Title: The Hypothalamic-Pituitary-Adrenocortical System and Sleep in Man
Author: Friess, E.; Wiedemann, K.; Steiger, A.; Holsboer, F.; 1995)
Journal: Adv Neuroimmunol; V. 5; Issue: 2; Pages: 111-25
Abstract: This review article summarizes the major findings about the interactions of human sleep structure and the hypothalamo-pituitary-adrenocortical (HPA) system under physiological and pathophysiological conditions, including studies that probe the sleep effects of systemically administered HPA hormones. Human sleep is regulated by a concerted action of various signal compounds acting at sleep-generating neurons whose central organization is not yet fully understood. During nocturnal sleep the endocrine system is remarkably active, the longest established finding being that growth hormone (GH) release is associated with the initiation of sleep and that there is a steep morning rise of cortisol (Weitzman et al., 1966; Takahashi et al., 1968). Moreover, the effects of exogenously administered corticosteroids and of their excessive endogenous release (e.g. Cushing’s disease) were recognized more than 20 years ago.
Notes: Journal Article
Author Address: Max-Planck-Institute of Psychiatry, Clinical Institute, Department of Psychiatry, Munich, Germany.
Abstract: Based on data obtained from the Tucson Epidemiologic Study of Chronic Lung Disease that included body weight, questionnaire responses, and spirometry, we found that among subjects with no respiratory symptoms, 28.0 percent reported insomnia (difficulty initiating or maintaining sleep) and 9.4 percent reported daytime sleepiness. Among subjects with respiratory symptoms, cough and/or wheeze, the rates of sleep complaints increased. With one symptom, 39.1 percent reported insomnia and 12.4 percent reported daytime sleepiness. With both symptoms, the rates were 52.8 percent and 22.8 percent, respectively. Overall, we found significant relationships between rates of respiratory symptoms and sleep complaints (trend chi 2 = 73.9, p < 0.001 for insomnia; trend chi 2 = 37.9, p < 0.001 for daytime sleepiness). In separate analyses, obesity, snoring, and a diagnosis of lung disease also influenced the rate of sleep complaints but, when we employed logistic regression, we found that obesity, respiratory symptoms, gender, and age were the only variables related to the risk of insomnia or daytime sleepiness.
Notes: Journal Article
Author Address: Department of Medicine, University of Arizona College of Medicine, Tucson 85724.
Abstract: Different medications can have significant effects on sleep quality and/or quantity. When prescribing medications it is important to be aware of these possible adverse effects of drugs. Disturbances of the sleep/wake cycle caused by medications can vary and include insomnia, daytime sleepiness, nightmares and changes in the sleep architecture. Psychotropic drugs are well known to have an effect on the sleep/wake cycle, but there is only limited information about the sleep effects of nonpsychotropic medications. Cardiovascular drugs, especially beta-blockers, which are widely used drugs, often change the sleep architecture and cause nightmares and insomnia. Both of these effects can be a potential source of noncompliance. Because of the complicated relationship between sleep, nocturnal asthma and antiasthmatic agents, the appropriate dosage and timing of medications should always be considered. Patients with Parkinson’s disease often experience disrupted sleep due to their disorder and the adverse effects of anti-parkinsonian medications.
Notes: Journal Article
Author Address: Institute of Behavioural Sciences, Semmelweis Medical University, Budapest, Hungary.
Abstract: Many physiological and behavioural functions have circadian rhythms – endogenous oscillations with a period of approximately 24 h that can occur even in the absence of sleep. We determined whether there is an endogenous circadian rhythm in breathing, metabolism and ventilatory chemosensitivity in humans. Ten healthy, adult males were studied throughout 4 days in a stable laboratory environment. After two initial baseline days (16 h wakefulness plus 8 h sleep) that served to achieve a steady state, subjects were studied under constant behavioural and environmental conditions throughout 41 h of wakefulness. Ventilation, metabolism and the magnitude of the hypercapnic ventilatory response (HCVR) were measured every 2 h. Individuals’ data were aligned according to circadian phase (core body temperature minimum; CBTmin) and averaged. In the group average data, there was a significant and large amplitude circadian variation in HCVR slope (average of +/-0.4 l min-1 mmHg-1; corresponding to +/-12.1 % of 24 h mean), and a smaller amplitude rhythm in the HCVR x-axis intercept (average of +/-1.1 mmHg; +/-2.1 % of 24 h mean). Despite a significant circadian variation in metabolism (+/-3.2 % of 24 h mean), there were no detectable rhythms in tidal volume, respiratory frequency or ventilation. This small discrepancy between metabolism and ventilation led to a small but significant circadian variation in end-tidal PCO2 (PET,CO2; +/-0.6 mmHg; +/-1.5 % of 24 h mean). The circadian minima of the group-averaged respiratory variables occurred 6-8 h earlier than CBTmin, suggesting that endogenous changes in CBT across the circadian cycle have less of an effect on respiration than equivalent experimentally induced changes in CBT. Throughout these circadian changes, there were no correlations between HCVR parameters (slope or x-axis intercept) and either resting ventilation or resting PET,CO2. This suggests that ventilation and PET,CO2 are little influenced by central chemosensory respiratory control in awake humans even when at rest under constant environmental and behavioural conditions. The characteristic change in PET,CO2 during non-rapid eye movement sleep was shown to be independent of circadian variations in PET,CO2, and probably reflects a change from predominantly behavioural to predominantly chemosensory respiratory control. This study has documented the existence and magnitude of circadian variations in respiration and respiratory control in awake humans for the first time under constant behavioural and environmental conditions. These results provide unique insights into respiratory control in awake humans, and highlight the importance of considering the phase of the circadian cycle in studies of respiratory control.
Notes: Clinical Trial
Author Address: Circadian, Neuroendocrine and Sleep Disorders Section, Brigham and Women’s Hospital, 221 Longwood Avenue, Boston, MA 02115-5817, USA. firstname.lastname@example.org
Title: Sleep Deprivation Per Se Does Not Decrease the Hypercapnic Ventilatory Response in Humans
Author: Spengler, C. M.; Shea, S. A.; (Date: Apr, 2000)
Journal: Am J Respir Crit Care Med; V. 161; Issue: 4 Pt 1; Pages: 1124-8
Abstract: Several studies have found that sleep deprivation reduces the hypercapnic ventilatory response (HCVR). Such results may have been affected by uncontrolled activities or environmental influences during the sleep deprivation period. The current study determined the “pure” effect of sleep deprivation on respiratory control under strictly controlled behavioral and environmental conditions. After 2 d of acclimation in the laboratory, 10 subjects maintained wakefulness (confirmed by EEG), a constant semirecumbent posture, ate regular small meals, had constant interaction with experimenters, and stayed in an environment with constant low light (10 lux) and constant room temperature for 41 consecutive hours. Measurements of HCVR, resting ventilation, V O(2) and V CO(2) were performed every 2 h. Comparisons were made of six pairs of measurements, with each pair separated by 24 h of sleep deprivation. None of the respiratory variables changed significantly with 24 h of sleep deprivation. Mean HCVR increased by 17% with sleep deprivation (3.12 versus 3.54 L x min(-1) x mm Hg(-1); not significant). These results show that sleep deprivation per se does not reduce the sensitivity of central chemoreceptors nor change resting ventilation or metabolism. The reduced HCVR after sleep loss found in previous studies may have been affected by uncontrolled activities or environmental influences during sleep deprivation periods.
Notes: Journal Article
Author Address: Circadian, Neuroendocrine, and Sleep Disorders Section, Brigham and Women’s Hospital, Boston, Massachusetts 02115, USA. email@example.com
Abstract: BACKGROUND: Chronic sleep debt is becoming increasingly common and affects millions of people in more-developed countries. Sleep debt is currently believed to have no adverse effect on health. We investigated the effect of sleep debt on metabolic and endocrine functions. METHODS: We assessed carbohydrate metabolism, thyrotropic function, activity of the hypothalamo-pituitary-adrenal axis, and sympathovagal balance in 11 young men after time in bed had been restricted to 4 h per night for 6 nights. We compared the sleep-debt condition with measurements taken at the end of a sleep-recovery period when participants were allowed 12 h in bed per night for 6 nights. FINDINGS: Glucose tolerance was lower in the sleep-debt condition than in the fully rested condition (p<0.02), as were thyrotropin concentrations (p<0.01). Evening cortisol concentrations were raised (p=0.0001) and activity of the sympathetic nervous system was increased in the sleep-debt condition (p<0.02). INTERPRETATION: Sleep debt has a harmful impact on carbohydrate metabolism and endocrine function. The effects are similar to those seen in normal ageing and, therefore, sleep debt may increase the severity of age-related chronic disorders.
Notes: Clinical Trial
Controlled Clinical Trial
Author Address: Department of Medicine, University of Chicago, IL 60637, USA.