Despite its advantages as a chronobiological technique, the ultra-short sleep/wake protocol remains underutilized in circadian rhythm research. The purpose of this study was to examine circadian rhythms of psychomotor vigilance (PVT), mood, and sleepiness in a sample (n = 25) of healthy young adults while they adhered to a 3-h ultra-short sleep/wake protocol. The protocol involved 1-h sleep intervals in darkness followed by 2-h wake intervals in dim light, repeated for 50–55 h. A 5-min PVT test was conducted every 9 h with the standard metrics of mean reaction time (RT; RTmean), median RT (RTmed), fastest 10% of responses (RT10fast), and the reciprocal of the 10% slowest responses (1/RT10slow). Subjective measures of mood and sleepiness were assessed every 3 h. A cosine fit of intra-aural temperature, assessed three times per wake period, established the time of the body temperature minimum (Tmin). Mood, sleepiness, and PVT performances were expressed relative to individual means and compared across eight times of day and across twelve 2-h intervals relative to Tmin. Significant time-of-day and circadian patterns were demonstrated for each of the PVT metrics, as well as for mood and sleepiness. Most mood subscales exhibited significant deterioration in day 2 of the protocol without an alteration of circadian pattern. However, neither sleepiness nor performance was worse on the second day of observation compared to the first day. These data provide further support for the use of the ultra-short sleep/wake protocol for measurement of circadian rhythms.

The objective of this study was to investigate the reliability and validity of the Pittsburgh Sleep Quality Index (PSQI) in a non-clinical sample consisting of younger and older adults. There has been little research validating the PSQI with respect to multinight recording as with actigraphy, and more validation is needed in samples not specifically selected for clinical disturbance. Also, the degree to which the PSQI scores may reflect depressive symptoms versus actual sleep disturbance remains unclear. One-hundred and twelve volunteers (53 younger and 59 older) were screened for their ability to perform treadmill exercises; inclusion was not based on sleep disturbance or depression. Internal homogeneity was evaluated by correlating PSQI component scores with the global score. Global and component scores were correlated with a sleep diary, actigraphy, and centers for epidemiological studies – depression scale scores to investigate criterion validity. Results showed high internal homogeneity. PSQI global score correlated appreciably with sleep diary variables and the depression scale, but not with any actigraphic sleep variables. These results suggest that the PSQI has good internal homogeneity, but may be less reflective of actual sleep parameters than a negative cognitive viewpoint or pessimistic thinking. The sleep complaints measured may often be more indicative of general dissatisfaction than of any specifically sleep-related disturbance.

Objective

To investigate whether a dose–response relationship existed between exercise and subjective sleep quality in postmenopausal women. This objective represents a post hoc assessment that was not previously considered.

Design

Parallel-group randomised controlled trial.

Setting

Clinical exercise physiology laboratory in Dallas, Texas.

Participants

437 sedentary overweight/obese postmenopausal women.

Intervention

Participants were randomised to one of four treatments, each of 6 months of duration: a non-exercise control treatment (n=92) or one of three dosages of moderate-intensity exercise (50% of VO2peak), designed to meet 50% (n=151), 100% (n=99) or 150% (n=95) of the National Institutes of Health Consensus Development Panel physical activity recommendations. Exercise dosages were structured to elicit energy expenditures of 4, 8 or 12 kilocalories per kilogram of body weight per week (KKW), respectively. Analyses were intent to treat.

Primary outcome measures

Continuous scores and odds of having significant sleep disturbance, as assessed by the Sleep Problems Index from the 6-item Medical Outcomes Study Sleep Scale. Outcome assessors were blinded to participant randomisation assignment.

Results

Change in the Medical Outcomes Study Sleep Problems Index score at 6 months significantly differed by treatment group (control: −2.09 (95% CI −4.58 to 0.40), 4 KKW: −3.93 (−5.87 to −1.99), 8 KKW: −4.06 (−6.45 to −1.67), 12 KKW: −6.22 (−8.68 to −3.77); p=0.04), with a significant dose–response trend observed (p=0.02). Exercise training participants had lower odds of having significant sleep disturbance at postintervention compared with control (4 KKW: OR 0.37 (95% CI 0.19 to 0.73), 8 KKW: 0.36 (0.17 to 0.77), 12 KKW: 0.34 (0.16 to 0.72)). The magnitude of weight loss did not differ between treatment conditions. Improvements in sleep quality were not related to changes in body weight, resting parasympathetic control or cardiorespiratory fitness.

Conclusion

Exercise training induced significant improvement in subjective sleep quality in postmenopausal women, with even a low dose of exercise resulting in greatly reduced odds of having significant sleep disturbance.

Trial registration number

clinicaltrials.gov identifier: NCT00011193.

Article summary

Article focus

Sleep disturbance is prevalent in postmenopausal women, with 35%–60% reporting significant sleep problems.

Effective, safe and easily available treatment options for disturbed sleep in postmenopausal women are lacking.

There has been equivocal evidence as to whether exercise improves sleep in postmenopausal women, though possible dose–response effects have been noted.

Key messages

Exercise resulted in significant improvement in subjective sleep quality in postmenopausal women, with reduced odds of having sleep disturbance at postintervention with even 50% of the recommended dose of exercise for adults.

The effects of exercise on sleep quality were independent of changes in body weight, resting parasympathetic control or cardiorespiratory fitness.

Strengths and limitations of this study

The study constitutes the largest randomised controlled trial on exercise and sleep quality, using a structured dose of exercise and a validated measure of sleep quality.

Only self-reported sleep was assessed; objective measurement of sleep, with either actigraphy or polysomnography, was not conducted.

Despite the high prevalence of sleep disturbance in the sample, participants were not selected on the basis of sleep complaints.

Perinatal depression is an important public health problem affecting 10% to 20% of childbearing women. Perinatal depression is associated with significant morbidity, and has enormous consequences for the wellbeing of the mother and child. During the perinatal period, treatment of depression, which could affect the mother and child during pregnancy and lactation, poses a complex problem for both mother and clinician. Bright light therapy may be an attractive treatment for perinatal depression because it is low cost, home-based, and has a much lower side effect profile than pharmacotherapy. The antidepressant effects of bright light are well established, and there are several rationales for expecting that bright light might also be efficacious for perinatal depression. This review describes these rationales, summarizes the available evidence on the efficacy of bright light therapy for perinatal depression, and discusses future directions for investigation of bright light therapy as a treatment for perinatal depression.

SUMMARY

The aim of this study was to investigate the effects of 8 weeks of moderate restriction of time in bed (TIB) on glucose tolerance and insulin sensitivity in healthy older self-reported long sleepers. Forty-two older adults (ages 50–70 years) who reported average sleep durations of ≥ 8.5 h per night were assessed. Following a 2-week baseline, participants were randomly assigned to two 8-week treatments: either (1) TIB restriction (n = 22), which involved following a fixed sleep schedule in which time in bed was reduced by 90 min compared with baseline; (2) a control (n = 18), which involved following a fixed sleep schedule but no imposed change of TIB. Sleep was monitored continuously via wrist actigraphy recordings, supplemented with a daily diary. Glucose tolerance and insulin sensitivity were assessed before and following the treatments. Compared with the control treatment, TIB restriction resulted in a significantly greater reduction of nocturnal TIB (1.39 ± 0.40 h versus 0.14 ± 0.26 h), nocturnal total sleep time (TST) (1.03 ± 0.53 h versus 0.40 ± 0.42 h), and 24-hr TST (1.03 ± 0.53 h versus 0.33 ± 0.43 h) from baseline values. However, no significant effect of TIB restriction was found for glucose tolerance or insulin sensitivity. These results suggest that healthy older long sleepers can tolerate 8 weeks of moderate TIB restriction without impairments in glucose tolerance or insulin sensitivity.

Circadian disruption has been linked with inflammation, an established cancer risk factor. Per3 clock gene polymorphisms have also been associated with circadian disruption and with increased cancer risk. Patients completed a questionnaire and provided a blood sample prior to undergoing a colonoscopy (n = 70). Adjusted mean serum cytokine concentrations (IL-6, TNF-alpha, gamma-INF, IL-I ra, IL-I-beta, VEGF) were compared among patients with high and low scores for fatigue (Multidimensional Fatigue Inventory), depressive symptoms (Beck Depression Inventory II), or sleep disruption (Pittsburgh Sleep Quality Index), or among patients with different Per3 clock gene variants. Poor sleep was associated with elevated VEGF, and fatigue-related reduced activity was associated with elevated TNF-alpha concentrations. Participants with the 4/5 or 5/5 Per3 variable tandem repeat sequence had elevated IL-6 concentrations compared to those with the 4/4 genotype. Biological processes linking circadian disruption with cancer remain to be elucidated. Increased inflammatory cytokine secretion may playa role.

Background

Most mammals are seasonal breeders whose gonads grow to anticipate reproduction in the spring and summer. As day length increases, secretion increases for two gonadotropins, luteinizing hormone (LH) and follicle stimulating hormone (FSH). This response is largely controlled by light. Light effects on gonadotropins are mediated through effects on the suprachiasmatic nucleus and responses of the circadian system. There is some evidence that seasonal breeding in humans is regulated by similar mechanisms, and that light stimulates LH secretion, but primate responses seem complex.

Methods

To gain further information on effects of bright light on LH and FSH secretion in humans, we analyzed urine samples collected in three experiments conducted for other goals. First, volunteers ages 18-30 years and 60-75 commenced an ultra-short 90-min sleep-wake cycle, during which they were exposed to 3000 lux light for 3 hours at balanced times of day, repeated for 3 days. Urine samples were assayed to explore any LH phase response curve. Second, depressed participants 60-79 years of age were treated with bright light or dim placebo light for 28 days, with measurements of urinary LH and FSH before and after treatment. Third, women of ages 20-45 years with premenstrual dysphoric disorder (PMDD) were treated to one 3-hour exposure of morning light, measuring LH and FSH in urine before and after the treatments.

Results

Two of the three studies showed significant increases in LH after light treatment, and FSH also tended to increase, but there were no significant contrasts with parallel placebo treatments and no significant time-of-day treatment effects.

Conclusions

These results gave some support for the hypothesis that bright light may augment LH secretion. Longer-duration studies may be needed to clarify the effects of light on human LH and FSH.

Background

The aim of this open trial was to examine the influence of acute bright light exposure on anxiety in older and young adults.

Methods

This study was ancillary to a complex 5-day laboratory experiment testing phase-responses to light at all times of the day. On 3 consecutive days, participants were exposed to bright light (3,000 lux) for 3 hours. The Spielberger State-Trait Anxiety Inventory (Form Y1) was administered 5 minutes before and 20 minutes after each treatment. Mean state anxiety before and after treatment were analyzed by age, sex, and time ANOVA. To avoid floor effects, only participants with baseline STAI levels of ≥ 25 were included.

Results

A significant anxiolytic effect of bright light was found for the mean data, as well as for each of the three days. No significant main effect of age, sex, or interaction of these factors with STAI change were found.

Conclusion

The results show consistent and significant (albeit modest) anxiolytic effects following acute bright light exposure in low anxiety adults. Further randomized, controlled trials in clinically anxious individuals are needed.

Background

The phase of a circadian rhythm reflects where the peak and the trough occur, for example, the peak and trough of performance within the 24 h. Light exposure can shift this phase. More extensive knowledge of the human circadian phase response to light is needed to guide light treatment for shiftworkers, air travelers, and people with circadian rhythm phase disorders. This study tested the hypotheses that older adults have absent or weaker phase-shift responses to light (3000 lux), and that women's responses might differ from those of men.

Methods

After preliminary health screening and home actigraphic recording baselines, 50 young adults (ages 18–31 years) and 56 older adults (ages 59–75 years) remained in light-controlled laboratory surroundings for 4.7 to 5.6 days, while experiencing a 90-min ultra-short sleep-wake cycle. Following at least 30 h in-lab baseline, over the next 51 h, participants were given 3 treatments with 3000 lux white light, each treatment for 3 h, centered at one of 8 clock times. The circadian rhythms of urinary aMT6s (a melatonin metabolite), free cortisol, oral temperature, and wrist activity were assessed at baseline and after treatment.

Results

Light (3000 lux for 3 h on 3 days) induced maximal phase shifts of about 3 h. Phase shifts did not differ significantly in amplitude among older and young groups or among women and men. At home and at baseline, compared to the young, the older adults were significantly phase-advanced in sleep, cortisol, and aMT6s onset, but not advanced in aMT6s acrophase or the temperature rhythm. The inflection from delays to advances was approximately 1.8 h earlier among older compared to young participants in reference to their aMT6s rhythm peaks, and it was earlier in clock time.

Conclusion

In these experimental conditions, 3000 lux light could shift the phase of circadian rhythms to about the same extent among older and young adults, but the optimal light timing for phase shifting differed. For an interval near 4 PM, bright light produced only negligible phase shifts for either age group.

Background

Our aims were to examine the influence of different bright light schedules on mood, sleep, and circadian organization in older adults (n = 60, ages 60–79 years) with insomnia and/or depression, contrasting with responses of young, healthy controls (n = 30, ages 20–40 years).

Methods

Volunteers were assessed for one week in their home environments. Urine was collected over two 24-hour periods to establish baseline acrophase of 6-sulphatoxymelatonin (aMT6s) excretion. Immediately following home recording, volunteers spent five nights and four days in the laboratory. Sleep periods were fixed at eight hours in darkness, consistent with the volunteers' usual sleep periods. Volunteers were randomly assigned to one of three light treatments (four hours per day) within the wake period: (A) two hours of 3,000 lux at 1–3 hours and 13–15 hours after arising; (B) four hours of 3,000 lux at 6–10 hours after arising; (C) four hours of dim placebo light at 6–10 hours after arising. Lighting was 50 lux during the remainder of wakefulness. The resulting aMT6s acrophase was determined during the final 30 hours in the laboratory.

Results

Neither mood nor total melatonin excretion differed significantly by treatment. For the three light treatments, significant and similar phase-response plots were found, indicating that the shift in aMT6s acrophase was dependent upon the circadian time of treatment. The changes in circadian timing were not significantly correlated to changes in sleep or mood.

Conclusion

The trial failed to demonstrate photoperiodic effects. The results suggest that even low levels of illumination and/or fixed timing of behavior had significant phase-shifting effects.