Sleep Test 2

Cardiovascular Physiological Changes

Heart rate is Process C-related and reaches its lowest point during the night when core body temperature is the lowest → RR interval on ECG increases

Parasympathetic system — decreased activity during the day and increased activity during the night since this system slows heart rate

Sympathetic system — increased activity during the day and decreased activity at night since this system increased heart rate

What makes the cyclical behavior occur for heart rate?

Sinoatrial node sends action potentials to make your heart beat (these action potentials depend on the activity of the node’s ion channels)

1. Molecular clock sends CR cues to the ionic channels of the sinoatrial node in the heart

• During the day: channels create the action potentials faster

• During the night: channels change so that it takes longer to generate the action potentials which slows heart rate

2. SCN coordinates the sinoatrial node’s molecular clock and syncs it to the sun so that the ion channels change on the 24-hour cycle

Blood Pressure

Blood pressure = cardiac output * peripheral resistance

Cardiac output — amount of blood heart puts out → heart rate * stroke volume

Peripheral resistance — resistance of blood flow created by friction of blood cells flowing against the blood vessels

Baroreflex

Buffers changes in blood pressure through a negative feedback loop

When blood pressure increases:

1. Baroreceptors increase firing rate to signal the brain that BP is high

2. Heartrate decreases to reduce cardiac output

3. Blood vessels expand in size to decrease peripheral resistance

^These result in a decrease in BP to return to normal state

When blood pressure decreases:

1. Baroreceptors decrease firing rate which signals the brain that BP is low

2. Heartrate increases to increase cardiac output

3. Blood vessels contract to increase peripheral resistance

^These result in an increase in BP to return to normal state

Blood Pressure Sensitivity

How much of a change in BP is needed to cause a change in regulator variables

• Higher sensitivity = smaller change in BP needed to evoke a response

• Low sensitivity = larger change in BP needed to evoke a response

During sleep: baroreflex becomes more sensitive → smaller changes in BP evoke responses when you are asleep

Blood Pressure Setpoint

The ideal level of BP to be maintained

During sleep: setpoint is lower

• Artificially increasing BP during sleep led to a lower setpoint of BP the following day b/c the baroreceptors were resisting the change during the night, and this activity continued through the next day

Endothelial Dysfunction

Flow-mediated dilation fails to occur → blood vessels do not expand in response to increase in BP

Study: normal sleep group vs. 2/3 sleep duration

• Results: normal sleep condition had appropriate flow-mediated dilation, but short sleep duration group had blood vessels remain the same size or constrict in response to the increase in BP

  • This failure to accommodate the increase in BP is problematic b/c that will lead to increased stress on the blood vessel walls, creating hypertrophic vessels, and eventually hypertension

Sleep and the Immune System

Bidirectional relationship since better sleep makes your immune system stronger while being sick drives you to sleep more

Innate immune system — rapid, non-specific response in which macrophages release cytokines to kill bacteria

• Increased activity during the day since most of the body’s needs are anti-inflammatory then, but suppressed at night

Adaptive immunity — slow, pathogen-specific response to store immune memories via antigens

• Suppressed during the day, but increased activity during the night (specifically during SWS)

  • Study: subjects who were sleep-deprived built significantly less antibodies after receiving the flu vaccine → no immune system memory was made

• Growth hormone and prolactin boost adaptive immunity during sleep

• Study: decreased sleep efficiency increased risk of developing the cold virus that participants were exposed to

Metabolism

Process 1:

1. When we eat, glucose levels in blood increase

2. Pancreas releases insulin to make fat cells which absorb glucose from blood → this brings our glucose levels back down

• Type-II diabetes: insulin resistance leads to high glucose b/c fat cells fail to absorb it from the blood

Process 2:

1. When glucose is low, pancreas releases glucagon

2. Liver releases glucose into the blood

Metabolism (Glucose) and Sleep

Body maintains a constant blood-glucose concentration during sleep b/c it becomes temporarily insulin-resistant at night → Process 2 is activated, but Process 1 is suppressed

• This is a Process-S relationship

Study: ??

Metabolism (Hormones) and Sleep

Study: normal sleep vs. sleep-deprived response to a continuous glucose infusion

Results: sleep-deprived group had significantly less leptin and more ghrelin circulating in their blood than the normal sleep group → their hormones were telling them that they were hungry while the normal group was satiated by the infusion

Energy balance hypothesis — original attempt to explain these results by saying that you are awake more, so you need to eat more food to maintain your energy

• BUT this is incorrect b/c sleep-deprivation does not affect resting metabolic rate or total energy expenditure

Evolutionary Mismatch Hypothesis

Environment in which our biological processes function today are not matched

• In the past, people did not deprive themselves of the things that they needed to survive (e.g. sleep and food), but we do that frequently today

Sleep and Physical Health Implications (short list)

• Inflammation goes up during wake and immunity goes down

• Leptin/ghrelin ratio goes down leading to increased appetite with tendency to consume calorically and fat dense foods but no increase in energy expenditure

• Insulin resistance

• Changes in baroreflex function

• Endothelial function

Evidence of Sleep-CVD Relationship

• Cardiac death/events typically occur early in the morning b/c waking up and going from supine position to standing shocks the body

• U-relationship between number of hours of sleep and mortality risk

  • Risk of mortality increases with both short and long sleep

    • Pathways to these increased risk are different though for each end → short sleep is associated with stress and leads to physical health issues while long sleep is often secondary to other underlying ailments that already increase mortality risk

Insomnia

For 3 nights of the week for more than a month, you have difficulty falling asleep, maintaining sleep, and sleep is non-restorative which leads to daytime dysfunction

• This has to be occurring despite having an adequate opportunity to sleep

Insomnia combined w/ short sleep duration has compounding effects on risk for cardiovascular disease → each problem has its own individual risk and they add on to each other

Emotions

Modal model generation:

1. Encounter a situation

2. Pay attention to the stimuli presented

3. Appraise the stimuli which determines our response

Sleep deprivation causes a negative bias in emotions

Sleep and Emotional Cues

Normal sleep group: responded to positive stimuli with pupil constriction (no fight/flight response), negative stimuli caused pupil dilation (fight/response), and neutral stimuli was a net zero movement of pupil diameter

Sleep-deprived group: negative stimuli caused a greater pupil dilation (greater fight/flight response) than was seen in the normal sleep group

• Also had an anticipatory response b/c their pupils started dilated during the cue session while the normal group did not show this

Sleep and Stress Reactivity

High stress condition: no difference in self-reported stress ratings between normal sleep and sleep-deprived

Low stress condition: sleep-deprived group rated twice as much stress as the normal group

Main takeaway: threshold for stress is much lower for sleep-deprived people

Sleep and Emotional Faces

Fearful face: sleep-deprived group had greater fear activation in the amygdala than did the normal sleep group

• Sleep deprivation decouples the ventral anterior cingulate cortex and amygdala → makes the amygdala more hyperactive → increased anxiety

• Sleep deprivation also disconnects the medial PFC and amygdala → makes amygdala more hyperactive → increases fight/flight response

Happy face: no difference between the two groups

Main takeaway: brain functionally reorganizes itself so that it becomes hypersensitive to negative stimuli and enhances the brain areas involved in fight/flight response

Sleep to Remember Hypothesis

Methods: participants were sleep-deprived or fully rested, learned a new list of words, slept, and then had to recall the words

Results: sleep-deprived group had much lower coding efficiency

• Sleep-deprived group recalled significantly more negative words than positive/neutral (but there was no difference between sleep-deprived and normal sleep in negative recall)

Main takeaway: sleep improves memory encoding

Sleep to Forget Hypothesis

Theory: REM sleep after a traumatic event correlates with less PTSD symptoms b/c it essentially serves as self-induced exposure therapy

• REM is like wake but cortisol and norepinephrine (stress hormone and neurotransmitter) are absent

• During REM, brain will recall memories that are tagged with stress, but this feeling will be absent since there is no norepinephrine or cortisol in this sleep stage

• Over time, the stress associated with these memories will go away since it is not felt when it’s recalled during REM

Evidence for this theory:

• Sleep-deprived group had decreased ??

REM and Mental Health

• People with depression had reduced REM latency → they got to REM faster than the control groups

• Different delta sleep ratios (# delta waves in first NREM period to # delta waves in second NREM period)

  • Normal: ratio is above 1 b/c sleep earlier in the night is NREM-heavy and transitions to REM-heavy later in the night

  • Depression: ratio is around or slightly less than 1

Sleep and Mental Health

Originally: sleep was studied to treat psychological disorders (rather than for studying sleep itself)

• Biomarker perspective — Sleep EEG could provide significant data and improve psychiatric diagnoses in the same way lab data was used in other specialties

  • REM latency as an indicator

Now:

• Transdiagnostic perspective and measuring global sleep dysfunction (rather than just REM latency)

  • Descriptively and mechanistically transdiagnostic

• Mutual maintenance — sleep could be an opportunity to use as treatment for psychiatric disorders

  • These treatments would also be more versatile b/c sleep could treat multiple disorders at once given that issues are associated with all types of disorders

Benca Mental Health Meta-Analysis

Found same patterns in all diagnostic categories → sleep differences compared to control group were present for all disorders, making it impossible to diagnose people solely by their sleep data

• Reduced total sleep time and sleep efficiency

• Longer sleep latency

• In affective disorders: reduced NREM sleep, shorter REM latency, most sleep disturbances

Drawbacks of this meta-analysis:

• Family history of participants was not accounted for

• Studies included but had different definitions of sleep variables

• No control for first night effects

• Overlapping subjects were included (being diagnosed w/ more than one of the disorders)

Baglioni Mental Health Meta-Analysis

Attempted to control for two drawbacks of Benca’s study (control of first night effects and overlapping subjects)

Takeaways:

• Sleep can’t be used as diagnosis method since specific sleep issues were present across many diagnoses → no single sleep variable was disease-specific

• REM pressure wasn’t present when controlling for co-morbidities, so this issue might not be due to the psychiatric disorder

• Pattern of sleep dysregulation may be a better biomarker for psychiatric disorder than using just a single/specific sleep measure