KIN240 Principles of Biobehavioral Health PDF

Notes KIN240: Principles of Biobehavioral Health Sleep Understanding the Biological Drive Despite general societal awareness that sleep relates to health, we still have relatively little understanding of why this is. However, some insight is provided by taking into consideration the underlying archi...

Notes KIN240: Principles of Biobehavioral Health Sleep Understanding the Biological Drive Despite general societal awareness that sleep relates to health, we still have relatively little understanding of why this is. However, some insight is provided by taking into consideration the underlying architecture of sleep and its hypothesized biological purpose. In doing so, the relationship between physical activity and sleep becomes almost an expected outcome. Sleep Health — A pattern of sleep–wakefulness, adapted to individual, social, and environmental demands, that promotes adequate functioning of physical, mental, and social processes. Characterized by subjective satisfaction with sleep, sustained alertness during waking hours, appropriate timing, and adequate efficiency and duration. The vast majority of research on sleep as it relates to health has focused upon the negative consequences of poor or restricted sleep rather than the potential benefits of good sleep. As such, the state of the literature is largely more focused on the idea of sleep deficiency — a deficit in the quantity or quality of sleep obtained versus the amount needed for optimal health. In many ways this orientation of sleep research reflects pre–1940's era perspectives of health (e.g., good sleep is the avoidance of problematic sleep; health as the absence/avoidance of illness, disease, and debilitating conditions). The idea of framing healthy sleep as only that which is necessary to promote adequate functioning appropriate for individual, social, and environmental demands (aligning with modern perspectives of health), is only starting to become integrated into this area of research. Accordingly, it is important to acknowledge that the present state of the literature provides minimal insights beyond this negative perspective — poor sleep is definitely bad, while good sleep is simply not bad. Nevertheless, evidence has consistently observed that poor sleep is related to greater overall mortality risk, heart disease, diabetes, and hypertension. © Michigan State University Chapter 9 78 Notes KIN240: Principles of Biobehavioral Health Sleep Time Duration [Time in Bed] — The duration of the period from going to bed to getting out of bed. Sleep Time Duration [Actual Sleep Time] — The total duration of the period in a non–awake state. The Canadian 24–hour Movement Guidelines recommendations for sleep specifically utilized the recommended sleep time duration from the National Sleep Foundation. These guidelines recommend 9 to 11 hours of sleep for children aged 5 to 13, 8 to 10 hours for children aged 14 to 17, and 7 to 9 hours of sleep for adults. The recommendation for sleep duration in adults similarly aligns with consensus statements by the American Academy of Sleep Medicine and the Sleep Research Society. However, an important point emphasized by the panel that created these guidelines for the National Sleep Foundation is that some individuals may deviate from the recommended times with no adverse (harmful or unfavorable) effects. However, individuals with sleep durations which excessively deviate from these recommended sleep durations may have serious health problems already or may be compromising their health and wellbeing by intentionally restricting sleep — if those behaviors are sustained for a long period. Additionally, another critical clarification is that although sleep time duration recommendations are used as the fundamental guideline behavior; this is simply a reflection of the evidence base surrounding the importance of sleep for health. Population level studies in this area do not typically differentiate between time in bed and actual sleep time. Since actual sleep time is less than the time spent in bed, these studies tend to bias data towards higher sleep duration estimates. Within research on the relationship between sleep, health, and wellbeing; there are five key dimensions of sleep known as SATED that are particularly relevant: Satisfaction with sleep, Alertness during waking hours, Timing of sleep, sleep Efficiency, and sleep Duration. The concept of Satisfaction with sleep or quality of sleep reflects the subjective assessment of sleep quality that is independent from the quantity of sleep obtained. So an individual who sleeps for a long duration may still report perceiving the sleep to be of low quality. This dimension of sleep has been found to be particularly important for mental health with individuals who chronically report poor quality sleep also exhibiting greater prevalence of anxiety and depression. Alertness reflects the ability to maintain attentive wakefulness during the day. Although it can seem odd to characterize a dimension of sleep as its absence; an individual will have greater difficulty maintaining attentive wakefulness during the day if poor sleep occurs. This dimension of sleep has been found to be an important factor in risks associated with © Michigan State University Chapter 9 79 Notes KIN240: Principles of Biobehavioral Health accidents, poor academic performance, and medication errors. Sleep Timing reflects the placement of sleep within the 24–day — the timing of going to bed/waking up, and the midpoint of sleep time. Across a number of investigations, later sleep timing and variability in sleep timing have been associated with adverse cardiometabolic health outcomes and greater risk of obesity; and is a critical issue in the context of shift workers and those with variable scheduling practices. Sleep continuity or Efficiency reflects the ease of falling and returning to sleep as well as the ability to sleep throughout the night without waking up. This dimension of sleep has been found to be particularly important in the regulation of perceptions of stress and emotional reactivity. The concept of sleep Duration represents a major dimension that is commonly assessed within population–level investigations but it has been argued that it may be the least relevant for health and wellbeing outside of circumstances associated with severe sleep restriction/deprivation. However, individuals who exhibit deviant patterns of sleep duration exhibit greater risk of mortality from all causes. Sleep — A reversible behavioral state of perceptual disengagement from and unresponsiveness to the environment. However, a more refined understanding of the relationship between sleep and health may be provided by assessing more specific components of sleep. The concept of sleep is based on both physiological and behavioral changes that occur during this state. Although sleep is often conceptualized as an inactive brain in an inactive body, there is a characteristic pattern to sleep whereby both the brain and body cycle through periods of greater activity. This pattern is referred to as Sleep Architecture and characterizes the stages of sleep into wakefulness (stage W), multiple stages of non–rapid eye movement sleep (NREM), and rapid eye movement sleep (REM). The wakefulness sleep stage (stage W) reflects the transition from fully alert wakefulness to drowsiness. If your father is sitting on the couch watching TV and starts to 'nod off', this is the sleep stage you are observing. If we were to put electrodes on his scalp to measure his brain activity using electroencephalography (EEG), we would be able to observe the hallmark of this sleep stage: the presence of a posterior dominant rhythm (also known as alpha rhythm or alpha bursts) within EEG activity that occurs when the eyes close. This pattern of activity reflects EEG activity within the 8 to 13 hertz frequency range that is relatively small over frontal brain regions and grows progressively larger over occipital (towards the back of the head) regions. When the © Michigan State University Chapter 9 80 Notes KIN240: Principles of Biobehavioral Health eyes are open this posterior dominant rhythm dissipates (goes away). Another facet of the wakefulness sleep stage is reactivity to external stimuli. In response to noises or other stimuli (such as changing what is playing on the TV), your father will still exhibit alterations in brain activity and reactive eye movements indicating general awareness of the external stimuli. Finally, during this stage the individual may exhibit hypnic jerks — irregular spontaneous or reactive movements of all or part of the body that can sometimes be accompanied by a sense of falling. Non–rapid eye movement (NREM) sleep encompasses a number of separate stages of sleep that are characterized by progressive decreases in responsiveness to external stimuli. Historically, the characterization of this aspect of sleep subdivided it into 4 distinct stages; however, the American Academy of Sleep Medicine (AASM) now classifies NREM sleep into 3 stages (N1, N2, N3) predominantly on the basis of EEG activity. The NREM Sleep stage 1 (N1) reflects the period in which an individual moves from drowsiness to light sleep, representing the first point at which an individual would be considered to be asleep. However, an individual can still be easily woken from this sleep stage and if they are, may not feel like they were asleep. So even though your father had officially fallen asleep while watching the TV; if you were to wake him, he would likely feel like he was just letting his eyes close for a bit and wasnt actually sleeping. The hallmark characteristic of this sleep stage is the presence of theta waves reflecting EEG activity within the 4 to 7 hertz frequency range as well as vertex sharp waves (which look somewhat like a sail boat) that are most prominent over central (the middle) regions. During this stage there is usually a reduction in muscle tone as muscles relax, slow eye movements, as well as initial reductions in body temperature, blood pressure, cardiac and ventilatory rate. The time it takes to transition from a state of wakefulness to this sleep stage is referred to as sleep onset latency. Individuals who take more than 60 minutes to transition from wakefulness to NREM Sleep stage 1 (N1) are considered to have poor sleep onset latency (trouble falling asleep). Whereas an individual who takes 15 to 30 minutes to transition to this stage is considered to have good sleep onset latency. NREM Sleep stage 2 (N2) reflects the second phase of light sleep. The hallmark characteristic of this sleep stage is the presence of sleep spindles which are bursts of EEG activity within the 11 to 16 hertz frequency range that present maximally over frontal and central regions. These sleep spindles are thought to reflect periods in which sensory inputs are 'disconnected' in the brain to optimize the process of long–term memory consolidation. A second hallmark characteristic of NREM Sleep stage 2 (N2) is the presence of K–complexes which are single positive and then negative deflections in the EEG activity © Michigan State University Chapter 9 81 Notes KIN240: Principles of Biobehavioral Health that present maximally over frontal regions. These K–complexes can occur either spontaneously or in response to an external stimulus in the environment — indicating that individuals retain some degree of environmental awareness during this sleep stage. NREM Sleep stage 3 (N3) combines the original 3rd and 4th stages of sleep and reflects a period of sleep known as deep sleep or slow wave sleep. If awakened during this sleep stage, the individual may experience grogginess (weariness, fatigue, dazed). The hallmark characteristic of this sleep stage is the presence of long, slow EEG activity known as delta waves within the 0.5 to 2 hertz frequency range that presents maximally over frontal regions. However, sleep spindles and K complexes may still occur during this sleep stage. During this stage movement of the eyes and body are not typically seen and body temperature, blood pressure, cardiac and ventilatory rate all fall to their lowest levels. Consistent with its name, rapid eye movement sleep (REM) is characterized by rapid eye movements that occur despite the eyes being in a closed state. Rapid eye movement sleep is considered the deepest stage of sleep, however the activity of the brain returns to nearly the same levels as those observed while awake as this stage is the period in which most dreams occur. During this stage of sleep, hyperpolarization of spinal motor neurons contributes to muscle immobility referred to as atonia and the abolishment of spinal reflexes. However, minor brief, jerky twitches of the body can still occur. During rapid eye movement, sleep brown adipose tissue becomes more active within tissues near the spinal cord contributing to increases in body temperature, and blood pressure, cardiac and ventilatory rate all increase to near the same levels observed during wakeful states. The transition between stages of sleep is often visualized using a hypnogram to depict the time spent within each stage of sleep. During sleep, individuals follow a typical sleep architecture pattern. The prototypical pattern is W to N1 to N2 to N3 then back to N2 before going into REM sleep. However, following the first sleep cycle this is often shortened to cycle from N2 to N3 then back to N2 before going into REM sleep. In humans, this sleep architecture pattern usually lasts around 90 to 100 minutes for each cycle and four to five sleep cycles are completed. But interestingly, the amount of time spent within each sleep stage varies by sleep cycle. Individuals will usually only spend five to ten minutes in NREM Sleep stage 1 (N1) and may not return to this stage for the remainder of the sleep. The time spent in NREM Sleep stage 2 (N2) and REM sleep is relatively minimal during initial sleep cycles and progressively increases during the duration of the sleep, such that the final REM stage can last almost an hour in some cases. In contrast, during the initial sleep cycles there is greater time spent in © Michigan State University Chapter 9 82 Notes KIN240: Principles of Biobehavioral Health NREM Sleep stage 3 (N3), but with successive cycles the time spent in this stage decreases and may even be absent. Exemplar Sleep Cycle Pattern W N1 N2 N3 N2 REM 25 10 15 40 15 15 15 35 20 25 1 2 25 30 25 35 Fourth Cycle 35 15 35 45 Fifth Cycle 40 First Cycle Second Cycle Third Cycle Minutes in each stage. The gold–standard approach for assessing sleep stages is through the use of polysomnography (PSG) which assesses EEG activity, blood oxygenation, heart rate, ventilatory rate, as well as leg and eye movements. This approach enables characterizing the specific attributes associate with each sleep stage that align with the criteria set forth by the American Academy of Sleep Medicine. However, the nature of this measurement approach means that sleep assessments must typically be done within specially equipped sleep laboratories that have staff appropriately trained in setting the person up and monitoring them while they sleep. More recent advances in technology have enabled the ability to bring many of these measures into home–based environments and even consumer–grade products exist which can incorporate EEG–based approaches into devices that could be self–applied for regular home–based monitoring of these aspects of sleep. Absent the use of EEG, approaches for assessing sleep stages such as those used by Fitbit and Apple watches rely upon integrating heart rate and accelerometry measures to try to differentiate what stage of sleep an individual may be in. Although these devices all claim to use proprietary algorithms for differentiating sleep stages, the fundamental approach used by all is relatively straightforward. Recall that in light sleep — NREM Sleep stage 1 (N1) and NREM Sleep stage 2 (N2) — there are reductions in heart rate but still the potential for the body to move. So if you are sleeping in this stage we should see some amount of movement (typically below that of normal day to day activity) but heart rate should be relatively low. In deep sleep (NREM Sleep stage 3; slow–wave sleep) heart rate is typically suppressed as is movement of the body. So if you are in this stage we should see exceptionally low movement as well as low heart rate. Within REM sleep, heart rate becomes elevated to similar levels as waking but movement of the body is suppressed. So if there is exceptionally little movement but an increase in heart rate this would indicate being in REM sleep. By combining measurement of movement using accelerometry and heart © Michigan State University Chapter 9 83 Notes KIN240: Principles of Biobehavioral Health rate it is possible to segment sleep stages into wakefulness (when there is both normal heart rate and movement is diminished relative to daily activity but more present than in deep sleep and REM sleep), light sleep (combining NREM Sleep stage 1 and stage 2), deep sleep (NREM Sleep stage 3; slow–wave sleep), and REM sleep. Why do we sleep? Among the fundamental mechanisms that coordinate and govern sleep (and conversely wakefulness), the most well known is the circadian rhythm. Circadian rhythms are highly heritable — about half of the variation in circadian rhythms is attributable to specific genetic factors — and predominately driven by daylight. Although the circadian system plays a critical role, the daily rhythms of sleep and wakefulness are highly influenced and in some cases even over–ridden by neural, behavioral, and environmental factors. At the most basic level, however, the regulation of sleep and wakefulness is the result of the effects of two opposing factors: circadian phase and homeostatic sleep pressure. Within the circadian system, the suprachiasmatic nucleus (SCN) of the hypothalamus serves as the central pacemaker that generally follows a 24–hour cyclic period and is fundamentally a biological clock. Interestingly, regardless of if an animal is awake during the day (diurnal) or awake at night (nocturnal), the activity of the suprachiasmatic nucleus (SCN) in the animal increases in response to daylight. Although the suprachiasmatic nucleus (SCN) is important, the critical hub of the circadian system is the dorsomedial hypothalamic nucleus (DMH) which receives inputs from the suprachiasmatic nucleus (SCN) as well as a number of other systems (receiving information regarding food, temperature, and social cues) to generate a coordinated and adaptable sleep–wake rhythm. The primary role of the dorsomedial hypothalamic nucleus (DMH) is in coordinating the generation of a wake–promoting signal through the ascending arousal system. The ascending arousal system follows two primary branches bringing online the motor and sensory pathway by way of the thalamus and the arousal promoting pathway by way of the locus coeruleus, dorsal and median raphe nuclei, and tuberomammillary nucleus. In contrast to what might be expected, the circadian wake promoting signal is relatively minimal following waking but becomes progressively stronger during the course of the day. The peak of this wake–promoting signal occurs between 7 and 10pm and then rapidly diminishes. When the signal from the dorsomedial hypothalamic nucleus (DMH) diminishes, the ventrolateral preoptic nucleus (VLPO) of the hypothalamus becomes active to promote sleep. The ventrolateral preoptic nucleus (VLPO) sends © Michigan State University Chapter 9 84 Notes KIN240: Principles of Biobehavioral Health inhibitory signals to the various pathways within the ascending arousal system to create a sleep–promoting signal. Upon onset of sleep, the circadian sleep–promoting signal is relatively minimal but becomes progressively stronger during the course of the sleep; peaking between 4 and 6am before rapidly diminishing. The interplay between neural circuits within the circadian system is commonly described as a flip–flop switch (also known as a rocker switch). This concept borrows from electrical engineering to describe a circuit that minimizes transitional states and therefore has abrupt transitions. Rather than wake–promoting and sleep–promoting pathways having distinct and fully independent systems that could potentially both be active at the same time, they are mutually inhibitory upon the other. When the dorsomedial hypothalamic nucleus (DMH) is activating the wake–promoting pathway, the dorsomedial hypothalamic nucleus (DMH) and the branches of the ascending arousal system serve to inhibit the ventrolateral preoptic nucleus (VLPO) to prevent the sleep–promoting pathway. But conversely, when the ventrolateral preoptic nucleus (VLPO) is activating the sleep–promoting pathway it serves to inhibit the branches of the ascending arousal system to prevent the wake–promoting pathway. This flip–flop circuit explains the relatively abrupt transitions between sleep and wake. The nature of this circuit, however, means that it is also prone to influence from homeostatic sleep pressure. The idea of homeostatic sleep pressure reflects the fundamental basis that humans accumulate a need to sleep during prolonged periods of wakefulness. This is colloquially referred to as sleep debt based upon evidence that inadequate sleep can appear to accumulate and increase the drive/pressure to obtain sleep. Although the specific mechanisms that contribute to increasing homeostatic sleep pressure are still unclear, it is generally thought that accumulation of adenosine may play a role. Adenosine is a byproduct of cellular metabolism and has been observed to accumulate during prolonged wakefulness. When injected near the ventrolateral preoptic nucleus (VLPO), adenosine causes rodent models to sleep. Conversely, the properties of caffeine cause it to block adenosine from binding to receptors resulting in maintaining a wakeful state. However, there may be multiple other mechanisms (referred to as somnogens) and inflammatory factors which accumulate during wakefulness that serve to activate the sleep–promoting pathway (or inhibit the wake–promoting pathway) to induce sleep. Accordingly, upon entering a waking state there should be very little homeostatic sleep pressure. Therefore, the circadian wake–promoting pathway need only be minimally active to maintain a wakeful state. However, as homeostatic sleep pressure accumulates throughout the © Michigan State University Chapter 9 85 Notes KIN240: Principles of Biobehavioral Health day, the activity in the circadian wake–promoting pathway needs to to proportionately increase. At some point, either driven by circadian influences or homeostatic sleep pressure, the flip–flop switch causes the sleep–promoting pathway to actively inhibit the wake–promoting pathway until sleep occurs. Since the homeostatic sleep pressure remains elevated the circadian sleep–promoting pathway need only be minimally active to maintain a sleeping state. However, as that homeostatic sleep pressure dissipates (goes away), the activity in the circadian sleep–promoting pathway needs to to proportionately increase to maintain the sleeping state. Why do we need to sleep? Despite the well–established research demonstrating that sleep is essential, such that sleep deprivation/restriction can result in both short and long–term consequences for health and wellbeing; the biological function of why we sleep remains unknown. Nevertheless, several theories of the function of sleep have been proposed. It is important to note that the major theories are not mutually exclusive. Specific aspects of sleep may provide opportunities for each of the underlying mechanisms proposed to play a role. Protective Field Theory of Sleep — The cyclic pattern of sleep balances the fundamental biological function of sleep with the need for environmental awareness. Since sleep represents the time when the organism is most vulnerable to predators and environmental risks, there is a biological imperative to minimize this risk. Although the protective field theory of sleep is often misunderstood as somehow relating to sleep in general, this theory is actually attempting to explain the biological basis for different sleep stages. During both NREM Sleep stage 3 (N3) and REM sleep, the organism exhibits exceptionally low muscle tone and upon awaking take the longest to return to fully conscious states. As such, the benefit of cycling through sleep stages — specifically separating NREM Sleep stage 3 (N3; slow–wave) and REM sleep with periods of NREM Sleep stage 2 (N2; light) sleep — is to provide an opportunity for greater environmental awareness and the ability to rapidly transition from sleep to fully awake states. It also explains why time spent in NREM Sleep stage 2 (N2; light) is relatively short during early phases of sleep but grows progressively longer with sleep duration. During early portions of the sleep, the individual is likely relatively safe — otherwise signals integrated into the dorsomedial hypothalamic nucleus (DMH) would be helping to keep the individual awake — but as sleep duration increases the environmental risks may have changed. Therefore, it is biologically advantageous to become more aware of external stimuli © Michigan State University Chapter 9 86 Notes KIN240: Principles of Biobehavioral Health as the sleep duration increases. As humans spend nearly half of their total sleep duration in NREM Sleep stage 2 (N2; light), this general degree of environmental awareness present within this sleep stage is biologically advantageous to avoid predation and increase survival. The assumption of this theory then is that light stages of sleep are not a biological necessity but rather exist as a protective field for NREM Sleep stage 3 (N3) and REM sleep which are necessary. Energy Conservation Theory of Sleep — Sleep enables an opportunity to adopt a low–energy state. Although there are a number of variants of energy conservation theories attributed to different individuals, the fundamental premise is that times when organisms sleep also tend to be times when it would be biologically advantageous to adopt a low–energy state. Although normal wakeful states represent periods of high energy expenditure, they also tend to represent periods in which there is greater opportunity for energy accumulation. Conversely, sleep behaviors tend to occur during periods when their is reduced opportunity for energy accumulation or when the risks associated with energy accumulation are elevated. For instance, as humans have relatively poor night vision, the ability to successfully acquire food without incurring injury during the night is diminished. Given this situation, it is preferable to enter into the low–energy state of sleep and to conserve energy as much as possible. Similarly, in other organisms, the relative timing of their sleep patterns (diurnal or nocturnal) tends to align with those periods when the food they eat is most abundantly available and the risks of obtaining that food are lower. Consistent with this theory, organisms with higher metabolic rates also tend to sleep for longer periods than organisms with lower metabolic rates. The benefit of entering into sleep is that metabolic rate during sleep tends to be 5 to 15% lower than during waking states. Although generally applicable to all stages of sleep, energy conservation theories tend to focus upon the idea of energetic trade–offs between sleep stages. Although the brain is highly active during REM sleep, the increased energy consumption is offset by the absence of motor function. During NREM Sleep stage 2 (N2; light sleep), the brain is less active so the body can allow motor function to resume while still maintaining this lower energy state. Although not always explicitly indicated, when discussing human sleep behaviors energy conservation theories will occasionally begin to incorporate aspects of the Protective Field Theory of Sleep into justifications for adopting a less efficient stage during light sleep. © Michigan State University Chapter 9 87 Notes KIN240: Principles of Biobehavioral Health Restorative Theory of Sleep — Sleep enables an opportunity for cellular renewal and regeneration that may not be possible during waking states. Restorative theories of sleep have also been presented in a number of forms and attributed to different individuals, but the underlying conceptual argument is that sleep provides an opportunity for the body and brain to allocate energetic resources towards restorative function. A key clarification is that these theories do not actually argue that cellular repair can only occur during sleep. Rather, some aspects of cellular repair and renewal may be more efficiently engaged in when the body is not awake and moving. The major evidence in support of this theory of sleep is that hormones released during sleep tend to have predominately anabolic (tissue building) function while catabolic hormones tend to be suppressed. Restorative theories of sleep tend to focus on NREM Sleep stage 3 (N3; slow–wave sleep) as this stage of sleep is considered particularly important for supporting musculoskeletal recovery and growth as well as promoting enhanced immune function. For instance, growth hormones are predominately released during this stage. Within the brain, protein synthesis has been found to be enhanced during slow–wave sleep; and deprivation of slow–wave sleep has been found to impair the growth of new neurons (neurogenesis). During periods of greater growth — such as during adolescence and pregnancy — time spent in slow–wave sleep is increased. In this sense, upon falling asleep the body spends a large portion of time within slow–wave sleep presumably to begin restorative function. The gradual reduction in time spent in slow–wave sleep over the course of the night would then be an expected occurrence reflecting a reduced need for cellular repair and renewal. REM sleep also appears to be a time when neural repair and regeneration processes occur, and is implicated as a period when oligodendrocytes (brain cells that generate and maintain myelin axonal coatings) are the most active. During REM sleep, astrocytes (glial cells that outnumber neurons 5 to 1 which are involved with regulating blood flow, altering neurotransmitters, and are involved in the maintenance of neurons) work to clear neural metabolic waste and promote flushing of neural tissues by shrinking and expanding. In this sense, the greater brain activity observed during REM sleep may reflect the restorative clearance of metabolic byproducts by microglia and astrocytes. As neuronal environments are improved and neurotransmitters are replaced, resting membrane potentials within neural tissues may be altered resulting in increased brain activity. Since this would presumably also increase the likelihood of unintentional firing of motor patterns, it would also explain why hyperpolarization of spinal motor neurons occurs as it would prevent these motor patterns © Michigan State University Chapter 9 88 Notes KIN240: Principles of Biobehavioral Health from eliciting movement. Such a perspective would similarly align with the observation that REM sleep is relatively short during early periods of the sleep, but as microglia and astrocytes are able to clear greater neural waste in the brain, the time spent in REM sleep increases. Memory Consolidation – Network Integrity Theory of Sleep — Sleep provides a period for the reorganization and strengthening of neural networks critical to support memory and daily function. Memory consolidation theories and synaptic–neuronal network integrity theories build upon research focusing on the relationship between sleep and cognitive function. Such research has investigated not only the role of sleep deprivation/restriction on memory/cognition but also on how time spent in specific stages of sleep impacts upon the ability to sustain information within long–term memory and maintain high–levels of cognitive performance. The fundamental conclusion is that sleep provides a critical period when neural networks underlying memory and high level cognitive processes reorganize and strengthen. In particular, both the time spent in NREM Sleep stage 3 (N3; slow–wave sleep) and the density of sleep spindles appear to be particularly important for supporting memory consolidation. Whereas time spent in REM sleep appears particularly important for consolidating emotionally charged memories and may promote better removal of irrelevant or unnecessary information from memory. As motor activity can impair or interfere with memory consolidation; during both NREM Sleep stage 3 (N3; slow–wave sleep) and REM sleep, motor outputs are suppressed potentially as a means of avoiding this issue. Influence of Physical Activity on Sleep Societally there tends to be a perception that individuals should avoid engaging in physical activity too close to when they go to bed. However, research in this area indicates that the beneficial influence of physical activity remains the same whether it is performed more than eight hours before bedtime, three to eight hours before, or less than three hours before bedtime. The exception being that engaging in physical activity within less than three hours of going to bed reduces the time spent within NREM Sleep stage 1 (N1), appearing to indicate that it may help individuals to fall asleep faster. Regardless of when the physical activity is engaged in, following even a single bout of physical activity there appears to be an increase in total sleep time, improved sleep efficiency, and a shift towards increasing the amount of time spent within NREM Sleep stage 3 (N3, slow–wave sleep) and decreasing the amount of time in REM sleep. Although no differences in the type of physical activities or the intensity of physical have been observed; for © Michigan State University Chapter 9 89 Notes KIN240: Principles of Biobehavioral Health moderate–to–vigorous intensities of physical activity, longer duration of activity (up to around 90 minutes) is associated with greater benefits. Similarly, overwhelming evidence indicates that habitual (chronic) physical activity engagement is associated with enhanced perceptions of sleep quality (satisfaction), increased daytime alertness, faster sleep onset latency, increased duration of sleep, and greater time spent within NREM Sleep stage 3 (N3, slow–wave sleep); generally mirroring the effects of a single bout of physical activity. Further, improvements in sleep associated with regular engagement in physical activity have also been observed within individuals with sleep disorders and has been found to be associated with a reduced need for the use of sleep medications. The beneficial effects of both acute and chronic physical activity engagement on sleep have been attributed to a number of potential mechanisms. Early research attributed these effects to thermogeneic responses (Thermogenic Hypothesis); whereby changes in core body temperature that occurred during activity served as a trigger to promote better sleep outcomes. The underlying concept was that the increase in core body temperature during activity were followed by rapid decreases in core body temperature following the cessation of the activity. This rapid decrease in body temperature serves as a somnogen to activate the sleep–promoting pathway to induce sleep more quickly. However, such explanations are a poor fit for observations that even physical activity eight hours prior to going to sleep has beneficial effects; and have come into question given that these effects still occur in context where body temperature does not rise during activity. It may also be that physical activity provides an opportunity for greater exposure to light (Light Exposure Hypothesis). As light therapy has been found to promote better sleep outcomes, the engagement in physical activity without outdoor settings during daylight hours or within well–lit gyms may contribute to the beneficial effects of physical activity on sleep. However, such a mechanism would suggest that individuals who choose to engage in physical activity during non–daylight hours or within low–light gym environments may minimize the beneficial influence of the activity engagement as it relates to sleep. Despite such attributions, the general perspective is that the beneficial relationship of physical activity for sleep may actually be the result of aligning with two hypothesized fundamental reasons why we sleep: energy conservation and body restoration. In the context of the energy conservation theory of sleep, the increased energy expenditure that occurs during physical activity requires an adaptive response to attempt to minimize total daily energy expenditure. So long as the physical activity is not excessive in duration (which might indicate a threat to survival); the energy expended during physical activity can © Michigan State University Chapter 9 90 Notes KIN240: Principles of Biobehavioral Health be potentially offset through sleep. Therefore, enabling the organism to enter sleep faster and spend more time within the most energy efficient stage of sleep is a reactive response ultimately in service of maintaining low energy expenditure. In the context of the restorative theory of sleep, physical activity places substantial stress upon physiological systems which then requires reparative processes to be engaged. So as the individual engages in more prolonged physical activity, metabolic byproducts are created and accumulate alongside inflammatory cytokines. There is also potential for the activity to induce skeletal muscle and tissue damage. The presence of these various metabolic and inflammatory markers may serve as somnogens to activate the sleep–promoting pathway to induce sleep more quickly. As a result of the activity, greater time must be spent within NREM Sleep stage 3 (N3; slow–wave sleep) to repair and regenerate the body. Finally, although it is commonly accepted that poor sleep contributes to impaired physical performance; the actual evidence indicates that poor sleep may not actually directly impact performance. Rather poor sleep contributes to a greater awareness of physical exertion and cognitive impairments associated with vigilance (being aware of potential dangers), sustaining attention, and emotional regulation. While these may impair physical performance in some circumstances, the larger issue is that each of these elements increase the relative risk of incurring an injury. Thus, it should come as no surprise that poor sleep is associated with a greater risk of incurring an exercise–related injury. Additional Resources: Hirshkowitz, M., Whiton, K., Albert, S. M., Alessi, C., Bruni, O., DonCarlos, L.,... & Hillard, P. J. A. (2015). National Sleep Foundation’s sleep time duration recommendations: Methodology and results summary. Sleep Health, 1(1), 40-43. http://dx.doi.org/10.1016/j.sleh.2014.12.010 Hirshkowitz, M. (2004). Normal human sleep: An overview. Medical Clinics, 88(3), 551-565. http://dx.doi.org/10.1016/j.mcna.2004.01.001 Saper, C. B., Scammell, T. E., & Lu, J. (2005). Hypothalamic regulation of sleep and circadian rhythms. Nature, 437(7063), 1257-1263. https://doi.org/10.1038/nature04284 © Michigan State University Chapter 9 91