10/11 - Consequences of Sleep Deprivation in Physiology and Human Performance

Question 1

What is mortality risk? Does sleep duration correlate with mortality risk in large population studies?

Answer 1

The risk that you’re going to die over a fixed period of time.

1. 12 (12% higher probability of dying relative to average sleepers) is relative risk for short sleepers
2. 3 (30% higher probability of dying) for long sleepers

Many other correlates in the variables you’re interested in (male, sick, overweight, poor etc.). Can be factored out.

Question 2

True or false? People that sleep less than 6-7 or more than 9-10 have increased mortality risk

What is the optimal time for sleep?

Answer 2

True

6.5 hours

Question 3

Increased sleep gives a higher risk for mortality. How is this studied? What is a problem in studying this?

Answer 3

Surrogate markers for illness used to study this (eg. obesity, vascular function, glucose metabolism, hormones etc.) and look at how sleep duration affects these things (in the laboratory). This works because we know these surrogate measure will lead to higher mortality through things like immune suppression etc.

Difficulty is that you can’t make people sleep ‘more,’ only less.

Question 4

What do you find when you let someone sleep for longer periods of times (eg. 14 hour nights)?

Answer 4

• Increase in mood
• Increase in Energy
• Decrease in fatigue

Unlikely that extra sleep is causing physiological damage that is increasing mortality risk.

Question 5

What is one explanation for longer sleep causing higher mortality? (3)

Answer 5

• People who sleep more might spend less time exercising
• Medical condition (eg. metabolic disorder that may not be diagnosed)
• Symptom of another condition (eg. Alzheimer’s, etc.)

Question 6

What happens when you partition long sleepers into different levels of exercise? Short sleepers?

Answer 6

You find that increased mortality rates is driven entirely by inactivity (least motor activity throughout day)

Short sleep affects mortality risk ‘independently’ of activity levels

Question 7

How can you demonstrate - experimentally - that activity levels determine mortality, and not longer sleep?

Answer 7

The Bradford-Hill criteria

List of criteria for determining if environmental dangers were actually related to cancer. Used when it’s impossible or unethical to experimentally study this (eg. getting people to smoke to assess lung cancer)

Question 8

If you restrict sleep (even acutely), what happens? (4)

Answer 8

People develop features of a metabolic syndrome

• Increased abdominal obesity (~BMI)
• Poor lipid regulation (elevated glycerol, TGs)
• Elevated blood pressure
• Increased insulin resistance

These all increase the risk of developing cardiovascular disease, cerebrovascular disease (stroke) and type II diabetes. Metabolic syndrome signs (above) are predictors for developing type II diabetes.

Question 9

True or false? The shorter your sleep, the higher your body mass index increase.

Why (maybe)?

Answer 9

True

• Increase in ghrelin (promotes food intake)
• Decrease in leptin (decrease food intake)

Question 10

What happens to calorie intake across the day in 5 hour and 9 hour sleep conditions?

Answer 10

5 hour: increased energy expenditure, increasing high fat, high carbohydrate snacks after dinner that more than compensated

9 hour: Burn less energy because awake less, at leass post dinner snacks

Question 11

True or false? The time you eat makes a difference

Answer 11

Mice studies suggest this is true. Gain more weight when fed during light phase. Eating at the wrong time increases fat deposition.

Question 12

In dieting Spaniards, did eating the big meal later (after 2:00 PM) cause weight gain?

Answer 12

Yes

Eating later associated with higher weight gain

Question 13

How do night owl type people (delayed phenotype) differ in terms of diet from early larks? What is the strongest predictor of how much they weighed?

Answer 13

Night owl type people in general have later preferred meal times and higher BMI than larks

• Shorter total sleep times
• Delay in sleep onset
• Ate more fast food and full sugar soft drinks
• Fewer fruits and vegetables

Strongest predictor of how much they weighed was how much they ate after 8:00 at night.

Question 14

Those who sleep little and have a delayed phenotype have metabolic profile close to ___?

Answer 14

People with type II diabetes, which have poor control of glucose levels and other impaired metabolic processes

Question 15

If you stay awake during your normal sleep phase, how many extra calories will you burn? Will staying awake extra make you lost weight?

Answer 15

135 kcal (not very much)

People who stay awake burn up more calories, but that only translates into weight loss if you don’t eat more (which you almost invariantly do). And people usually choose worse foods.

Question 16

How is blood glucose levels for people who spend less time sleeping?

Answer 16

They have elevated glucose levels throughout the night and glucose levels stay up higher after meals than people who have long sleep (sign of insulin resistance)

Normal insulin response is really important in preventing type II diabetes (obesity, brain damage, heart damage, kidney damage, circulation in hands and sleep etc.)

Question 17

True or false? If you sleep more, you are less likely to be overweight

Answer 17

False, by changing your sleep you can’t demonstrate weight decrease (no data to suggest this).

Once you’ve gained weight, you’re no longer susceptible to increasing sleep and losing weight. However, it will prevent further weight gain.

Question 18

What does cortisol from cortex do? How/why is this important in the modern day and how does it relate to sleep?

Answer 18

• Mobilizes glucose
• Increase blood pressure
• Activates immune system

Acts with adrenalin from adrenal gland to prepare for flight or fight. In today’s society, not faced with stress events, but continuous stress. Elevated cortisol levels linked with chronic stress, causes hippocampal damage (memory, depression, especially during aging), cardiovascular issues etc.

Body produces circadian rhythms of cortisol every day. When you’re sleeping, cortisol levels drop

Question 19

During the day, when do cortisol levels rise and drop? How does sleep deprivation affect this?

Answer 19

Peak of cortisol when waking up, and second peak just after wakening.

Drop in cortisol during onset and progression of sleep. Begins to fall in afternoon.
- Sustained elevated cortisol in afternoon when sleep deprived (bad!)

Question 20

How does menstrual phase modulate cortisol response to sleep restriction in:

Follicular phase (beginning of ovulation):
Luteal phase (end of ovulation):

Answer 20

Follicular phase: less cortisol when waking than baseline (odd) but elevated cortisol in afternoon (expected)

Luteal phase: Small increase in cortisol after waking, NO elevation in cortisol levels in afternoon and evening (odd)

High progesterone levels in luteal phase may have some effect.

Question 21

Early studies said cytokines are suppressed by sleep loss, and particularly interleukin 6 (IL6) and interleukin 12 (IL12) and tumour necrosis factor (TNF), while other cytokines got increased.

What is the real case?

Answer 21

All inflammatory cytokines are increased during sleep loss

Question 22

What is evidence that sleep loss impacts the immune system?

Answer 22

• People often report getting colds after sleep deprivation studies
• Increased risk of pneumonia
• People who spontaneously get less than 6 hours a night have less clinical protection from immunization of hepatitis B, compared to those who get more than 7 hours
• People who report less than 7 hours a night have a 3x increase in developing a cold in response to exposure of rhinovirus
• Immunized people against influenza, that have been deprived to 4 hours of sleep a night for 4 nights, looking at them ten days later, they show less antibody production than those who get a normal amount of sleep
• Blunted antibody response when you keep someone awake all night after immunization

Question 23

Depressed people have hyperactive immune system. How might this be related to sleep?

Answer 23

• Depression also linked to short, interrupted sleep with reduction in slow waves.
• People who have viral infection have negative mood state, reduced energy levels and interrupted and short sleep similar to that seen in depression.
• If you treat people for depression (clinical pathology eradicated), sometimes they will have lingering poor sleep that can be associated with relapse. If you treat someone for depression AND insomnia, they have much better outcomes than people just treated for depression.

Question 24

What is the most common sleep disorder around the world?

Answer 24

Sleep apnea

apnea = not breathing

Obstructed sleep apnea (breathing obstructed causing sleep loss)

Question 25

What happens during sleep apnea?

Answer 25

An individual loses muscle tone in airway muscles around neck. If they are overweight and older, that increases the pressure to shut down airway.

Stop breathing for periods of times, lasting for seconds or minutes, hundreds of times a night. When they stop breathing, they produce more CO2 in brain, with less oxygen. Causing them to wake up with snorting arousals.

Severe disruption of sleep causing increased daytime sleepiness.

Question 26

What is hypopnea? What is this measured as in sleep apnea?

Answer 26

Less breathing than normal. A reduction in airflow, rather than complete block.

The index to measure this is called apnea hypopnea index (A.H.I.) and it is #-occurences/hour

Question 27

What is the apnea hypopnea index (AHI) for mild sleep apnea?

Answer 27

over 5 occurrences per hour

Question 28

True or false? Old people are more susceptible to sleep apnea. Why?

Answer 28

True. Because their airways are more susceptible to collapse.

Question 29

What are five pathologies associated with sleep apnea?

Answer 29

• Increase in hypertension
• Stress on vascular/respiratory system
• Heart goes into irregular fibrillation
• High risk of heart attack and stroke
• Stress on brain from lack of oxygen (decades of sleep apnea can cause brain damage)

Question 30

How is sleep apnea treated?

Answer 30

With surgery or CFAP that opens the airways.

Question 31

What percent of sleep apnea people also have hypertension?

Answer 31

50%

40% of those have obstructed sleep apnea

Question 32

What does sleep apnea lead to in terms of chronic sleep loss (4) and chronic nocturnal hypoxia and vascular stresses?

Answer 32

Chronic sleep loss

• Impaired quality of life of patient and partner
• Daytime sleepiness
• Increased car accidents
• Increased mortality

Chronic nocturnal hypoxia and vascular stresses
- Systemic and pulmonary hypertension
- Atrial and ventricular fibrillation
(a few more, see slides)

Question 33

Aggregation of platelets can block off blood vessels. When are platelets most ‘sticky?’ When are normal people most protected for heart attacks, and when are sleep apnea people most vulnerable?

Answer 33

In the early morning.

Normal: protected during sleep

Sleep apnea: Increase risk during sleep phase (increase tension in vascular system during cessation of breathing)

Question 34

True or false? Daytime blood pressure predicts risk for heart attack.

Answer 34

False. Nighttime blood pressure is best predictor for cardiac disease.

Dipping, (high blood pressure during day, low at night). Non-dipping is very high predictor of cardiac disease. Increased rise in blood pressure periodically with sleep apnea episodes during night increases risk.

Daily BP rhythms is the best predictor of cardiac disease.

Question 35

True or false? Sleep apnea can lead to vascular damage. Which, regardless of blood pressure, results in increased risk for heart attack.

Answer 35

True

Question 36

How are strokes related to dipping and sleep apnea?

Answer 36

• More strokes associated with non-dippers and inversed dippers.
• Intracerebral hemorrhages associated very strongly with extreme dippers
• Cerebral infarction (more common) associated with inverse-dipping and non-dipping

(dipping is elevated BP during day, decreased at night - which is ‘normal’)

Question 37

Disruption of normal melatonin levels is associated as a possible treatment for effects of sleep apnea. How? (4)

Answer 37

• Aging associated with decreased melatonin receptor levels in SCN
• People who take a single dose of melatonin during the day or night for 3 weeks causes an immediate decrease in nocturnal blood pressure (increased dipping). Don’t see a reduction in the first night.
• Melatonin acts through different receptors to increase/decrease blood pressure in animal models. Action seen above is probably not directly pharmaceutical, as the effect isn’t seen for several weeks.
• Hypothesized that melatonin is actually acting on the SCN (not on blood vessels) to produce dipping effect. Melatonin may be improving amplitude of SCN oscillation.

Question 38

What is fatal familial insomnia?

Answer 38

A prion disease, where prions degenerate brain.

No SWS, no sleep spindles. Lots of stage 1 sleep and daytime sleepiness. Degeneration continues to death. Cognitive losses, and loss of circadian rhythms.

Postpartum dissection shows that thalamic nuclei are severely damaged, explaining loss of SWA.

Not an example of sleep loss killing. Prion kills you through degeneration of autonomic nervous system.

Question 39

What is the primary reason for admission of old person to nursing home?

Answer 39

Alzheimer’s leads to nocturnal disturbances and confusion that can cause problems. Can’t cope with sleep problems at home, because caregivers need sleep.

Only about half of geriatricians ask patients about sleep problems!

Question 40

If you simple keep mice awake (sleep deprive them), what begins to instantly accumulate in their brain?

Answer 40

Beta amyloid

it gets reduced when you sleep.

If you block hypocretin receptors, you get a reduction in beta amyloid (probably from more sleep, ie. narcolepsy like symptoms)

Question 41

The rate of clearance of beta amyloid is faster during ____ and ____

Answer 41

Anaesthesia and sleep

Question 42

What is the MSL test?

Answer 42

A test of sleep latency.

Wake up in morning, have breakfast. Couple hours and they are allowed to fall asleep (time). Keep doing this over 2 hours intervals in a darkened environment conducive to sleeping.

Question 43

How does shortened sleep effect sleep onset latency?

Answer 43

Sleep onset latency is proportional to the shortness of sleep

Eg. shorter sleep = shorter latency

Question 44

People who have very short MSLT latency to sleep, show what? How does this differ from long latency people?

Answer 44

Increase in sleep length and latency to fall asleep also lengthens

Sounds like someone with a sleep deficit.

Long latency people show a little latency increase after 6 days.

Question 45

When given lots of time to sleep, how do habitual short sleeper and habitual long sleepers differ?

Answer 45

Short sleepers continuously sleep longer than long sleepers. Indicating that they are chronically sleep deprived.

These people show no signs of sleep deprivation.

Question 46

What is the psychomotor visual task (PVT)?

Answer 46

• Very easy to administer
• No learning/improvement effect
• You set a limit between a time range at random intervals, an indicator appears and the subject presses a button as fast as they can.
• It measures attention

Question 47

How does restricted sleep effect the psychomotor visual task (PVT)?

Answer 47

Reduction in sleep reliably causes lapses in PVT performance, as if the brain sometimes ‘turns off.’

Question 48

What does a reduction in PVT performance due to sleep restriction suggest?

Answer 48

There are cognitive costs associated with wakefulness

Question 49

How do subjective measures of sleepiness (eg. KSS) differ from objective (eg. PVT)

Answer 49

One people get into a state of sleep deprivation, they consider that as normal. There is not a linear self aware report of sleepiness vs. days of sleep restriction.

After a few days of sleep restriction, they do not detect increased sleep loss. They feel like they ‘get used to it.’

The PVT test shows continuous decrease in performance, objective measures show ‘your body doesn’t get used to it’

Question 50

How does sustained waking effect objective and subjective performance?

Answer 50

Objective: Circadian system kicks in and improves alertness at certain times (brings you almost back to baseline in some cases)

Subjective: You feel sleepier for a bit, but then this feeling flattens out.

Conclusion: We are really bad at detecting our own sleep loss

Question 51

Driving after being awake for 16 and 22 hours is the same as driving with blood alcohol level of?

Answer 51

16 hours: 0.05 blood alcohol (pulled over)
22 hours: 0.10 blood alcohol (intoxicated)
29 hours: >0.05 (due to circadian rhythm)

hours of sleep loss might be less important than the fact that you’re trying to drive at 5am

Question 52

Why are sleep deprivation effects most severe at night

Answer 52

Combination of sleep deprivation combined with circadian phase where attention is low

Question 53

True or false? Chronic sleep deprivation can’t be made up by a good night of sleep

Answer 53

True

Question 54

When the same people are tested weeks apart with the same sleep deprivation period, they are consistent in performance between the two testings. Why? How did this compare with KSS sleepiness test?

Answer 54

• Not due to baseline sleep deprivation before forced deprivation
• Tested them a week later to rule that this wasn’t just a random fluke
• Conclusion: A characteristic of the individual that is consistent over time

Performance wasn’t really related to KSS sleepiness (people have a poor sense of what their ability will be like and how sleepy they actually are). Not even variability in performance is reflected in variability in how sleepy you are.

Question 55

How do self reported caffeine sensitive vs. caffeine insensitive people show impact of sleep loss on PVT performance?

Answer 55

Caffeine sensitivity: worse performance at night, but caffeine help performance

Caffeine insensitive: Better performance at night, but caffeine doesn’t really help

The more sensitive you are to caffeine, the more sensitive you are to the effects of sleep loss

Hypothesized to be genetic. Differences in adenosine receptors.

Question 56

How are population based statistics effective for measuring effects of sleep loss?

Answer 56

Most people don’t have clear examples of sleep effecting mortality or injury etc. However when you sample a population you see a correlation between accidents and sleep loss, due to extended shifts, night shifts etc.

Question 57

Why have many accidents over the past years occurred at night?

Answer 57

Cognitive deficits due to lack of sleep. Eg. Chernobyl, 3 Mile Island etc.

Commonly from long shifts (eg. over 24 hours)`

Question 58

Why are reduced work-hour shifts in healthcare sometimes seen as negative?

Answer 58

Because more hand-overs result in more mistakes, lost information etc.

Plus, it’s felt that education of residence suffers from reduced time spent on shifts.

Question 59

How is shift work more deleterious than jet lag?

Answer 59

With jet lag, you eventually do adjust, as there are entrainers and other people in sync with you.

Shift workers live on local time, even when they’re working on another time. Melatonin is not compatible with the work they’re trying to do. Melatonin disruption and suppression will prevent it from helping the body (eg. free radical scavenging, anti-cancer), possibly explaining for poor health. The other source of poor health is from crappy nutrition in hospitals late at night (eg. vending machines). As well as drugs during the night to keep them awake, and drugs during the day to make them sleep.

Question 60

What two different consequences of working at night affect job performance and safety during the night shift?

Answer 60

• Curtailed sleep (fighting circadian rhythm)

- Displaced sleep (increased homeostatic drive).

Question 61

What impact does working more adverse shifts have on driving safety?

Answer 61

Increased risk of motor vehicle accidents. 6x increase in near-misses, 2.3 increase in actual accidently, increased falling asleep driving or stopped at a red light.

Question 62

What are the benefits of limiting the work hours of medical residents and who receives those benefits?

Answer 62

Reduced chance of burnout, less work, better personal wellbeing.

Question 63

What are the costs of limiting the work hours of medical residents and who bears the burden of those costs?

Answer 63

Less education at hospital, poor communication during patient handover reduces care quality.

Question 64

How can society best balance the risks and benefits associated with having people in various professions working during the night?

Answer 64

Hire more medical personnel and give them shorter shifts.

Question 65

How do the effects of shift work resemble those of jet lag? Why is it even more difficult to adjust to adverse shift work schedules than to adjust to the effects of jet lag?

Answer 65

They both involve trying to function out of your body’s phase and generate similar symptoms. However with shift work, there is no adjusting, environmental cues stay largely unchanged. Everyone else around you is following their normal daily lives while you have to follow yours, while if you fly to Tokyo you will eventually adjust to the lighting and to what everyone else is doing when they’re doing it.

Question 66

Why might shift workers try not to adjust their schedules and physiology to accommodate work at night?

Answer 66

It would conflict with their desire to socialize during the day and do other daily chores.

Question 67

Which health problems are increased in frequency among long-term shift workers? (5)

Answer 67

• Heart disease
• Metabolic disorders
• Cancer
• Miscarriages
• Various chronic conditions.

Question 68

How much sleep do people need? Which criteria have been applied to attempt to answer this question?

Answer 68

In clinical settings, the typical definition of ‘required sleep’ is the duration an individual needs in order to wake refreshed, feel well rested, and function without excessive sleepiness throughout the day.

• One study reported that waking EEG recordings from short sleepers (defined as getting less than 6 h nightly) show more theta and low-frequency alpha frequencies (which are associated with increased sleep drive) than long sleepers (>9 h), suggesting that they have an ongoing accumulated sleep debt
• Another tool that has been used to assess whether people need more sleep than they get is the Multiple Sleep Latency Test (MSLT)

Question 69

According to surveys, how much sleep do most people get?

Answer 69

Around 7-7.5

Question 70

Describe the procedures of the Multiple Sleep Latency Test (MSLT).

Answer 70

• Individuals first undergo a PSG study overnight and then are allowed to lie in a quiet, darkened bedroom for a maximum of 20 min while PSG recordings are obtained at 2 h intervals 4 or 5 times throughout the day.
• Participants are instructed to try to fall asleep or not to resist sleep onset.
• In one large sample of healthy people with no sleep complaints, sleep onset latencies averaged ~11 min in those under 30 and closer to 13 min in those older than 30
• This test is used frequently in sleep laboratories to assess whether an individual is showing excessive daytime sleepiness by determining how often and how quickly they fall asleep during the daytime tests
• Unusually short latencies are usually considered a sign of prior insufficient sleep or a specific sleep disorder, such as narcolepsy.

Question 71

What evidence supports the idea that the Multiple Sleep Latency Test (MSLT) is a valid measure of how much accumulated sleep loss/need people have?

Answer 71

Evidence from studies in which sleep need is deliberately manipulated.

• Restricting sleep for one night to durations ranging from 5 down to 1 h results in a linearly increasing propensity to fall asleep during the following daytime tests.
• Similarly, chronic restriction to 5 h sleep nightly for 1 to 7 days causes a linear increase over days in the tendency to fall asleep during daytime MSLTs

Question 72

Do self-reported short sleepers need less sleep or do they only get less sleep? What is the evidence obtained from MSLT studies that support your conclusion?

Answer 72

Sleep onset latencies during the MSLT immediately lengthened for those with initial short latencies but not for those with long latencies; the latter group did show some latency increase by the 6th day of testing.

• These results suggest that short MSLT latencies reflect chronic mild sleep deprivation that can be reversed by extending sleep time. It is important to note that these individuals had no sleep complaints, and that the short-latency group that apparently had an accumulated sleep debt reported that they slept spontaneously ~7 h on average, which would generally be considered in the normal range
• Those with spontaneous short sleep showed very short MSLT sleep onset latencies, suggesting high sleep drive. In addition, they lengthened sleep durations, often quite dramatically
• The increase in sleep duration was negatively correlated with the length of habitual reported sleep, strongly implying that short sleepers carry a larger sleep debt, rather than needing less sleep

Question 73

Discuss the advantages and disadvantages of the PVT in assessing the impact of sleep loss on human performance.

Answer 73

Advantages

• Brief and easy to administer
• Little learning performance increase
• Sensitive to sleep loss
• Reliable results for individual testing

Disadvantages
- It is very different from the more complicated and intellectually demanding tasks to which one would like to generalize; namely, those most workers perform under conditions of restricted sleep.

Without the ability to maintain attention on the task at hand and keep from drifting off into sleep, one cannot effectively fly an airplane, perform a surgical procedure, drive a truck, memorize a formula or monitor the control panels in a nuclear power station.

Question 74

If people are restricted to 4 h sleep nightly for two weeks, what durations of different sleep stages do they show during their sleep opportunities and how do these values relate to what they show when they have 8 h nightly sleep opportunities?

Answer 74

• SWS not strongly effected
• Very shortened stage 2 and REM sleep

These results indicate that people tend to selectively protect time in SWS when the opportunity for total sleep time is restricted. This observation is consistent with evidence we reviewed earlier that periods of sleep deprivation result in immediate increases in slow EEG frequencies when sleep is again allowed.

Question 75

What is the impact on PVT performance of chronic restriction to different durations of sleep opportunity?

Answer 75

These studies found that PVT performance is progressively degraded over successive days of sleep restriction, and that the rapidity with which deficits emerge is directly related to the degree of sleep restriction

• Compared to 3 h time in bed (TIB), deficits emerge more slowly when participants have 5 or 7 h TIB nightly and may become relatively stable late in the deprivation period.
• A mathematical comparison of these sleep restriction effects to those resulting from total sleep deprivation led to the conclusion that the deficits that emerged are best characterized as being directly related not to cumulative hours of sleep lost, but rather to the ‘excess’ hours of waking over the days of restricted sleep
• Suggesting that the principal impact on the ability to maintain attention results from the accumulated neural consequences of extended wakefulness, which are apparently not compensated for sufficiently during the restricted sleep opportunities, even when SWS durations are preserved.

Question 76

How do objective and subjective assessments of the impact of sleep loss compare during chronic partial sleep restriction?

Answer 76

There was considerable dissociation between the patterns of increasing functional deficits and the patterns of increasing self-reported sleepiness. For example, during the later stages of a 14 day study of sleep restriction, deficits in PVT performance increased steeply in those restricted to 6 and especially 4 h of time in bed nightly. In contrast to this pattern, subjective sleepiness increased at only a very slow rate after the first few days; thus, there was little difference in subjective sleepiness ratings between days 10 and 14 of restriction to 4 h sleep nightly, while the lapses in PVT performance continued to increase over those days

Question 77

How do objective and subjective assessments of the impact of sleep loss compare during an acute 40 h period of sleep deprivation?

Answer 77

When individuals were sleep deprived for 40 h beginning with the time of usual waking and were tested for both PVT lapses in performance and subjective sleepiness, they showed increasing subjective sleepiness up to ~24 h of waking, and then stable ratings over the next 16 h during the next day, even though PVT performance began to improve during that period because of the circadian phase of testing

These results may reflect a general dissociation between objective and subjective measures of sleepiness. But another factor to consider is that participants would be aware of how they had rated their own sleepiness previously, and may have continued to rate themselves as roughly equally sleepy when they knew they had not had a chance to sleep. In either case, subjective reports of sleepiness are often a poor predictor of performance quality, and neither is a simple function of the number of hours of wakefulness.

Question 78

Cohen et al. (2010) studied the effects of chronic, mild sleep restriction using a forced desynchronization protocol. What did the PVT performance results indicate about how sleep reverses the effects of acute versus chronic sleep restriction? What do the performance deficits observed indicate about how circadian effects interact with homeostatic sleep deficits?

Answer 78

Over 3 weeks of these schedules, those with the shorter sleep opportunities showed increasingly poor PVT performance overall.
- However when performance at different circadian phases was compared, there was little performance deficit during the subjective day, while performance during the late, subjective night (when melatonin levels were high) deteriorated throughout the study and was principally responsible for the overall effect of sleep restriction.

These finding demonstrate the importance of circadian factors in determining the impact on performance of chronic, mild sleep restriction

Question 79

How did Von Dongen et al. (2004) try to assess whether differences in PVT performance during sleep deprivation are related to the following factors: effects of prior sleep history; characteristic individual differences in sensitivity to sleep loss; and random variation?

Answer 79

In this study, participants were tested for PVT performance (and other tasks) during 36 h of sleep deprivation after they had first undergone modest sleep restriction (6 h in bed nightly) or were sleep satiated (12 h in bed nightly) for a week, in order to address the issue of potential baseline differences in sleep satiation. The 12 h ‘sleep satiation’ condition was also repeated at least two weeks apart from the other tests. As had been seen in earlier studies, the number of lapses during 36 h of sleep deprivation (shown as performance over the last 24 h of the period) varied among individuals

Individuals performed consistently (mostly), not due to random variation.

These data indicate that performance differences among participants represent stable traits of these individuals during sleep deprivation, not random variability, nor the effects of prior sleep history. Other research supports the idea that responses to sleep loss are characteristic of individuals. Those who showed the largest deficits in cognitive performance when restricted to 3 h sleep nightly for 7 nights also showed the worst deficits in response to acute total sleep deprivation.

Question 80

Are inter-individual differences in self-ratings of sleepiness during sleep deprivation
attributable to:
- Prior sleep history before sleep deprivation?
- Random factors?
- Or individual
differences in perception of sleepiness?

Answer 80

Individual differences in perceptino of sleepiness

Question 81

How is deprivation of sleep fundamentally different from deprivation of any other target of motivated behaviour?

What potential confound does this fact introduce into any study of the effects of sleep deprivation?

Answer 81

No external resources are needed to satisfy the drive to sleep: left to its own devices, an organism satisfies its sleep need through internal processes. If it cannot get to its usual sleep location, it will fall asleep wherever it is

To deprive an organism of sleep requires not removal of a resource, but some form of active intervention to keep it awake. In addition, the longer an organism is sleep deprived, the more likely it is to fall asleep, and the more vigorous or frequent must be the interventions to prevent sleep.

Question 82

Describe the ‘flowerpot’ and ‘multiple flowerpot’ methods of sleep deprivation.

What are the advantages and disadvantages of each?

Answer 82

The ‘flowerpot’ method, involves placing an animal (rat or cat, usually) on an overturned flowerpot set in a shallow pool of water. The reduction of postural muscle tone that normally accompanies sleep onset causes the animal to fall off the small flowerpot bottom and into the water. The fall, and the fact these species are averse to being immersed in water, causes them to awaken. So the animals are compelled to stay awake in order to avoid the negative consequences of falling asleep.
- One unintended consequence of the flowerpot method is that the animal must remain virtually immobile on the flowerpot, as well as staying awake. To control for the impact of immobility, multiple flowerpots may be placed near enough to each other so that an animal can move among them, but far enough apart so that they cannot stretch out between them, and thus cannot fall asleep. This approach permits some movement, but the animal still has the experience of reduced mobility as well as occasional immersion in the water. Thus, not all factors other than a reduction in sleep amounts have been controlled for.

Question 83

What are the principal physiological symptoms associated with long-term sleep
deprivation in rats using the DOW method?

Answer 83

The experimental rats, but not the controls, developed a variety of physiological abnormalities over the days of the study, including hair loss and skin lesions, disruption of body temperature regulation resulting in explosive increases in heat loss, digestive system ulcers, and weight loss, despite showing very significant increases in food intake. These symptoms reflected seriously disturbed physiological functions, especially in relation to temperature control and metabolic homeostasis. After 11 days of the study, the first experimental animal died, and none survived chronic sleep deprivation for more than 32 days, while all of the control animals survived

Question 84

Summarize evidence that chronic, repeated interruption of sleep with modest sleep
reduction may also have severe physiological consequences.

Answer 84

• the pattern of disk rotation generated as a result of the sleep attempts of experimental rats in previous DOW studies was played back to rats chronically in a fixed temporal pattern. This fixed schedule of rotations was also designed to ensure that no long sleep bouts could occur and that sleep was irregularly and repeatedly interrupted
• experimental rats began to develop major metabolic abnormalities and gradually started to sleep even less than the time allowed. Their food and water intake started to climb while their body weights declined steeply; they also developed skin ulcers, hair loss and atrophy of adipose tissues. The control rats showed no changes in intake and only the typical slow increase in body weight shown by normal adult rats in a laboratory. During the sixth cycle, two rats died. These results are surprising given the relatively modest sleep reductions (at least initially) and the periodic recovery days. (Rats were, however, also maintained on a high-fat diet, and it is not clear whether or how this might have contributed to their pathology.) These findings suggest that chronic severe interruption of sleep, along with relatively minor reductions in total sleep time, can also have very serious metabolic consequences.

Question 85

Describe the ‘gentle handling’ approach to sleep deprivation and its strengths and
limitations.

Answer 85

This approach involves an experimenter responding immediately to EEG and/or postural evidence of sleep onset by introducing novel objects into an animal’s environment, moving bedding or other objects near the animal, or gently blowing on the animal to keep it from sleeping. This approach is very effective for relatively short-term deprivation studies and certainly minimizes the stressful components. In fact, there seems to be no increase in cortisol release (a hallmark of typical stress responses) during this gentler form of sleep deprivation. It is doubtful, however, that it would continue to be effective for many days, because it is likely that the pressure to sleep would eventually overwhelm animals’ responsiveness to these relatively mild environmental disturbances.

Question 86

How is the term ‘stress’ used and how do these multiple usages further complicate
interpretation of the role of stress as a factor in sleep deprivation?

Can we study the physiological effects of sleep deprivation independently of those of
stress?

Answer 86

The potential ‘stressors’ in a sleep deprivation study could include the following: the external conditions imposed to prevent sleep (e.g., immobility on a small flowerpot); the direct physiological damage resulting from the sleep deprivation method (e.g., consequences of repeated falls into water); the direct physiological damage resulting from the loss of sleep; and the homeostatic and allostatic physiological adaptations that represent the responses of the body to either the physical provocations involved or the sleep loss itself.

It may not be possible to determine which physiological consequences are linked to stress and which to sleep loss, and it may not be important to try: stress responses may be inevitable mediators of some of the devastating physiological effects of sustained, long-term sleep loss.

Question 87

What were the major behavioural and physiological effects documented in the case
of Randy Gardner during his 11 days of sleep deprivation?

Discuss some ideas about why he recovered quickly from his 11 days of sleep loss,
while rats become severely debilitated and may even die from similar durations of
sleep loss.

Answer 87

• Cognitive decline and irritability
• One explanation is that the effects of sleep loss enforced by human experimenters and the mechanics of the DOW system generate debilitating stress responses that were not experienced by a person who was voluntarily depriving himself of sleep, apparently with a good deal of positive attention as well as social and medical support. As already discussed, it is very difficult or impossible to separate the effects of sleep loss from those of the associated experience of stress.
• losing 11-32 days of sleep for a rat may be equivalent to losing 390-960 days for a human, due to metabolic differences

Question 88

Discuss whether some people never sleep and what might account for self-reports of
this phenomenon.

Answer 88

These reports, however, are anecdotal and not accompanied by objective evidence of such sleep patterns.

Two people were tested, both slept through the night but denied it. Diagnosed with sleep state misperception (SSM).

SSM not uncommon for insomnia patients

Question 89

What findings from van den Berg et al. (2008) with respect to the comparison of self-report to actigraphic findings on sleep duration point to unsuspected factors that can bias self-reports of sleep?

Answer 89

indicated that about 1/3 of participants self-reported total sleep durations that differed by more than 1 h (in either direction) from the durations estimated by actigraphy for the same time period. The direction of these differences also depended on sleep quality in a surprising way. People whose actigraphic data showed that they had relatively poor sleep generated self-reports that overestimated how long they slept, relative to the actigraphy results. On the other hand, those who self-reported poor sleep tended to underestimate how long they had slept, relative to the actigraphy results.

This report also described an unexpected sex difference. Actigraphic recordings indicated that women slept on average about 15 min more than men, but sleep diaries indicated that women reported getting about 15 min less sleep than men