep and wakefulness in mice by simultaneous EEG/EMG recordings. The piezoelectric films detect the animal's movements with high sensitivity and the regularity of the piezo output signal, related to the regular breathing movements characteristic of sleep, serves to automatically determine sleep. Although the system is commercially available (Signal Solutions LLC, Lexington, KY), this is the first statistical validation of various aspects of sleep. DESIGN: EEG/EMG and piezo signals were recorded simultaneously during 48 h. SETTING: Mouse sleep laboratory. PARTICIPANTS: Nine male and nine female CFW outbred mice. INTERVENTIONS: EEG/EMG surgery. MEASUREMENTS AND RESULTS: The results showed a high correspondence between EEG/EMG-determined and piezo-determined total sleep time and the distribution of sleep over a 48-h baseline recording with 18 mice. Moreover, the piezo system was capable of assessing sleep quality (i.e., sleep consolidation) and interesting observations at transitions to and from rapid eye movement sleep were made that could be exploited in the future to also distinguish the two sleep states. CONCLUSIONS: The piezo system proved to be a reliable alternative to electroencephalogram/electromyogram recording in the mouse and will be useful for first-pass, large-scale sleep screens for genetic or pharmacological studies. CITATION: Mang GM, Nicod J, Emmenegger Y, Donohue KD, O'Hara BF, Franken P. Evaluation of a piezoelectric system as an alternative to electroencephalogram/electromyogram recordings in mouse sleep studies.
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INTRODUCTION: The aim of this study was to evaluate if there is a significant effect of lunar phases on subjective and objective sleep variables in the general population. METHODS: A total of 2125 individuals (51.2% women, age 58.8 ± 11.2 years) participating in a population-based cohort study underwent a complete polysomnography (PSG) at home. Subjective sleep quality was evaluated by a self-rating scale. Sleep electroencephalography (EEG) spectral analysis was performed in 759 participants without significant sleep disorders. Salivary cortisol levels were assessed at awakening, 30 min after awakening, at 11 am, and at 8 pm. Lunar phases were grouped into full moon (FM), waxing/waning moon (WM), and new moon (NM). RESULTS: Overall, there was no significant difference between lunar phases with regard to subjective sleep quality. We found only a nonsignificant (p = 0.08) trend toward a better sleep quality during the NM phase. Objective sleep duration was not different between phases (FM: 398 ± 3 min, WM: 402 ± 3 min, NM: 403 ± 3 min; p = 0.31). No difference was found with regard to other PSG-derived parameters, EEG spectral analysis, or in diurnal cortisol levels. When considering only subjects with apnea/hypopnea index of <15/h and periodic leg movements index of <15/h, we found a trend toward shorter total sleep time during FM (FM: 402 ± 4, WM: 407 ± 4, NM: 415 ± 4 min; p = 0.06) and shorter-stage N2 duration (FM: 178 ± 3, WM: 182 ± 3, NM: 188 ± 3 min; p = 0.05). CONCLUSION: Our large population-based study provides no evidence of a significant effect of lunar phases on human sleep.
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To evaluate the effect of smoking habits on sleep, data from 1492 adults referred to the Sleep Institute were accessed and divided into 3 categories of smoking status: current, former and non-smokers. Categories of pack-years (<15 and ≥15) defined smoking severity. The association of smoking status and smoking severity with sleep was analyzed for sleep parameters, especially apnea and hypopnea index (AHI) ≥5, more than 5% of total sleep time (TST) spent with oxyhemoglobin saturation (SaO2) <90%, and arousal index. The arousal index was higher among current (21 ± 17) and former smokers (20 ± 17) than non-smokers (17 ± 15; P < 0.04). Former smokers had a higher percent of TST at SaO2 <90% than non-smokers (9 ± 18 vs 6 ± 13; P < 0.04). Former smokers with pack-years ≥15 compared to <15 exhibited higher AHI (22 ± 24 vs 16 ± 21; P < 0.05) and arousal index (22 ± 19 vs 18 ± 15; P < 0.05). Current smokers with pack-years ≥15 compared to <15 exhibited higher arousal index (23 ± 18 vs 18 ± 16; P < 0.05) and percent of TST at SaO2 <90% (11 ± 17 vs 6 ± 13; P < 0.05). Smoking status and pack-years were not associated with AHI ≥5 on logistic regression analysis, but current smokers with pack-years ≥15 were 1.9 times more likely to spend more than 5% of TST at SaO2 <90% than non-smokers (95%CI = 1.21-2.97; P = 0.005). The variability of arousal index was influenced by gender, AHI and current smokers with pack-years ≥15 (all P < 0.01). Smoking habits seem to be associated with arousal and oxyhemoglobin desaturation during sleep, but not with AHI. The effect was more pronounced in current than former smokers.
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Inter-individual differences in the phase of the endogenous circadian rhythms have been established. Individuals with early circadian phase are called morning types; those with late circadian phase are evening types. The Horne and Östberg Morningness-Eveningness Questionnaire (MEQ) is the most frequently used to assess individual chronotype. The distribution of MEQ scores is likely to be biased by several fact, ors, such as gender, age, genetic background, latitude, and social habits. The objective of the present study was to determine the effect of different social synchronizers on the sleep/wake cycle of persons with different chronotypes. Volunteers were selected from a total of 1232 UFPR undergraduate students who completed the MEQ. Thirty-two subjects completed the study, including 8 morning types, 8 evening types and 16 intermediate types. Sleep schedules were recorded by actigraphy for 1 week on two occasions: during the school term and during vacation. Sleep onset and offset times, sleep duration, and mid-sleep time for each chronotype group were compared by the Mann-Whitney U-test separately for school term and vacation. School term and vacation data were compared by the Wilcoxon matched-pair test. Morning types showed earlier sleep times and longer sleep duration compared with evening types (23:00 ± 44 and 508.9 ± 50.27 vs 01:08 ± 61.95 and 456.44 ± 59.08, for the weekdays during vacation). During vacation, the subjects showed later sleep times, except for the morning types, who did not exhibit differences for sleep onset times. The results support the idea that social schedules have an impact on the expression of circadian rhythmicity but this impact depends on the individual chronotype.
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Sleep is important for the recovery of a critically ill patient, as lack of sleep is known to influence negatively a person’s cardiovascular system, mood, orientation, and metabolic and immune function and thus, it may prolong patients’ intensive care unit (ICU) and hospital stay. Intubated and mechanically ventilated patients suffer from fragmented and light sleep. However, it is not known well how non-intubated patients sleep. The evaluation of the patients’ sleep may be compromised by their fatigue and still position with no indication if they are asleep or not. The purpose of this study was to evaluate ICU patients’ sleep evaluation methods, the quality of non-intubated patients’ sleep, and the sleep evaluations performed by ICU nurses. The aims were to develop recommendations of patients’ sleep evaluation for ICU nurses and to provide a description of the quality of non-intubated patients’ sleep. The literature review of ICU patients’ sleep evaluation methods was extended to the end of 2014. The evaluation of the quality of patients’ sleep was conducted with four data: A) the nurses’ narrative documentations of the quality of patients’ sleep (n=114), B) the nurses’ sleep evaluations (n=21) with a structured observation instrument C) the patients’ self-evaluations (n=114) with the Richards-Campbell Sleep Questionnaire, and D) polysomnographic evaluations of the quality of patients’ sleep (n=21). The correspondence of data A with data C (collected 4–8/2011), and data B with data D (collected 5–8/2009) were analysed. Content analysis was used for the nurses’ documentations and statistical analyses for all the other data. The quality of non-intubated patients’ sleep varied between individuals. In many patients, sleep was light, awakenings were frequent, and the amount of sleep was insufficient as compared to sleep in healthy people. However, some patients were able to sleep well. The patients evaluated the quality of their sleep on average neither high nor low. Sleep depth was evaluated to be the worst and the speed of falling asleep the best aspect of sleep, on a scale 0 (poor sleep) to 100 (good sleep). Nursing care was mostly performed while the patients were awake, and thus the disturbing effect was low. The instruments available for nurses to evaluate the quality of patients’ sleep were limited and measured mainly the quantity of sleep. Nurses’ structured observatory evaluations of the quality of patients’ sleep were correct for approximately two thirds of the cases, and only regarding total sleep time. Nurses’ narrative documentations of the patients’ sleep corresponded with patients’ self-evaluations in just over half of the cases. However, nurses documented several dimensions of sleep that are not included in the present sleep evaluation instruments. They could be classified according to the components of the nursing process: needs assessment, sleep assessment, intervention, and effect of intervention. Valid, more comprehensive sleep evaluation methods for nurses are needed to evaluate, document, improve and study patients’ quality of sleep.
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Sleep bruxism (SB) is characterized by repetitive and coordinated mandible movements and non-functional teeth contacts during sleep time. Although the etiology of SB is controversial, the literature converges on its multifactorial origin. Occlusal factors, smoking, alcoholism, drug usage, stress, and anxiety have been described as SB trigger factors. Recent studies on this topic discussed the role of neurotransmitters on the development of SB.Thus, the purpose of this study was to detect and quantify the urinary levels of catecholamines, specifically of adrenaline, noradrenaline and dopamine, in subjects with SB and in control individuals.Urine from individuals with SB (n = 20) and without SB (n = 20) was subjected to liquid chromatography. The catecholamine data were compared by Mann-Whitney's test (p a parts per thousand currency sign 0.05).Our analysis showed higher levels of catecholamines in subjects with SB (adrenaline = 111.4 A mu g/24 h; noradrenaline = 261,5 A mu g/24 h; dopamine = 479.5 A mu g/24 h) than in control subjects (adrenaline = 35,0 A mu g/24 h; noradrenaline = 148,7 A mu g/24 h; dopamine = 201,7 A mu g/24 h). Statistical differences were found for the three catecholamines tested.It was concluded that individuals with SB have higher levels of urinary catecholamines.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)