Effect of treating severe nasal obstruction on the severity of obstructive sleep apnoea.

An association between mouth breathing during sleep and increased propensity for upper airway collapse is well documented, but the effect of treatment for nasal obstruction on mouth breathing during sleep and simultaneous obstructive sleep apnoea (OSA) severity has not been described previously. A randomised single blind placebo- and sham-controlled crossover study of treatment (topical decongestant and external dilator strip) for nasal obstruction was carried out in 10 patients (nine males; mean+/-SEM 46+/-5 yrs) with nasal obstruction and OSA. All patients had normal acoustic pharyngometry. The effect of treatment on nasal resistance, mouth breathing during sleep and OSA severity was quantified. Treatment of nasal obstruction was associated with a dramatic and sustained reduction in nasal resistance and the oral fraction of ventilation during sleep (mean (95% confidence interval) absolute reduction in oral fraction 30% (12-49)). Improvements in sleep architecture were observed during active treatment, and there was a modest reduction in OSA severity (change in apnoea-hypopnoea index 12 (3-22)). In conclusion, treating nasal obstruction reduced mouth breathing during sleep and obstructive sleep apnoea severity, but did not effectively alleviate obstructive sleep apnoea.

Effect of nasal or oral breathing route on upper airway resistance during sleep.

Healthy subjects with normal nasal resistance breathe almost exclusively through the nose during sleep. This study tested the hypothesis that a mechanical advantage might explain this preponderance of nasal over oral breathing during sleep. A randomised, single-blind, crossover design was used to compare upper airway resistance during sleep in the nasal and oral breathing conditions in 12 (seven male) healthy subjects with normal nasal resistance, aged 30+/-4 (mean+/-SEM) yrs, and with a body mass index of 23+/-1 kg x m2. During wakefulness, upper airway resistance was similar between the oral and nasal breathing routes. However, during sleep (supine, stage two) upper airway resistance was much higher while breathing orally (median 12.4 cmH2O x L(-1) x s(-1), range 4.5-40.2) than nasally (5.2 cmH2O x L(-1) x s(-1), 1.7-10.8). In addition, obstructive (but not central) apnoeas and hypopnoeas were profoundly more frequent when breathing orally (apnoea-hypopnoea index 43+/-6) than nasally (1.5+/-0.5). Upper airway resistance during sleep and the propensity to obstructive sleep apnoea are significantly lower while breathing nasally rather than orally. This mechanical advantage may explain the preponderance of nasal breathing during sleep in normal subjects.

Oral contraceptives alter sleep and raise body temperature in young women.

Female reproductive steroids, oestrogen and progesterone, not only affect reproductive function, but also thermoregulation and sleep. Chronic administration of synthetic steroids, as occurs in women taking oral contraceptives, may affect these regulatory systems differently from endogenous oestrogen and progesterone. We therefore investigated body temperature and sleep in ten young women taking oral contraceptives, in the active and placebo phases of the contraceptive pack, and compared them to a group of nine women with ovulatory cycles, in the mid-follicular and mid-luteal phases. Body temperature was raised throughout 24 h in the women taking oral contraceptives in the active phase, and in the naturally cycling women in the luteal phase, compared to the follicular phase. The women taking oral contraceptives in the placebo phase, however, continued to have raised body temperatures, similar to those in the active phase, indicating a prolonged action of synthetic reproductive steroids on body temperature. Sleep also was influenced by the endogenous and synthetic reproductive steroids, but independently of body temperature. The women taking oral contraceptives had more stage-2 non-rapid eye movement sleep in the active phase, both compared to their placebo phase and the naturally cycling women. The naturally cycling women, however, had more slow wave sleep in the luteal phase compared to the contraceptive group of women. Exogenous reproductive steroids therefore influence body temperature and sleep differently from endogenous progesterone and oestrogen.

Sleep and 24 hour body temperatures: a comparison in young men, naturally cycling women and women taking hormonal contraceptives.

Body temperature has a circadian rhythm, and in women with ovulatory cycles, also a menstrual rhythm. Body temperature and sleep are believed to be closely coupled, but the influence on their relationship of gender, menstrual cycle phase and female reproductive hormones is unresolved. We investigated sleep and 24 h rectal temperatures in eight women with normal menstrual cycles in their mid-follicular and mid-luteal phases, and in eight young women taking a steady dose of oral progestin and ethinyl oestradiol (hormonal contraceptive), and compared their sleep and body temperatures with that of eight young men, sleeping in identical conditions. All subjects maintained their habitual daytime schedules. Rectal temperatures were elevated throughout 24 h in the luteal phase compared with the follicular phase in the naturally cycling women, consistent with a raised thermoregulatory set-point. Rectal temperatures in the women taking hormonal contraceptives were similar to those of the naturally cycling women in the luteal phase. Gender influenced body temperature: the naturally cycling women and the women taking hormonal contraceptives attained their nocturnal minimum body temperatures earlier than the men, and the naturally cycling women had blunted nocturnal body temperature drops compared with the men. Sleep architecture was essentially unaffected by either menstrual cycle phase or gender. The women taking hormonal contraceptives had less slow wave sleep (SWS), however, than the naturally cycling women. Gender, menstrual cycle phase and hormonal contraceptives significantly influenced body temperature, but had only minor consequences for sleep, in the young men and women in our study.

Sleep and daytime sleepiness in retinitis pigmentosa patients.

OBJECTIVE: We examined sleep, daytime sleepiness and the ability to stay awake during the day in patients affected with retinitis pigmentosa (RP), to further delineate the role of photoreceptors in the circadian cycle. METHODS: Twelve individuals diagnosed with RP (40 +/- 8 years) And 12 normally sighted healthy individuals (39 +/- 7 years) matched for age, body mass index (BMI) and sex were selected for the study. Participants had their sleep recorded on two consecutive nights and were monitored on the two following days. On the first day, their ability to stay awake and on the second, their sleep propensity were assessed using the Maintenance of Wakefulness Test (MWT) and the Multiple Sleep Latency Test (MSLT), respectively. Self-report measures were obtained using the Pittsburgh Sleep Quality Index (PSQI), the Epworth Sleepiness Scale (ESS), and the Toronto Hospital Alertness Test (THAT). RESULTS: Subjective daytime sleepiness (ESS: 9 +/- 5 vs. 6 +/- 4, P=0.053) and objectively measured sleep propensity (MSLT: 10 +/- 5 vs. 17 +/- 3 min, P < 0.000) were significantly higher in RP patients than controls, whilst their alertness (THAT: 29 +/- 9 vs. 38 +/- 7, P=0.016) and ability to stay awake (MWT: 21 +/- 9 vs. 29 +/- 2 min, P=0.006) were significantly reduced. Retinitis pigmentosa participants had more disturbed nighttime sleep, with significantly more awakenings (arousal index: 14 +/- 8 vs. 8 +/- 6 h, P=0.039), and tended to have less rapid eye movement (REM) sleep (19 +/- 5 vs. 22 +/- 3%, P=0.094). CONCLUSION: Patients with RP have increased daytime sleepiness, reduced alertness and more disturbed nighttime sleep of poorer quality than their normally sighted counterparts, suggesting an influence of photoreceptor degeneration on the circadian cycle.

Preliminary randomized double-blind placebo-controlled trial of tryptophan combined with fluoxetine to treat major depressive disorder: antidepressant and hypnotic effects.

OBJECTIVE: Because the initial phase of treatment of depression with a selective serotonin reuptake inhibitor is often complicated by a delayed onset of action of the antidepressant or severe insomnia or both, we investigated whether tryptophan, an amino acid with both antidepressant-augmenting and hypnotic effects, would benefit patients with depression at the beginning of treatment with fluoxetine. DESIGN: Randomized, double-blind, placebo-controlled trial. PATIENTS: Thirty individuals with major depressive disorder. INTERVENTIONS: Treatment over 8 weeks with 20 mg of fluoxetine per day and either tryptophan (2 to 4 g per day) or placebo. OUTCOME MEASURES: Mood was assessed using the 29-item Hamilton Depression Rating Scale (HDRS-29) and the Beck Depression Inventory (BDI). Laboratory sleep studies were done at baseline and after 4 and 8 weeks of treatment using standard procedures. RESULTS: During the first week of treatment, there was a significantly greater decrease in HDRS-29 depression scores, and a similar trend in BDI scores, in the tryptophan/fluoxetine group than in the placebo/fluoxetine group. No significant differences were noted at later time points. With respect to sleep measures, there was a significant group-by-time interaction for slow-wave sleep at week 4. Further analysis revealed a significant decrease in slow-wave sleep after 4 weeks of treatment in the placebo/fluoxetine group, but not in the tryptophan/fluoxetine group. No cases of serotonin syndrome occurred, and the combination was well tolerated, although the 4 g per day dosage of tryptophan produced daytime drowsiness. CONCLUSIONS: Combining 20 mg of fluoxetine with 2 g of tryptophan daily at the outset of treatment for major depressive disorder appears to be a safe protocol that may have both a rapid antidepressant effect and a protective effect on slow-wave sleep. Further large-scale studies are needed to confirm these initial findings.

Beneficial physiological and performance responses to a month of restricted energy intake in healthy overweight women.

Changes in mood, performance, cortisol, and physiological variables with a month-long energy restricting diet (3.347 MJ/day) were studied in nine overweight (mean mass 71.2 +/- 8 kg; body mass index 26.1 +/- 2.8 kg/m(2)), healthy premenopausal (age 20-36 years) women. Measurements were taken in the 2 weeks before the diet (baseline) and again in the final 2 weeks of the diet to attenuate menstrual cycle differences. A reduction in energy intake and concomitant weight loss (5.80 +/- 1.65 kg) were accompanied by a significant decline in systolic blood pressure (5.4%), heart rate (7.6%), and cortisol concentration (13.6%). Fatigue and vigour on the Profile of Mood States (POMS) questionnaire were adversely affected; however, subjective assessments of mood, concentration, temperature sensitivity, appetite, and sleep quality using visual analogue scales, were not significantly altered during the month-long period of energy restriction. Motor performance, as assessed by hand-eye coordination, improved with both a reduction in mean reaction time and improved accuracy in response to visual stimuli. The very low-energy diet appeared to be neither physiologically nor psychologically stressful. Beneficial effects were evident with a reduction in BMI, reduced risk of cardiovascular stress, improved motor performance, and a decline in physiological stress with dieting success.

High nocturnal body temperatures and disturbed sleep in women with primary dysmenorrhea.

Primary dysmenorrhea is characterized by painful uterine cramps, near and during menstruation, that have an impact on personal life and productivity. The effect on sleep of this recurring pain has not been established. We compared sleep, nocturnal body temperatures, and hormone profiles during the menstrual cycle of 10 young women who suffered from primary dysmenorrhea, without any menstrual-associated mood disturbances, and 8 women who had normal menstrual cycles. Dysmenorrheic pain significantly decreased subjective sleep quality, sleep efficiency, and rapid eye movement (REM) sleep but not slow wave sleep (SWS), compared with pain-free phases of the menstrual cycle and compared with the controls. Even before menstruation, in the absence of pain, the women with dysmenorrhea had different sleep patterns, nocturnal body temperatures, and hormone levels compared with the controls. In the mid-follicular, mid-luteal, and menstrual phases, the dysmenorrheics had elevated morning estrogen concentrations, higher mean in-bed temperatures, and less REM sleep compared with the controls, as well as higher luteal phase prolactin levels. Both groups of women had less REM sleep when their body temperatures were high during the luteal and menstrual phases, implying that REM sleep is sensitive to elevated body temperatures. We have shown that dysmenorrhea is not only a disorder of menstruation but is manifest throughout the menstrual cycle. Furthermore, dysmenorrheic pain disturbs sleep, which may exacerbate the effect of the pain on daytime functioning.

Energy content of the evening meal alters nocturnal body temperature but not sleep.

Meals of varying energy content and episodes of sleep influence body temperature. We compared the effect of an evening meal, varying from high-energy (11.91 +/- 0.86 MJ) to average (5.74 +/- 0.88 MJ) and a 10-h fast (no evening meal), on nocturnal body temperature and sleep. Seven healthy men (20-24 years, mean body mass index of 23.4 +/- 2.6 kg/m2) reported to the laboratory for an evening meal at 2000 h having consumed similar amounts of food before 1300 h. After completing the meal, subjective hunger ratings were assessed, and a venous blood sample taken. The subjects spent 4 nonconsecutive nights (an adaptation night, followed by either of the two meal conditions or the fast in random order) in the sleep laboratory when polysomnographic recordings were made from 2300 to 0700 h. Meal energy content and serum concentrations of insulin, triglyceride, and low-density lipoproteins (LDL) varied significantly. Lower rectal temperatures were measured during the fast than following the meals. Over the 8-h recording period, thermal response indices (TRI) varied with higher body temperatures following the higher energy meal. Similar rectal temperatures were attained by the end of the sleep periods. There were no significant differences in any of the subjective or objective sleep measures. The physiological responses associated with the transient dietary changes of an evening meal or a 10-h fast altered nocturnal body temperature but did not significantly affect sleep of good sleepers when sleep was initiated 2 to 3 h after finishing the meal.

A comparison of subjective estimates of sleep with objective polysomnographic data in healthy men and women.

Twenty healthy men and women had their sleep recorded objectively, using polysomnography on 3 nonconsecutive nights. Following each night, the subjects assessed their sleep onset latency and number of awakenings, subjectively. Self-ratings were compared with objective measures of sleep onset latency (SOL), calculated as the time from lights-out to the first continuous minute of stage 2 sleep, and the number of awakenings which lasted 1 minute or longer on the polysomnograms. Apart from the first night, the subjects overestimated the time that it took them to fall asleep, despite sleep onset being scored as the latency to stage 2, rather than stage 1 sleep. On all 3 nights, the subjects underestimated the number of awakenings when compared to objective criteria. Although the subjects were consistent in their errors of estimation of their sleep compared to polysomnographic assessments over the three nights, the between-individual variation was large, so that objective and subjective ratings of SOL and awakenings were not correlated. The young men and women in our study, who were free of medication or sleep complaints, perceived their sleep inaccurately when compared to objective polysomnographic recordings.

Different nocturnal body temperatures and sleep with forced-air warming in men and in women taking hormonal contraceptives.

We studied how forced-air warming, conventionally used to control body temperature during and after anaesthesia, affected the nocturnal rectal temperatures and sleep composition of young men and women. Seven healthy women who were taking oral or injection contraceptives, and six healthy men spent 3 nights in a controlled environment: an adaptation night followed by 2 nights when they slept under either a down duvet (baseline) or a quilt perfused with warm air (hot). Repeated analysis of variance (ANOVA) revealed significant gender differences in the body temperature responses. On the baseline night, despite sleeping under the same conditions, the women did not show a nocturnal drop in body temperature as shown by the men. Forced-air warming increased body temperature to a similar extent in the men and the women, and resulted in enhanced hyperthermia in the women, and blunted the drop in body temperature in the men, compared to their baseline nights. The significant increases in body temperature had no consequences, however, for the subjective sleep quality of either the men or women, and only minor consequences for objective sleep composition. Both men and women had increased amounts of Stage 2 sleep on the hot night (P < 0.04). In addition, the women had reduced rapid eye movement (REM) sleep when compared to their baseline night (P < 0.04). Our results confirm that in a passive thermal environment, women who are taking oral or injection contraceptives have higher nocturnal body temperatures than men. Also, as sleep architecture was minimally affected by the increases in body temperature of between 0.2 and 0.3 degree C on the hot night in the men and women, and subjective sleep quality was unaffected, our results question the existence of a tight association between sleep and body temperature.

Menstrual factors in sleep.

The changing endocrine profile in premenopausal women alters aspects of sleep and circadian rhythms. Subjectively women appear to feel a greater need for sleep and report poor and insufficient sleep more often than men. This greater sleep requirement may manifest with a higher amplitude of slow-wave sleep in the EEG in women. Healthy young women, with biphasic body temperature rhythms of ovulatory menstrual cycles, have more stage 2 sleep, higher spindle frequency activity and less rapid-eye movement (REM) sleep when progesterone predominates in the luteal phase. These sleep-EEG changes may largely be caused by neurosteroids acting on the brain. Sleep regulatory mechanisms, indicated by the onset to sleep, slow-wave sleep (SWS) and slow-wave activity, appear to be unaffected by menstrual phase in women with normal cycles. Women with premenstrual mood symptoms have more stage 2 sleep and seemingly less SWS and REM sleep, a blunted circadian rhythm of melatonin and an earlier minimum body temperature than asymptomatic women. Subjective repercussions include increased daytime sleepiness, lethargy and fatigue. Treatment strategies for menstrual-associated complaints include using oral contraceptives and sleep deprivation but the physiology and pharmacology of normal menstrual changes, the disorders and their treatment need to be better understood.

Effects of training volume on sleep, psychological, and selected physiological profiles of elite female swimmers.

Excessive training is reported to cause sleep disturbances and mood changes. We examined sleep and psychological changes in female swimmers across a competitive swimming season, that is, at the start of the season (onset), during peak training period (peak), and after a precompetition reduction in training (taper). For each phase, polysomnographic recordings, body composition, psychological parameters, and swimming performance were obtained. A daily training log and sleep diary were maintained for the entire study period. Sleep onset latency (SOL) time awake after sleep onset, total sleep time (TST), and rapid eye movement (REM) sleep times were similar at all three training levels. Slow wave sleep (SWS) formed a very high percentage of total sleep in the onset (26%) and peak (31%) training periods, but was significantly reduced following precompetition taper (16%), supporting the theory that the need for restorative SWS is reduced with reduced physical demand. The number of movements during sleep was significantly higher at the higher training volumes, suggesting some sleep disruption. In contrast to other studies, mood deteriorated with a reduction in training volume and/or impending competition.

An evaluative study of the short-term effects of once-daily, sustained-release theophylline on sleep in nocturnal asthmatics.

OBJECTIVE: To examine the effects of once-daily, sustained-release theophylline on sleep patterns in nocturnal asthmatics. DESIGN: Double-blind, randomised, cross-over, placebocontrolled trial over 22 days. Seven-day period to establish therapeutic levels of theophylline (11.8 +/- 3 mg/l); 8-day cross-over period of 4 days' placebo or theophylline; 7-day baseline period. Electrophysiological sleep patterns, overnight bronchoconstriction and arterial O2 saturation monitored on nights 7, 11 and 15. SETTING: Sleep Laboratory, Medical School, University of the Witwatersrand. PATIENTS: Twelve volunteers who met the criteria for asthma, had previously used theophylline, were clinically stable and had a history of nocturnal awakenings caused by asthma were enrolled. OUTCOME MEASURES: Sleep-onset latency (SOL), within-sleep wakefulness (WSW), rapid eye movement sleep (REM), slow-wave sleep (SWS), peak expiratory flow rate (PEFR) and arterial oxygen saturation. RESULTS: SOL increased on theophylline--12 minutes (range 7-9 minutes) compared with placebo--6 minutes (range 3-11 minutes); WSW increased from 33 minutes (range 17-66 minutes) on placebo to 72 minutes (range 35-150 minutes) on theophylline. REM sleep was unaltered. SWS decreased in 10-12 patients, but this difference was not significant. Early morning PEFR was significantly better on theophylline in all study limbs. CONCLUSION: Our findings show that while once-daily, sustained-release theophylline improves bronchodilation in nocturnal asthmatics, it increases nocturnal wakefulness and decreases sleep efficiency during short-term treatment. This may, however, not be a long-term effect.

Sleep and the sleep electroencephalogram across the menstrual cycle in young healthy women.

Cyclic changes in hormones, body temperature, and metabolic rate characterize the menstrual cycle. To investigate whether these changes are associated with changes in sleep and the sleep electroencephalogram (EEG), a total of 138 sleep episodes from 9 women with no premenstrual syndrome symptoms were recorded every second night throughout one ovulatory menstrual cycle and analyzed in relation to menstrual phase. Ovulation and menstrual cycle stage were confirmed by measurements of temperature, urinary LH, and midluteal plasma levels of estrogen and progesterone. No significant variation across the menstrual cycle was observed for subjective ratings of sleep quality and mood as well as for objective measures of total sleep time, sleep efficiency, sleep latency, rapid eye movement sleep latency, and slow wave sleep. In nonrapid eye movement sleep, EEG power density in the 14.25-15.0 hertz band, which corresponds to the upper frequency range of the sleep spindles, exhibited a large variation across the menstrual cycle, with a maximum in the luteal phase. The data show that in healthy young women, sleep spindle frequency activity varies in parallel with core body temperature, whereas homeostatic sleep regulatory mechanisms, as indexed by the time course of EEG slow wave activity are not substantially affected by the menstrual cycle.

The influence of ipsapirone, a 5-HT1A agonist, on sleep patterns of healthy subjects.

Ipsapirone is a new pyrimidinylpiperazine ligand specific for 5-HT1A receptors, with potential therapeutic use in affective disorders. Because 5-HT is involved in the regulation of sleep, we investigated the effect of ipsapirone hydrochloride on sleep patterns in 18 normal, healthy subjects of both sexes. Compared to placebo, ipsapirone 5 mg administered by mouth three times daily for 14 days decreased rapid eye movement (REM) sleep duration and, by the tenth day of treatment, began to reduce slow wave sleep (SWS) duration. The decrease in REM sleep occurred in the first 3 h of sleep. The latency to REM sleep was increased from the first night following ipsapirone administration, remained increased throughout the 14 days of administration, and fell to equal latency on placebo immediately administration ended. Subjective assessments of sleep revealed no differences between ipsapirone and placebo. Our experiments confirm a role of 5-HT1A receptors in sleep. The effects of ipsapirone on the sleep patterns of patients with affective disorders still need to be determined.

Prolonged endurance exercise and sleep disruption.

To determine whether exercise duration effects the recovery sleep following exercise, eight fit male endurance athletes, ages 23-42 yr, had their sleep electrophysiologically studied. This was done on four separate occasions: after a day on which no specific exercise was performed; after a day of a 15-km run; after a 42.2-km run day; after a day in which the athletes participated in a strenuous ultra-triathlon. Sleep patterns following the no exercise day and the 15-km and the 42.2-km run days were similar. The sleep pattern of the ultra-triathlon day when compared with the other three days showed significantly increased wakefulness and delayed and decreased rapid eye movement (REM) sleep. The duration of slow wave sleep (SWS) in the first 6 h after lights out, however, was no different. The increased wakefulness and decreased REM clearly indicate increased stress after the ultra-triathlon. REM sleep appears to be a more sensitive index of exercise induced stress than SWS.

Restricted energy intake affects nocturnal body temperature and sleep patterns.

Changes in nocturnal body temperature, sleep patterns, and blood variables with energy restriction (3347 kJ/d) were studied in nine overweight (body mass index 26.1 +/- 2.8) premenopausal women aged 20-36 y. Variables were measured both 2 wk before and in the final 2 wk of 4-wk dieting. Data collected 28 d apart were compared to attenuate menstrual cycle differences. Subjects lost 8 +/- 4% of their initial body mass after 4 wk of energy restriction and plasma triiodothyronine (T3) was significantly reduced from 5.9 +/- 0.7 to 5.1 +/- 0.6 pmol/L (P < 0.05). The implied suppression of heat production (metabolic rate) with reduced T3 may account for the observed decrease in minimum nocturnal rectal temperature (from 36.5 +/- 0.3 to 36.3 +/- 0.3 degree C, P < 0.05). Furthermore, dieting significantly altered sleep patterns; sleep onset latency was lengthened and slow-wave sleep decreased (P < 0.05). These changes may be indicative of reduced restorative/biosynthetic requirements. It thus appears that energy restriction results in a hypometabolic state that affects nocturnal body temperature and sleep patterns.