Article

Bonnet MH, Arand DL. 24-Hour metabolic rate in insomniacs and matched normal sleepers. Sleep 18: 581-8

Dayton VA Hospital, Wright State University, Ohio, USA.
Sleep (Impact Factor: 5.06). 10/1995; 18(7):581-8.
Source: PubMed

ABSTRACT Groups of 10 objectively defined insomniacs and age-, sex- and weight-matched normal sleepers were evaluated on sleep, performance, mood, personality and metabolic measures over a 36-hour sleep laboratory stay. Insomniacs were defined to have increased wake time during the night but also had decreased stage 2 and rapid eye movement sleep. As expected insomniacs reported increased confusion, tension and depression and decreased vigor on the profile of mood states mood scale throughout the evaluation period as compared to the normals. Insomniacs also had decreased memory ability on the short-term memory test and the MAST. These performance and mood differences were not secondary to sleepiness because the insomniacs also had significantly increased multiple sleep latency test (MSLT) values throughout the evaluation period. In conjunction with the consistent mood, performance and MSLT differences during the day and the sleep differences at night, whole body VO2, measured at intervals across the day and throughout one night of sleep, was consistently elevated at all measurement points in the insomniacs as compared to the normals. The nocturnal increase in metabolic rate remained even after metabolic values from periods during the night containing wake time or arousals were eliminated from the data set. It was concluded that patients who report chronic insomnia may suffer from a more general disorder of hyperarousal (as measured here by a 24-hour increase in metabolic rate) that may be responsible for both the daytime symptoms and the nocturnal poor sleep. Future studies need to explore 24-hour insomnia treatment strategies that decrease hyperarousal.

Download full-text

Full-text

Available from: Michael H Bonnet, Sep 01, 2015
3 Followers
 · 
141 Views
 · 
800 Downloads
  • Source
    • "Notwithstanding, brain mechanisms of insomnia have remained elusive, hampering the development of effective treatments. The symptoms of insomnia are not limited to sleep and may best be summarized as a round-the-clock state of hyper-arousal (Bonnet and Arand, 1995). Indeed, subjective hyper-arousal indices like tension, irritability, hypersensitivity and behavioural hyper-responsivity are complemented by physiological indices of hyper-arousal. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Insomnia is prevalent, severe and partially heritable. Unfortunately, its neuronal correlates remain enigmatic, hampering the development of mechanistic models and rational treatments. Consistently reported impairments concern fragmented sleep, hyper-arousal and executive dysfunction. Because fronto-striatal networks could well play a role in sleep, arousal regulation and executive functioning, the present series of studies used an executive task to evaluate fronto-striatal functioning in disturbed sleep. Patients with insomnia showed reduced recruitment of the head of the left caudate nucleus during executive functioning, which was not secondary to altered performance or baseline perfusion. Individual differences in caudate recruitment were associated with hyper-arousal severity. Seed-based functional connectivity analysis suggested that attenuated input from a projecting orbitofrontal area with reduced grey matter density contributes to altered caudate recruitment in patients with insomnia. Attenuated caudate recruitment persisted after successful treatment of insomnia, warranting evaluation as a potential vulnerability trait. A similar selective reduction in caudate recruitment could be elicited in participants without sleep complaints by slow-wave sleep fragmentation, providing a model to facilitate investigation of the causes and consequences of insomnia.
    Brain 11/2013; 137(2). DOI:10.1093/brain/awt329 · 10.23 Impact Factor
  • Source
    • "Patients with insomnia, despite lacking night sleep and day-time fatigue, are at a higher state of alertness than those who have appropriate sleep, which has also been demonstrated by the fact that patients with insomnia have longer sleep latency than a control group consisting of ordinary people who sleep upon an execution of latency repeat inspection. This suggests that insomnia is an over-alertness obstacle ranging for 24 hours, and not one limited only to nighttime [78]. As another piece of evidence of over-alertness, patients with insomnia have an increased metabolic rate for 24 hours, their sympathetic nervous system is relatively exacerbated [78], and their adrenal cortex hormone and cortisol density are markedly increased compared to ordinary people [2]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: The purpose of this study was to review potential, physiological, hormonal and neuronal mechanisms that may mediate the sleep changes. This paper investigates the literatures regarding the activity of the hypothalamic-pituitary-adrenal (HPA) axis, one of the main neuroendocrine stress systems during sleep in order to identify relations between stress and sleep disorder and the treatment of stress-induced insomnia. Sleep and wakefulness are regulated by the aminergic, cholinergic brainstem and hypothalamic systems. Activation of the HPA and/or the sympathetic nervous systems results in wakefulness and these hormones including corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), cortisol or corticosterone, noradrenaline, and adrenaline, are associated with attention and arousal. Stress-related insomnia leads to a vicious circle by activating the HPA system. An awareness of the close interaction between sleep and stress systems is emerging and the hypothalamus is now recognized as a key center for sleep regulation, with hypothalamic neurontransmitter systems providing the framework for therapeutic advances. An updated understanding of these systems may allow researchers to elucidate neural mechanisms of sleep disorder and to develop effective intervention for sleep disorder.
    12/2012; 21(4):141-50. DOI:10.5607/en.2012.21.4.141
  • Source
    • "Two weeks of partial sleep deprivation (5.5 hours) decreased resting metabolic rate and increased RQ in a randomized, cross-over study109 (Table 1). In contrast, subjects with chronic insomnia had increased metabolic rate.127 We have recently shown that poor sleep quality was associated with higher REE, a higher RQ, and an activation of the stress system in obese subjects with short sleep duration.128 "
    [Show abstract] [Hide abstract]
    ABSTRACT: In the last 50 years, the average self-reported sleep duration in the United States has decreased by 1.5-2 hours in parallel with an increasing prevalence of obesity and diabetes. Epidemiological studies and meta-analyses report a strong relationship between short or disturbed sleep, obesity, and abnormalities in glucose metabolism. This relationship is likely to be bidirectional and causal in nature, but many aspects remain to be elucidated. Sleep and the internal circadian clock influence a host of endocrine parameters. Sleep curtailment in humans alters multiple metabolic pathways, leading to more insulin resistance, possibly decreased energy expenditure, increased appetite, and immunological changes. On the other hand, psychological, endocrine, and anatomical abnormalities in individuals with obesity and/or diabetes can interfere with sleep duration and quality, thus creating a vicious cycle. In this review, we address mechanisms linking sleep with metabolism, highlight the need for studies conducted in real-life settings, and explore therapeutic interventions to improve sleep, with a potential beneficial effect on obesity and its comorbidities.
    Annals of the New York Academy of Sciences 07/2012; 1264(1):110-34. DOI:10.1111/j.1749-6632.2012.06655.x · 4.31 Impact Factor
Show more