ENTRIES A–Z
Philip Winn in Dictionary of Biological Psychology, 2003
Slow-wave sleep refers to quiet sleep in the mammal during which slow waves are recorded from the ELECTROENCE-PHALOGRAM (EEG). These slow waves range in frequency from 0.1 to 4 Hz. The waves from 1 to 4 Hz are termed DELTA WAVES, whereas more recently the waves below 1 Hz have been termed the slow oscillation. In fact, the delta waves ride on top of the slow oscillation. Slow waves increase in incidence and amplitude in a progression from sleep onset to the full development of slow wave sleep and thus in what has been divided into four stages in humans. In addition, another activity which occurs at a higher frequency (12-14 Hz) and with increasing then decreasing amplitude to form a spindle-like shape evoking the name SLEEP SPINDLE, occurs in the early stages of sleep. Thus in humans, a loss of alpha activity (marking relaxed wakefulness) occurs in stage 1, spindles riding on slower waves in stage 2 and a progressive increase in delta riding on slower waves in stages 3 and 4. Slow-wave sleep is referred to as QUIET SLEEP because there are few movements in deep slow-wave sleep, in contrast to REM SLEEP, when the eyes move and the extremities twitch or move. In addition, it was originally believed that no mental activity occurred during slow-wave sleep, in contrast to REM sleep, when DREAMING was shown to occur. However subsequent studies found that mental activity does occur in slow-wave sleep. This sleep mentation is reported as dream-like but described as less vivid and bizarre than the dreams of REM sleep.
Sleep Disorders in Older Adults
K. Rao Poduri in Geriatric Rehabilitation, 2017
A large meta-analysis of 65 overnight studies representing 3577 subjects across the entire age spectrum reported that, with age, the percentage time of REM sleep decreased, while the percentages of light sleep (stage 1 and stage 2 sleep) increased [5]. Furthermore, slow-wave sleep (SWS) had a gradual and linear decrease of 2% per decade in young and middle-aged adults. When only reviewing studies of elderly participants, SWS remained constant after the age of 60 years with no significant continued change with age [5]. Finally, men aged 16–83 years had an average decrease in the total sleep time of 27 minutes per decade from midlife into late age [6]. While these age-related changes are well documented, their consequences are not fully understood or extensively researched. However, in the current theoretical framework, such changes in sleep architecture are considered nonpathological and might reflect age-related neural degeneration [7].
The Internal Milieu Brain and Body
Rolland S. Parker in Concussive Brain Trauma, 2016
Hypocretins: The hypocretin system and the circadian seem to exchange activation. The hypocretins are two peptides that are synthesized exclusively in the lateral, posterior, and perifornical hypothalamus. They project to such monoaminergic centers as the LC noradrenergic, raphe nucleus (serotonergic), and ventral tegmental (dopaminergic) areas. Hypocretin is an excitatory neuropeptide that activates multiple neuromodulatory systems involved in the regulation of sleep-wake behavior. It activates neuromodulatory cell groups during wakefulness, but less so during slow-wave sleep. Its role during REM sleep is uncertain. While low hypocretin levels have been observed after head trauma, and may result in sleepiness, disturbed capacity to sleep seems more characteristic. Hypocretins may be important in HPA regulation during arousal, and in vagally mediated gastric acid secretion, SNS activation, and cardiovascular function (increased BP and heart rate). This arousal effect may modulate autonomic and sensory functions of the spinal cord, promote energy consumption, produce hyperthermia, and simulate sympathetic tone (Taheri et al., 2006).
Physical Activity and Cognition: A Mediating Role of Efficient Sleep
Published in Behavioral Sleep Medicine, 2018
Kristine A. Wilckens, Kirk I. Erickson, Mark E. Wheeler
Awakenings during sleep are less likely to occur during the deepest stage of sleep, slow-wave sleep (Neckelmann & Ursin, 1993). Slow-wave sleep involves neural synchrony predominantly over the prefrontal cortex, reflecting synchronized depolarizing of neurons (Steriade et al., 1993). Such neural synchrony over the prefrontal cortex may potentiate synapses within networks important for executive control. Slow-wave sleep has been shown to increase with exercise (Kline et al., 2013), and is linked to executive control and memory consolidation (Anderson & Horne, 2003; Mander et al., 2013; Wilckens et al., 2016). One proposed mechanism supporting a link between physical activity and sleep is the restoration hypothesis, which proposes that energy expenditure stimulates a restoration process whereby sleep allows the body and brain to recuperate (Buman & King, 2010; Driver & Taylor, 2000; Lopez, 2008). Accordingly, slow-wave sleep has been proposed to preferentially “restore” prefrontal cortex function (Anderson & Horne, 2003; Maquet et al., 1997; Muzur, Pace-Schott, & Hobson, 2002; Picchioni, Duyn, & Horovitz, 2013; Wilckens et al., 2016). Additionally, low sleep efficiency may reflect the disruption of multiple sleep features involved in cognition, including stage N2 spindles and rapid eye movement sleep. Future research will determine whether the sleep mechanism linking physical activity with executive control is synchronized neural firing, a restoration processes, or a combination of sleep features working together to enhance executive control.
Does breaking up prolonged sitting when sleep restricted affect postprandial glucose responses and subsequent sleep architecture? – a pilot study
Published in Chronobiology International, 2018
Grace E. Vincent, Sarah M. Jay, Charli Sargent, Katya Kovac, Michele Lastella, Corneel Vandelanotte, Nicola D. Ridgers, Sally A. Ferguson
In this study, regularly breaking up prolonged sitting with light-intensity walking was associated with small increases in stage N3 sleep (slow-wave sleep) and a decrease in stage N2 sleep and WASO. These findings partially support one previous study which investigated sleep of hypertensive adults using sit–stand desks compared to continuous sitting across two simulated 8-h workdays (Kline et al. 2017). Some subjective (WASO, sleep-onset latency and awakenings) but not objective (measured by wrist-actigraphy) improvements in sleep quality were reported (Kline et al. 2017). A recent review of the previous literature showed that acute exercise results in small increases in slow-wave sleep (Chennaoui et al. 2015). Slow-wave sleep plays a crucial role in recovery and sleep consolidation (Roth 2009), but the mechanisms linking physical activity and increases in slow-wave sleep are unclear. Further, it is unknown what characteristics of the physical activity (e.g. intermittent, amount) in the current study contributed to the increase in slow-wave sleep. The observed increase in the amount of slow-wave sleep with subsequent days of sleep restriction is supported by previous literature (Wu et al. 2010). Further research is needed to explore what aspects of breaking up sitting have benefits for subsequent sleep.
Association between sleep disorders and morning blood pressure in hypertensive patients
Published in Clinical and Experimental Hypertension, 2018
Xinran Li, Jiangbo Li, Kai Liu, Shenzhen Gong, Rufeng Shi, Pei Pan, Yujie Yang, Xiaoping Chen
The general characteristics of the subjects are shown in Table 1. Overall, our sample had a mean age of 57.4 ± 15.4 years (n = 144), 63.9% of the subjects were males, and 48.6% of the subjects had diabetes. Higher night-time systolic BP (SBP) (P < 0.001), night-time diastolic BP (DBP) (P < 0.001) and FBG (P = 0.033) existed in the morning hypertension group. The sleep characteristics of subjects are shown in Table 2. Compared with normal sleep characteristics, which are over 95% sleep efficiency, 47%-60% proportion of light sleep and 13%-23% proportion of slow wave sleep (28), our subjects showed decreases in sleep efficiency and the proportion of slow wave sleep, increases in the proportion of light sleep and MI. There were no significant differences between subjects with and without morning hypertension in the parameters of sleep architecture and sleep respiratory and severity of OSA (all P > 0.05) (Table 2).
Related Knowledge Centers
- Delta Wave
- Electroencephalography
- Explicit Memory
- Eye Movement
- Memory Consolidation
- Neocortex
- Rapid Eye Movement Sleep
- Muscle Tone
- NON-Rapid Eye Movement Sleep
- Neuron