HEALTH PSYCHOLOGY II
Central question: How do the mind and the body influence each other?
Homeostatic Regulation
Homeostatic Regulation = the organism’s ability to keep its internal environment stable, despite
changes in the external environment (ex. temperature, blood pH, oxygen pressure, blood glucose)
Central nervous system = interface for interaction with external environment
‘Stress’ = threat to homeostasis, threat to the balance
o Stressor: physical or psychological
Psychological stressor = top-down, signals begin in brain (e.g. anticipation of pain,
exam)
Physical stressor = bottom-up, outside signals enter our brains (e.g. cold)
Both are threats to homeostasis and set responses in motion
o Compensatory stress response = body's adaptive mechanism to counteract stress,
maintain balance (homeostasis), and survive by activating protective systems (like the
HPA axis) to repair damage, manage energy, or alter functions
Chronic activation can lead to disease
Feedback control: negative loops counteract a stimulus (like temperature regulation or blood sugar) to restore
balance, and positive loops amplify a signal (like childbirth or blood clotting) for quick completion, all
orchestrated by nerves and hormones to keep vital functions in check.
Temperature
o Core body temp is around 37°C: in the hypothalamus there is a set point expecting
that temperature, but when the temp is higher then nervous system signals dermal
blood vessels to dilate and sweat glands to secrete -> body heat is lost to environment
-> body temp drops back to 37°C
o If the temp goes below 37°C, the nervous system signals blood vessels to constrict
and sweat glands to remain active -> body heat conserved
Still cold: NS signals muscles to contract to generate body heat -> back to
37°C
Blood pressure
o Baroreceptors in our heart notice high blood pressure: signal sent up via the
glossopharyngeal nerve to the brain stem, which sends a signal via the vagus nervus
toward the heart to adjust its rate
Blood pH levels/ arterial carbon dioxide pressure (PaCO2):
o Increase in blood pH is detected by chemoreceptors -> less stimulation of respiratory
centers -> decreased ventilation -> blood CO² increases, causing a decrease in blood
pH => homeostasis maintained
o Decrease in blood pH is detected by chemoreceptors -> more stimulation of
respiratory centers -> increased ventilation -> blood CO² decreases, causing an
increase in blood pH => homeostasis maintained
Feedforward control: body initiates actions before physiological changes or signals from
environment
Perturbations are being anticipated & corrected before they occur
Classical conditioning as a viable mechanism, for example “Exercise Hyperpnea”: the
increase in ventilation and heart rate occur at the onset of physical exercise, even before an
increase in PaCO2
1
,A hierarchy of homeostastic controls (!)
We can divide homeostatic regulation into five layers beginning at the lower levels in the system:
1. Organs and their local reflexes: Organs can
regulate their own functions using built-in
reflexes that need no higher level of control to
function effectively
2. Autonomic and endocrine messengers: The
autonomic nervous system and the endocrine
system form two channels of descending
communication from the central nervous system
to the individual organs
3. Brainstem regulation: The brainstem regulates
autonomic outputs to the organs through a
complex network of reflex centers
4. Hypothalamic integrations: The hypothalamus
regulates endocrine messengers to the body. It
also coordinates actions of the brainstem
autonomic nuclei.
5. Inputs from higher brain centers: Brain areas
above the hypothalamus have inputs from the
external world and can use this information to
form emotions, memories, and awareness. These
higher processes can then alter the activities of the hypothalamus and brainstem
Intrinsic control mechanisms
On the organ level, there are intrinsic control mechanisms:
Organ adapts its functioning on its own in response to slow, local changes
Example: Frank Starling Mechanism
o If returning (venous) blood volume increases then atrium chambers fill more before next beat
o More effective filling of atria creates more wall stretch and more muscle fiber tension
o More vigorous contraction on next beat
o Left ventricle empties more completely → more effective blood flow into aorta (balloon in
class)
o => Heart responses to flow demands caused by systemic circulation
The existence of intrinsic cardiac controls means that if the heart is deprived of its autonomic
innervation and its endocrine inputs, it will continue to supply blood to all tissues of the body.
It will maintain adequate blood flow completely on its own and without external control, as
long as conditions remain constant.
Autonomic controls and brainstem regulations
This type of control is dependent on the Autonomic Nervous System (ANS):
Viscera (inner organs like heart) have limited awareness & voluntary control ->
a person does not control their heart rate, so it works autonomically
“Negative” feedback mechanisms
ANS is composed of:
o Sensory pathways (afferent)
o Motor pathways (efferent)
o Divisions: sympathetic (SNS), parasympathetic (PNS), (enteric)
2
, Each division has sensory pathways from organs via ganglia to brainstem (afferent) and 4
response components (efferent):
o (a) descending autonomic and pre-ganglionic fibers (hypothalamus/brainstem →
intermediolateral cell column of spinal cord)
o (b) ganglia are collections of cell bodies (like a relay station for as-/descending signals, also part
of local regulation system/reflexes)
o (c) postganglionic fibers (messages more elaborated than in preganglionic fibers)
o (d) neuroeffector junctions: postganglionic fiber/receptor at target tissue (nerve
impulse → motor action)
Sympathetic division of ANS:
Signals sent out from thoracic
and lumbar region of spinal cord
1:10 pre- vs postganglionic
nerves
o General, broad influence
on viscera
o Extensive linkages across
widely distributed
ganglia
o Closely integrated
actions across different
organs (‘in sympathy’)
Neurotransmission:
o Acetylcholine (preganglionic)
o Norepinephrine (postganglionic): smooth muscle cells, cardiac muscles and pace
maker – activating function
o Except:
(a) sympathetic preganglionic nerves release acetylcholine at adrenal medulla
→ release of catecholamines (nor-/epinephrine) into blood
(b) sympathetic nerves release acetylcholine at sweat glands (hands, feet)
More active during stress → Crucial for fight/flight responses
Parasympathetic (vagal) division of ANS:
Signals sent out not from spinal cord but from pons and medulla
Ganglia more specific and nearer to target organ
1:3 pre- vs postganglionic nerves: localized, specific actions directed at one organ
Neurotransmission
o Acetylcholine (preganglionic)
o Acetylcholine (postganglionic): smooth
muscle cells & cardiac muscle and pace
maker – inhibitory influence
Less active during stress
Supporting energy conservation, reproduction,
digestion
3
, Autonomic control of heart rate:
Reciprocal manner of organ function example
Blue: parasympathetic outflow to SA node, via vagus nervus: heart rate
decreases
Red: sympathetic outflow to SA node: heart rate increases
Electrocardiogram (ECG/EKG): registration of electrical activity of the heart
Willem Einthoven: Nobelprice Medicine 1924
Heart rate (HR)
o Expressed in ‘beats per minute’ (bpm)
o Count number of R-peaks per minute
Heart period (HP)
o Interbeat interval (IBI) in msec
o Time between R-peaks (R-R interval)
Heart rate variability (HRV):
IBI series can be graphed to show the HRV
Reason for variability: vagal influences on
SA-node occur at respiratory rhythm
o Respiratory ‘gating’ of autonomic
outflow
o Only vagal influences allow for such
rapid fluctuations in heart rate
Respiratory Sinus Arrhythmia (RSA) =
variations in heart rate at respiratory rhythm
o Inspiration: less vagal outflow, heart
accelerates (O² to lungs to blood)
o Expiration: more vagal outflow, heart decelerates
Time Domain Measures to analyze HRV:
o Root Mean Square of Successive Differences (rMSSD) represents short term
variation of heart rhythm
o rMSSD ↑ = ↑ vagal input
o rMSSD ↓ = ↓ vagal input
Frequency Domain Measures to analyze HRV:
o Ultra low frequency (ULF) < 0.00335 Hz: circadian rhythms, other long term changes
in heart rhythm
o Very low frequency (VLF) = 0.00336-0.04 Hz: sympathetic + vagal effects, thermo
regulation, vasomotoric, …
o Low frequency (LF) = 0.041-0.15 Hz: tonic sympathetic + vagal effects, blood
pressure regulation, …
o High frequency (HF) = 0.151-0.40 Hz: vagal input; but not exclusively (also
moderated by respiration)
General significance of HRV: indicates the individual flexibility of the heart activity to fit
endogenous and exogenous demands
o => A greater HRV is associated with better mental and physiological health
o HRV (RSA) correlates with for example stress, depression & anxiety, cardiac
mortality, emotional regulation and executive functioning
4
Central question: How do the mind and the body influence each other?
Homeostatic Regulation
Homeostatic Regulation = the organism’s ability to keep its internal environment stable, despite
changes in the external environment (ex. temperature, blood pH, oxygen pressure, blood glucose)
Central nervous system = interface for interaction with external environment
‘Stress’ = threat to homeostasis, threat to the balance
o Stressor: physical or psychological
Psychological stressor = top-down, signals begin in brain (e.g. anticipation of pain,
exam)
Physical stressor = bottom-up, outside signals enter our brains (e.g. cold)
Both are threats to homeostasis and set responses in motion
o Compensatory stress response = body's adaptive mechanism to counteract stress,
maintain balance (homeostasis), and survive by activating protective systems (like the
HPA axis) to repair damage, manage energy, or alter functions
Chronic activation can lead to disease
Feedback control: negative loops counteract a stimulus (like temperature regulation or blood sugar) to restore
balance, and positive loops amplify a signal (like childbirth or blood clotting) for quick completion, all
orchestrated by nerves and hormones to keep vital functions in check.
Temperature
o Core body temp is around 37°C: in the hypothalamus there is a set point expecting
that temperature, but when the temp is higher then nervous system signals dermal
blood vessels to dilate and sweat glands to secrete -> body heat is lost to environment
-> body temp drops back to 37°C
o If the temp goes below 37°C, the nervous system signals blood vessels to constrict
and sweat glands to remain active -> body heat conserved
Still cold: NS signals muscles to contract to generate body heat -> back to
37°C
Blood pressure
o Baroreceptors in our heart notice high blood pressure: signal sent up via the
glossopharyngeal nerve to the brain stem, which sends a signal via the vagus nervus
toward the heart to adjust its rate
Blood pH levels/ arterial carbon dioxide pressure (PaCO2):
o Increase in blood pH is detected by chemoreceptors -> less stimulation of respiratory
centers -> decreased ventilation -> blood CO² increases, causing a decrease in blood
pH => homeostasis maintained
o Decrease in blood pH is detected by chemoreceptors -> more stimulation of
respiratory centers -> increased ventilation -> blood CO² decreases, causing an
increase in blood pH => homeostasis maintained
Feedforward control: body initiates actions before physiological changes or signals from
environment
Perturbations are being anticipated & corrected before they occur
Classical conditioning as a viable mechanism, for example “Exercise Hyperpnea”: the
increase in ventilation and heart rate occur at the onset of physical exercise, even before an
increase in PaCO2
1
,A hierarchy of homeostastic controls (!)
We can divide homeostatic regulation into five layers beginning at the lower levels in the system:
1. Organs and their local reflexes: Organs can
regulate their own functions using built-in
reflexes that need no higher level of control to
function effectively
2. Autonomic and endocrine messengers: The
autonomic nervous system and the endocrine
system form two channels of descending
communication from the central nervous system
to the individual organs
3. Brainstem regulation: The brainstem regulates
autonomic outputs to the organs through a
complex network of reflex centers
4. Hypothalamic integrations: The hypothalamus
regulates endocrine messengers to the body. It
also coordinates actions of the brainstem
autonomic nuclei.
5. Inputs from higher brain centers: Brain areas
above the hypothalamus have inputs from the
external world and can use this information to
form emotions, memories, and awareness. These
higher processes can then alter the activities of the hypothalamus and brainstem
Intrinsic control mechanisms
On the organ level, there are intrinsic control mechanisms:
Organ adapts its functioning on its own in response to slow, local changes
Example: Frank Starling Mechanism
o If returning (venous) blood volume increases then atrium chambers fill more before next beat
o More effective filling of atria creates more wall stretch and more muscle fiber tension
o More vigorous contraction on next beat
o Left ventricle empties more completely → more effective blood flow into aorta (balloon in
class)
o => Heart responses to flow demands caused by systemic circulation
The existence of intrinsic cardiac controls means that if the heart is deprived of its autonomic
innervation and its endocrine inputs, it will continue to supply blood to all tissues of the body.
It will maintain adequate blood flow completely on its own and without external control, as
long as conditions remain constant.
Autonomic controls and brainstem regulations
This type of control is dependent on the Autonomic Nervous System (ANS):
Viscera (inner organs like heart) have limited awareness & voluntary control ->
a person does not control their heart rate, so it works autonomically
“Negative” feedback mechanisms
ANS is composed of:
o Sensory pathways (afferent)
o Motor pathways (efferent)
o Divisions: sympathetic (SNS), parasympathetic (PNS), (enteric)
2
, Each division has sensory pathways from organs via ganglia to brainstem (afferent) and 4
response components (efferent):
o (a) descending autonomic and pre-ganglionic fibers (hypothalamus/brainstem →
intermediolateral cell column of spinal cord)
o (b) ganglia are collections of cell bodies (like a relay station for as-/descending signals, also part
of local regulation system/reflexes)
o (c) postganglionic fibers (messages more elaborated than in preganglionic fibers)
o (d) neuroeffector junctions: postganglionic fiber/receptor at target tissue (nerve
impulse → motor action)
Sympathetic division of ANS:
Signals sent out from thoracic
and lumbar region of spinal cord
1:10 pre- vs postganglionic
nerves
o General, broad influence
on viscera
o Extensive linkages across
widely distributed
ganglia
o Closely integrated
actions across different
organs (‘in sympathy’)
Neurotransmission:
o Acetylcholine (preganglionic)
o Norepinephrine (postganglionic): smooth muscle cells, cardiac muscles and pace
maker – activating function
o Except:
(a) sympathetic preganglionic nerves release acetylcholine at adrenal medulla
→ release of catecholamines (nor-/epinephrine) into blood
(b) sympathetic nerves release acetylcholine at sweat glands (hands, feet)
More active during stress → Crucial for fight/flight responses
Parasympathetic (vagal) division of ANS:
Signals sent out not from spinal cord but from pons and medulla
Ganglia more specific and nearer to target organ
1:3 pre- vs postganglionic nerves: localized, specific actions directed at one organ
Neurotransmission
o Acetylcholine (preganglionic)
o Acetylcholine (postganglionic): smooth
muscle cells & cardiac muscle and pace
maker – inhibitory influence
Less active during stress
Supporting energy conservation, reproduction,
digestion
3
, Autonomic control of heart rate:
Reciprocal manner of organ function example
Blue: parasympathetic outflow to SA node, via vagus nervus: heart rate
decreases
Red: sympathetic outflow to SA node: heart rate increases
Electrocardiogram (ECG/EKG): registration of electrical activity of the heart
Willem Einthoven: Nobelprice Medicine 1924
Heart rate (HR)
o Expressed in ‘beats per minute’ (bpm)
o Count number of R-peaks per minute
Heart period (HP)
o Interbeat interval (IBI) in msec
o Time between R-peaks (R-R interval)
Heart rate variability (HRV):
IBI series can be graphed to show the HRV
Reason for variability: vagal influences on
SA-node occur at respiratory rhythm
o Respiratory ‘gating’ of autonomic
outflow
o Only vagal influences allow for such
rapid fluctuations in heart rate
Respiratory Sinus Arrhythmia (RSA) =
variations in heart rate at respiratory rhythm
o Inspiration: less vagal outflow, heart
accelerates (O² to lungs to blood)
o Expiration: more vagal outflow, heart decelerates
Time Domain Measures to analyze HRV:
o Root Mean Square of Successive Differences (rMSSD) represents short term
variation of heart rhythm
o rMSSD ↑ = ↑ vagal input
o rMSSD ↓ = ↓ vagal input
Frequency Domain Measures to analyze HRV:
o Ultra low frequency (ULF) < 0.00335 Hz: circadian rhythms, other long term changes
in heart rhythm
o Very low frequency (VLF) = 0.00336-0.04 Hz: sympathetic + vagal effects, thermo
regulation, vasomotoric, …
o Low frequency (LF) = 0.041-0.15 Hz: tonic sympathetic + vagal effects, blood
pressure regulation, …
o High frequency (HF) = 0.151-0.40 Hz: vagal input; but not exclusively (also
moderated by respiration)
General significance of HRV: indicates the individual flexibility of the heart activity to fit
endogenous and exogenous demands
o => A greater HRV is associated with better mental and physiological health
o HRV (RSA) correlates with for example stress, depression & anxiety, cardiac
mortality, emotional regulation and executive functioning
4
