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The aim of this study was to investigate the effects of sleep deprivation on autonomic and endocrine functions during the day and on exercise tolerance in the evening. Ten healthy young males completed two, 2-day control and sleep deprivation trials. For the control trial, participants were allowed normal sleep from 23:00 to 07:00 h. For the sleep deprivation trial, participants did not sleep for 34 h. Autonomic activity was measured from 19:00 h on day 1 to 16:00 h on day 2 by frequency-domain measures of heart rate variability. Endocrine function was examined by measuring adrenocorticotropic hormone and cortisol from venous blood samples collected on day 2 at 09:00, 13:00, and 17:00 h and immediately after an exercise tolerance testing. Autonomic regulation, particularly parasympathetic regulation estimated from the high-frequency component of heart rate variability analysis, was significantly higher in the sleep deprivation trial than in the control trial in the morning and afternoon of day 2. Plasma adrenocorticotropic hormone concentrations were significantly higher at 09:00 and 13:00 h of day 2 under sleep deprivation. Heart rate during exercise was significantly lower following sleep deprivation. Therefore, the effects of sleep deprivation on autonomic regulation depend on the time of the day.
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http://dx.doi.org/10.1080/02640414.2012.733824 | DOI Listing |
J Neurosci Methods
September 2025
Department of Biosciences and Bioinformatics, School of Science, Xi'an Jiaotong-Liverpool University, Suzhou, China; Suzhou Key Laboratory on Neurobiology and Cell Signaling, School of Science, Xi'an Jiaotong-Liverpool University, Suzhou, China.
Background: Affective disorders represent a major global health burden. Animal models are widely used for modeling brain disorders and neuroactive drug discovery. A novel powerful tool in translational neuroscience research, zebrafish provide multiple behavioral assays relevant to anxiety-like and depression-related conditions (including despair-like behavior, a common feature in depression).
View Article and Find Full Text PDFJ Agric Food Chem
September 2025
Department of Food Science and Engineering, Ningbo University, Ningbo 315211, P.R. China.
Sleep deprivation (SD) is a major contributor to cognitive impairment, often accompanied by central neuroinflammation and gut microbiota dysbiosis. The tryptophan (TRP) pathway, activated via indoleamine 2,3-dioxygenase (IDO), serves as a critical link between immune activation and neuronal damage. Umbelliferone (UMB), a naturally occurring coumarin compound, possesses anti-inflammatory, antioxidant, and microbiota-modulating properties.
View Article and Find Full Text PDFJ Appl Physiol (1985)
September 2025
Department of Kinesiology and Sport Management, Texas Tech University, Lubbock, Texas, United States of America.
Consistent sleep patterns are associated with better cardiovascular health, while sleep loss is known to impair vascular function. This study examined whether consistent sleep could improve vascular function and mitigate the negative effect of 25-hour total sleep deprivation. Sixteen healthy adults (10 females, 6 males; 34 ± 9 years; BMI: 25 ± 3 kg/m²) completed a randomized crossover study involving two 12-night sleep conditions, habitual sleep and a consistent sleep/wake schedule that were separated by a 1-2-week washout.
View Article and Find Full Text PDFSleep
September 2025
Department of Neuroscience, Karolinska Institutet, Sweden.
Sleep Adv
July 2025
Department of Anatomy and Neurobiology, Boston University School of Medicine, Boston, MA 02118, United States.
The mismatch between rising sleep need and the fluctuating ability to fall asleep underlies insomnia-the most common sleep disorder-yet remains poorly understood. While sleep need increases steadily with time awake, sleep propensity-the likelihood of transitioning from wake to sleep-follows a bimodal pattern, peaking in the mid-afternoon, dipping in the evening, and rising again near bedtime. Building on our previously developed wave model of sleep dynamics, we extend this homeostatic framework to the waking period and show that it predicts the observed bimodal sleep propensity curve.
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