Successful physical exercise-induced weight loss is modulated by habitual sleep duration in the elderly: results of a pilot study.

Although it is widely accepted that physical exercise promotes weight loss, physical exercise alone had been found to result in only marginal weight loss compared to no treatment. Interestingly, both subjective and objective sleep duration have been shown to be negatively correlated to the body mass index (BMI). Despite this growing evidence of a relation between sleep duration and body weight, the role of habitual sleep duration in physical exercise-induced weight loss has not been studied so far. Twenty-two healthy elderly good sleepers aged 61-76 years (mean 68.36 years, 55 % female, BMI mean 25.15 kg/m2) either took part in a 12-week aerobic endurance training (3 × 30 min/week) or in a relaxation control (2 × 45 min/week). The BMI was assessed prior to and after intervention. Subjects maintained sleep logs every morning/evening during the training period, allowing for calculation of habitual sleep duration. Besides a significant main effect of the type of training, a significant interaction of type of training and habitual sleep duration was observed: while after treadmill training subjects who slept less than 7.5 h/night during intervention reduced their BMI by nearly 4 %, a comparable decrease in the BMI was found neither in subjects who slept more than 7.5 h nor after relaxation training independent of sleep duration. Sleep duration itself did not change in any group. Although results should be interpreted with caution due to the small sample size, this is the first study to indicate that physical exercise might compensate for disturbed body weight regulation associated with short sleep duration.

Sleep-dependent memory consolidation and its implications for psychiatry.

Both sleep disturbance and memory impairment are very common in psychiatric disorders. Since sleep has been shown to play a role in the process of transferring newly acquired information into long-term memory, i.e., consolidation, it is important to highlight this link in the context of psychiatric disorders. Along these lines, after providing a brief overview of healthy human sleep, current neurobiological models on sleep-dependent memory consolidation and resultant opportunities to manipulate the memory consolidation process, recent findings on sleep disturbances and sleep-dependent memory consolidation in patients with insomnia, major depression, schizophrenia, and post-traumatic stress disorder are systematically reviewed. Furthermore, possible underlying neuropathologies and their implications on therapeutic strategies are discussed. This review aims at sensitizing the reader for recognizing sleep disturbances as a potential contributor to cognitive deficits in several disorders, a fact which is often overlooked up to date.

Insomnia complaints and substance use in German adolescents: did we underestimate the role of coffee consumption? Results of the KiGGS study.

The purpose of the study was to study the associations of tobacco, alcohol, marijuana, and coffee use and insomnia complaints (IC) in adolescents with special consideration of the influence of coffee consumption on these relationships. 7698 Subjects aged 11-17 years were investigated in a cross-sectional study within the German Health Interview and Examination Survey for Children and Adolescents. Self-report questionnaires were distributed to the participants. Hierarchical regression analyses were performed to assess possible effects of coffee consumption on the association of tobacco, alcohol, and marijuana use with IC. Common risk factors for insomnia were included in the adjusted analyses. Tobacco, alcohol, marijuana and coffee use displayed significant bivariate associations with IC. After adjusting the first three substances for coffee consumption, their associations with IC were reduced considerably. After additionally adjusting for other potential confounders (age, gender, socio-economic status, externalizing and internalizing psychiatric problems, media use, bodyweight, medical condition), frequent coffee consumption, high alcohol intake and frequent smoking contributed to the prediction of IC in male subjects while frequent coffee consumption and high alcohol intake predicted the occurrence of IC in females. Coffee consumption could be an important risk factor for IC in adolescents and it significantly affects the association of smoking, alcohol, and marijuana with IC. Future research that includes long-term studies about psychoactive substance use (PSU) and sleep should also consider coffee consumption. Parents, educators, clinicians, and researchers should be aware of the potentially hazardous influence of PSU, especially coffee, alcohol and tobacco, on sleep in young individuals.

Relationships of peripheral IGF-1, VEGF and BDNF levels to exercise-related changes in memory, hippocampal perfusion and volumes in older adults.

Animal models point towards a key role of brain-derived neurotrophic factor (BDNF), insulin-like growth factor-I (IGF-I) and vascular endothelial growth factor (VEGF) in mediating exercise-induced structural and functional changes in the hippocampus. Recently, also platelet derived growth factor-C (PDGF-C) has been shown to promote blood vessel growth and neuronal survival. Moreover, reductions of these neurotrophic and angiogenic factors in old age have been related to hippocampal atrophy, decreased vascularization and cognitive decline. In a 3-month aerobic exercise study, forty healthy older humans (60 to 77years) were pseudo-randomly assigned to either an aerobic exercise group (indoor treadmill, n=21) or to a control group (indoor progressive-muscle relaxation/stretching, n=19). As reported recently, we found evidence for fitness-related perfusion changes of the aged human hippocampus that were closely linked to changes in episodic memory function. Here, we test whether peripheral levels of BDNF, IGF-I, VEGF or PDGF-C are related to changes in hippocampal blood flow, volume and memory performance. Growth factor levels were not significantly affected by exercise, and their changes were not related to changes in fitness or perfusion. However, changes in IGF-I levels were positively correlated with hippocampal volume changes (derived by manual volumetry and voxel-based morphometry) and late verbal recall performance, a relationship that seemed to be independent of fitness, perfusion or their changes over time. These preliminary findings link IGF-I levels to hippocampal volume changes and putatively hippocampus-dependent memory changes that seem to occur over time independently of exercise. We discuss methodological shortcomings of our study and potential differences in the temporal dynamics of how IGF-1, VEGF and BDNF may be affected by exercise and to what extent these differences may have led to the negative findings reported here.

Differential effect of an anticholinergic antidepressant on sleep-dependent memory consolidation.

STUDY OBJECTIVES: Rapid eye movement (REM) sleep is considered critical to the consolidation of procedural memory - the memory of skills and habits. Many antidepressants strongly suppress REM sleep, however, and procedural memory consolidation has been shown to be impaired in depressed patients on antidepressant therapy. As a result, it is important to determine whether antidepressive therapy can lead to amnestic impairment. We thus investigated the effects of the anticholinergic antidepressant amitriptyline on sleep-dependent memory consolidation. DESIGN: Double-blind, placebo-controlled, randomized, parallel-group study. SETTING: Sleep laboratory. PARTICIPANTS: Twenty-five healthy men (mean age: 26.8 ± 5.6 y). INTERVENTIONS: 75 mg amitriptyline versus placebo. MEASUREMENTS/RESULTS: To test memory consolidation, a visual discrimination task, a finger-tapping task, the Rey-Osterrieth Complex Figure Test, and the Rey Auditory-Verbal Learning Test were performed. Sleep was measured using polysomnography. Our findings show that amitriptyline profoundly suppressed REM sleep and impaired perceptual skill learning, but not motor skill or declarative learning. CONCLUSIONS: Our study is the first to demonstrate that an antidepressant can affect procedural memory consolidation in healthy subjects. Moreover, considering the results of a recent study, in which selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors were shown not to impair procedural memory consolidation, our findings suggest that procedural memory consolidation is not facilitated by the characteristics of REM sleep captured by visual sleep scoring, but rather by the high cholinergic tone associated with REM sleep. Our study contributes to the understanding of potentially undesirable behavioral effects of amitriptyline.

Declarative memory consolidation during the first night in a sleep lab: the role of REM sleep and cortisol.

While the consolidation of declarative memory is supported by slow wave sleep (SWS) in healthy subjects, it has been shown to be associated with rapid eye movement (REM) sleep in patients with insomnia. Sleep during a subject's first night in an unfamiliar environment is often disturbed, and this so-called first-night effect (FNE) has often been used as a model of transient insomnia. Additionally, sleeping for the first time in an unfamiliar environment can lead to increased cortisol secretion, and declarative memory consolidation likely depends on low cortisol levels, especially during the early part of the night. Accounting for intersubject variability in the FNE, we examined the relationship between sleep stages, cortisol secretion and declarative memory performance in 27 healthy young men. Declarative memory performance improved significantly after sleep. Whereas memory performance during the learning session and retrieval testing was strongly associated with cortisol secretion, the overnight gain was not. Post hoc analyses indicated that the overnight gain appears to be modulated by the extent of the FNE: a significant overnight improvement in memory performance was found only in subjects with a weak FNE (n=12). In these subjects, no association was found between any sleep stage and the improvement observed in their memory performance. In subjects with a strong FNE (n=12), however, the overnight change in memory performance was associated with the proportion of REM sleep and the total number of REMs. Disturbed sleep in an unfamiliar environment therefore appears to affect the memory consolidation process.

Precueing imminent conflict does not override sequence-dependent interference adaptation.

Interference effects are largely reduced after cognitive conflicts in previous trials. This sequence-dependent interference adaptation is often seen as a consequence of strategic executive control. We sought to investigate whether sequential modulations are comparable with cue-induced strategic adjustments in spatial interference tasks. If so, reliable cues indicating the next compatibility condition should override effects caused by prior events. To this end, cues were introduced in a spatial stimulus-response compatibility task and a Simon task that either indicated the upcoming trial compatibility (rule cues) or the target position, which was not related to the S-R rule (position cues). The proportion of valid cues was either completely or predominantly valid. In both tasks cueing benefits for absolutely reliable rule cues were clearly present. Remarkably, sequential modulations were not influenced by effective rule cueing and vice versa. Even absolutely reliable information about prospective control demands did not cancel out sequence-dependent interference adaptation. In addition, the contingent negative variation-an event-related brain potential in the cue-target interval that is related to response preparation and readiness-showed additive effects of preceding compatibility and cue reliability. The present results indicate that processes underlying sequence-dependent interference adaptation differ from cue-induced strategic processes of cognitive control.