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Circadian Rhythm
Published in Mehwish Iqbal, Complementary and Alternative Medicinal Approaches for Enhancing Immunity, 2023
The seminar was co-sponsored by four national institutes of health, including the NIA (National Institute of Aging), NIAAA (National Institute of Alcohol Abuse and Alcoholism), NHLBI (National Heart, Lung and Blood Institute) and NIAID (National Institute of Allergy and Infectious Diseases), considering a wide interest and identifying that sleep-based and circadian research carved across traditional regulations of academia (Haspel et al., 2020). Sleep is a natural and physiological phenomenon that demonstrates restorative and modulatory characteristics (Benington & Heller, 1995; Mackiewicz et al., 2007). The response of the immune system is controlled by three physiological processes, i.e. wakefulness, REM (rapid eye movement) sleep and NREM (non-rapid eye movement) sleep (Imeri & Opp, 2009).
Altitude, temperature, circadian rhythms and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Henning Wackerhage, Kenneth A. Dyar, Martin Schönfelder
The 24 h sleep-wake cycle is another circadian clock-regulated process that can impact exercise performance, as well as adaptations and recovery after training (98). Intriguingly, sleep quality has also been linked to skeletal muscle clock function. In constant darkness Bmal1 knockout mice are completely arrhythmic, which also impacts their sleep quality and recovery after sleep deprivation (99). To identify the organ responsible for these changes, researchers re-introduced constitutively high levels of BMAL1 in different organs of Bmal1 knockout mice (100). This kind of supraphysiological BMAL1 rescue in the brain did not restore normal sleep, suggesting that Bmal1 expression outside the brain may be responsible. They next expressed a constitutively high BMAL1 gene selectively in skeletal muscles of the otherwise Bmal1-deficient mice. This was sufficient to restore the amount of NREM (Non rapid eye movement) sleep and improve the ability to recover from sleep loss. While these data showed that skeletal muscle-specific BMAL1 can affect sleep, the precise mechanisms by which muscle communicates with the brain, the key organ for sleep, remain unidentified.
Sleep disorders and pregnancy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Numerous studies have examined changes in sleep architecture during pregnancy with variable findings (20–24). Most of these studies were however consistent in noting lighter and more disrupted sleep as pregnancy progresses. Wake after sleep onset increased from the second to third trimester, where as REM sleep decreased from the first trimester to second (24,25). Brunner et al. also found, by spectral analysis, a progressive decrease in EEG power density in non-rapid eye movement sleep (25).
Interaction between slow wave sleep and elevated office blood pressure in non-hypertensive obstructive sleep apnea patients: a cross-sectional study
Published in Blood Pressure, 2023
Ning Xia, Hao Wang, Lin Zhang, Xiao-Jun Fan, Xiu-Hong Nie
The interaction between sleep and hypertension has become apparent over past years. Sleep disorders have been confirmed to elevate blood pressure (BP) and develop hypertension [1–3], which is the most common prevalent risk factor for cardiovascular diseases [4]. Sleep comprises of two states, including rapid eye movement sleep and non-rapid eye movement sleep [5]. Slow wave sleep (SWS), one part of non-rapid eye movement sleep, increases vagal tone and reduces sympathetic tone, which consequently decreases heart rate and BP [6,7]. Experimental studies showed that SWS deprivation significantly attenuated nocturnal blood pressure decline [8]. Further prospective population-based studies supported the same conclusion [9,10]. Fung et al. [9] found incident hypertension was associated with decreased SWS percentage after multiple adjustments in a cohort of elderly men. Consistently, another study observed lower levels of percentage SWS increased odds of incident hypertension in both men and women independent of potential confounders [10].
Dieckol is a natural positive allosteric modulator of GABAA-benzodiazepine receptors and enhances inhibitory synaptic activity in cultured neurons
Published in Nutritional Neuroscience, 2021
Sangoh Kwon, Jong Hoon Jung, Suengmok Cho, Kwang-Deog Moon, Jaekwang Lee
Phlorotannin supplement (PS) is a marine polyphenol that is derived from brown algae. Previous studies have reported that PS possesses many potential health benefits, such as anti-diabetic, anti-cancer, anti-oxidation, and antibacterial effects [10,11]. In addition, PS has exhibited sleep-promoting effects. For example, phlorotannin extract from Ecklonia cava reduces sleep latency and increases sleep duration by promoting non-rapid eye movement sleep (NREMS) in mice [12–15]. Phlorotannins (dieckol, eckol, eckstolonol, and triphlorethol A) have been characterized as ligands of the GABAA-BZD receptor. A study of binding assays with GABAAR and in vivo sleep assays with flumazenil (FZL), a direct BZD antagonist, have indicated that phlorotannin extracts included dieckol may inhibit synaptic networks by increasing GABAergic transmission via binding to the BZD site on GABAARs [12]. Although each single molecules in E. cava showed a possibility to work on inhibitory synapse in brain through GABAA-BZD receptors, nevertheless, direct functional evidence for the effect of a single compound from PS or its extract in enhancing GABAAR activation via the BZD site is unclear.
Rethinking the use of hypnotics for treatment of insomnia in the elderly
Published in Expert Opinion on Pharmacotherapy, 2021
A common belief is that humans need less sleep as they age. No evidence for this exists, however. Indeed, it is more likely that age-related disorders (co)affecting the nervous system, as well as psychotropic medications, spoil the quality of sleep, leading to an increased need for sleep time in order to fulfill its functions. For reasons only partly understood, some sleep parameters change with healthy aging [10,11]: during midlife, between the ages of 35 and 50 years, deep slow wave sleep (SWS) is replaced by lighter NREM (non-rapid eye movement) sleep, whereas in late life, after the age of 70, REM sleep declines and sleep becomes more fragmented. These changes are paralleled by hormonal variations. Less SWS sleep coincides with reduced levels of growth hormone, whereas less REM sleep coincides with increased cortisol levels in the evening. Experimental evidence indicates that a homeostatic sleep drive is responsible for midlife changes in SWS and changes in growth hormone production, whereas REM and cortisol changes are due to flattening of the circadian drive to sleep and wakefulness. This flattening of endogenously generated 24-h variation is also thought to result in instability of REM sleep and sleep fragmentation in later life [11,12].