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group_3_presentation_2_-_how_sleep_influences_the_body [2020/02/27 20:16] mehmoodm [Consequences of Sleep Deprivation] |
group_3_presentation_2_-_how_sleep_influences_the_body [2020/02/27 22:35] (current) gorganir |
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| Sleep consists of two main phases, non‐rapid‐eye‐movement sleep (NREM) and rapid‐eye‐movement (REM) sleep. A measure of vigilance can be obtained by measuring brain electrical activity with electroencephalography (EEG). In EEG, waking is characterized by low‐amplitude, high‐frequency waves. During NREM sleep, the amplitude of EEG waves increases and the frequency decreases, while in REM sleep, EEG is indistinguishable from waking state. These states can be separated based on muscle activity (measured using electromyography, EMG) and saccadic eye movements (measured using electro‐oculography, EOG). During waking, muscle activity is high; in NREM sleep, it decreases; and in REM sleep, it practically disappears. | Sleep consists of two main phases, non‐rapid‐eye‐movement sleep (NREM) and rapid‐eye‐movement (REM) sleep. A measure of vigilance can be obtained by measuring brain electrical activity with electroencephalography (EEG). In EEG, waking is characterized by low‐amplitude, high‐frequency waves. During NREM sleep, the amplitude of EEG waves increases and the frequency decreases, while in REM sleep, EEG is indistinguishable from waking state. These states can be separated based on muscle activity (measured using electromyography, EMG) and saccadic eye movements (measured using electro‐oculography, EOG). During waking, muscle activity is high; in NREM sleep, it decreases; and in REM sleep, it practically disappears. | ||
| - | <box 40% round center|> {{ :group3img13.png?400 |}} </box| Figure 5. EEG of different stages of sleep (Porkka‐Heiskanen et al., 2013)> | + | <box 40% round center|> {{ :group3img13.png?400 |}} </box| Figure 4. EEG of different stages of sleep (Porkka‐Heiskanen et al., 2013)> |
| During REM sleep, eyes undergo characteristic rapid movements, of which the state has got its name. A finer division of NREM sleep is based on the proportion of the low‐frequency, high‐amplitude waves (called slow‐wave activity, SWA). NREM sleep is divided into three stages (S1, S2 and S3) in increasing order of SWA. Sleep stages alternate in the course of the night in a regular manner: sleep starts by S1 and deepens via S2 to S3 and then proceeds to REM sleep. After the REM sleep period, the cycle starts from the beginning. The duration of one sleep cycle is about 90 min. The sleep stages calculated across the night are often presented as a hypnogram, which describes the order and duration of each sleep stage. During SWA sleep, virtually all cortical neurons are engaged in a slow (<1 Hz) oscillation consisting of alternating ON and OFF periods. During ON periods, cortical cells are depolarized and fire action potentials at a high rate, while during OFF periods, cells are hyperpolarized and silent. (Porkka-Heiskanen et al., 2013) | During REM sleep, eyes undergo characteristic rapid movements, of which the state has got its name. A finer division of NREM sleep is based on the proportion of the low‐frequency, high‐amplitude waves (called slow‐wave activity, SWA). NREM sleep is divided into three stages (S1, S2 and S3) in increasing order of SWA. Sleep stages alternate in the course of the night in a regular manner: sleep starts by S1 and deepens via S2 to S3 and then proceeds to REM sleep. After the REM sleep period, the cycle starts from the beginning. The duration of one sleep cycle is about 90 min. The sleep stages calculated across the night are often presented as a hypnogram, which describes the order and duration of each sleep stage. During SWA sleep, virtually all cortical neurons are engaged in a slow (<1 Hz) oscillation consisting of alternating ON and OFF periods. During ON periods, cortical cells are depolarized and fire action potentials at a high rate, while during OFF periods, cells are hyperpolarized and silent. (Porkka-Heiskanen et al., 2013) | ||
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| The two‐process model says that a homeostatic process (Process S) interacts with a process controlled by the circadian pacemaker (Process C), with time‐courses derived from physiological and behavioural variables. The model simulates successfully the timing and intensity of sleep in diverse experimental protocols. Electrophysiological recordings from the suprachiasmatic nuclei (SCN) suggest that Processes S and C interact continuously. A deficiency of Process S was proposed to account for both depressive sleep disturbances and the antidepressant effect of sleep deprivation (Borbely et al., 2016). The homeostatic process represents the need for sleep. It increases while awake and decreases while sleeping. The circadian rhythm depends on the suprachiasmatic nucleus. It is entrained in the external light-dark cycle, firing most rapidly during the light period, under the regulation of a special class of light‐sensitive retinal ganglion cells that contain the photopigment melanopsin. The C process would increase during the sleep state, thus ensuring continued sleep despite the diminishing homeostatic need for it toward the end of the sleep cycle (Saper et al., 2005). | The two‐process model says that a homeostatic process (Process S) interacts with a process controlled by the circadian pacemaker (Process C), with time‐courses derived from physiological and behavioural variables. The model simulates successfully the timing and intensity of sleep in diverse experimental protocols. Electrophysiological recordings from the suprachiasmatic nuclei (SCN) suggest that Processes S and C interact continuously. A deficiency of Process S was proposed to account for both depressive sleep disturbances and the antidepressant effect of sleep deprivation (Borbely et al., 2016). The homeostatic process represents the need for sleep. It increases while awake and decreases while sleeping. The circadian rhythm depends on the suprachiasmatic nucleus. It is entrained in the external light-dark cycle, firing most rapidly during the light period, under the regulation of a special class of light‐sensitive retinal ganglion cells that contain the photopigment melanopsin. The C process would increase during the sleep state, thus ensuring continued sleep despite the diminishing homeostatic need for it toward the end of the sleep cycle (Saper et al., 2005). | ||
| - | <box 40% round center|> {{ :group3img15.png?400 |}} </box| Figure 6. Two process model of sleep regulation (Patanaik, 2015)> | + | <box 40% round center|> {{ :group3img15.png?400 |}} </box| Figure 5. Two process model of sleep regulation (Patanaik, 2015)> |
| Sleep is regulated by the interaction of a variety of neurotransmitter systems in the brainstem, forebrain, and hypothalamus. A core region that is active during REM sleep is the subcoeruleus nucleus (SubC). It is hypothesized that glutamatergic SubC neurons regulate REM sleep and its defining features such as muscle paralysis and cortical activation. REM sleep paralysis is initiated when glutamatergic SubC cells activate neurons in the ventromedial medulla (VMM), which causes the release of GABA and glycine onto skeletal motoneurons. REM sleep timing is controlled by the activity of GABAergic neurons in the ventrolateral periaqueductal gray and dorsal paragigantocellular reticular nucleus as well as melanin-concentrating hormone neurons in the hypothalamus and cholinergic cells in the laterodorsal and pedunculo-pontine tegmentum in the brainstem (Fraigne et al., 2015). | Sleep is regulated by the interaction of a variety of neurotransmitter systems in the brainstem, forebrain, and hypothalamus. A core region that is active during REM sleep is the subcoeruleus nucleus (SubC). It is hypothesized that glutamatergic SubC neurons regulate REM sleep and its defining features such as muscle paralysis and cortical activation. REM sleep paralysis is initiated when glutamatergic SubC cells activate neurons in the ventromedial medulla (VMM), which causes the release of GABA and glycine onto skeletal motoneurons. REM sleep timing is controlled by the activity of GABAergic neurons in the ventrolateral periaqueductal gray and dorsal paragigantocellular reticular nucleus as well as melanin-concentrating hormone neurons in the hypothalamus and cholinergic cells in the laterodorsal and pedunculo-pontine tegmentum in the brainstem (Fraigne et al., 2015). | ||
| - | <box 40% round center|> {{ :group3img16.png?400 |}} </box| Figure 7. How the brain is involved in sleep regulation (Porkka‐Heiskanen et al., 2013)> | + | <box 40% round center|> {{ :group3img16.png?400 |}} </box| Figure 6. How the brain is involved in sleep regulation (Porkka‐Heiskanen et al., 2013)> |
| =====Conclusion - How To Improve Sleep Quality===== | =====Conclusion - How To Improve Sleep Quality===== | ||
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| Harvard Health Publishing. (n.d.). Blue light has a dark side. Retrieved from | Harvard Health Publishing. (n.d.). Blue light has a dark side. Retrieved from | ||
| https://www.health.harvard.edu/staying-healthy/blue-light-has-a-dark-side | https://www.health.harvard.edu/staying-healthy/blue-light-has-a-dark-side | ||
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| + | How Does Circadian Rhythm Impact Pilots? | Travel Blog. (2019, April 27). APR Travel Blog. https://www.airportparkingreservations.com/blog/circadian-rhythm-aviation/ | ||
| How to get a great nap. (2018, November 20). Retrieved from | How to get a great nap. (2018, November 20). Retrieved from | ||
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| Spadola, C. E., Guo, N., Johnson, D. A., Sofer, T., Bertisch, S. M., Jackson, C. L., … Redline, S. | Spadola, C. E., Guo, N., Johnson, D. A., Sofer, T., Bertisch, S. M., Jackson, C. L., … Redline, S. | ||
| - | (2019). Evening intake of alcohol, caffeine, and nicotine: night-to-night associations with | + | (2019). Evening intake of alcohol, caffeine, and nicotine: night-to-night associations with sleep duration and continuity among African Americans in the Jackson Heart Sleep Study. Sleep, 42(11). doi: 10.1093/sleep/zsz136 |
| - | sleep duration and continuity among African Americans in the Jackson Heart Sleep | + | |
| - | + | ||
| - | Study. Sleep, 42(11). doi: 10.1093/sleep/zsz136 | + | |
| Stickgold, R. (2005). Sleep-dependent memory consolidation. Nature, 437(7063), 1272–1278. | Stickgold, R. (2005). Sleep-dependent memory consolidation. Nature, 437(7063), 1272–1278. | ||
