UNIT 3 Flashcards
what are the major functions of Cardiovascular system?
transport O2 and nutrients
Removes Co2 and other waste
transport hormones and other molecules
regulate body temperature
maintain acid-based balance
What systems does the cardiovascular system work with?
pulmonary system through cardiorespitory and cardiopulmonary
What makes up the CV system?
channels or tubes (blood vessels)
pump (heart)
fluid medium (blood/plasma)
arteries function
caries blood away from the heart
arterioles function
smallest arteries
resistance vessels: greatest ability to regulate pressure
capillaries function
smallest and most numerous vessels that allow for exchange between blood tissues
veins function
blood travels towards heart
exception: pulmonary vein
venules function
small vessels that connect to capillaries
pulmonary circuit
right side of heart
pumps deoxygenated blood and returns oxygenated
low pressure system
systemic circuit
left side of heart
pump oxygenated blood and returns deoxygenated
high pressure bc it’s long/large
where does the right atrium receive blood from?
superior vena cava
inferior vena cava
coronary sinus
what does the right atrium eject blood through?
tricuspid valve
What does the right atrium eject blood to?
right ventricle
Where does the right ventricle receive blood from?
right atrium
what does the right ventricle eject blood through?
pulmonic valve
what does the right ventricle eject blood to?
pulmonary artery and pulmonary circulation
where does the left atrium receive blood from?
pulmonary veins
what does the left atrium eject blood through?
mitral (bicuspid) valve
what does the left atrium eject blood to?
left ventricle
where does the left ventricle receive blood from?
left atrium
what does the left ventricle eject blood through?
aortic valve
What does the left ventricle eject blood to?
aorta and systemic circulation
AV valves
separates atria from ventricles
allow movement of blood from atria to ventricles
semilunar valves
allow movement of blood from ventricles to aorta and pulmonary artery
blood flow through pulmonary circulation (right heart)
Superior/inferior vena cavae -> right atrium -> tricuspid (AV) valve -> right ventricle -> pulmonary valve -> pulmonary arteries -> lungs
DEOXYGENATED
blood flow through systemic circulation (left heart)
Lungs -> pulmonary veins -> left atrium -> mitral (AV) valve -> left ventricle -> aortic valve -> aorta
OXYGENATED
muscular lays of the heart wall
epicardium: outer layer
myocardium: responsive for contractions
endocardium
Blood supply to cardiac muscles
receives blood supply via coronary arteries
high demand for oxygen and nutrients: doesn’t do anaerobic metabolism
heart receives “just enough” blood to function
blockage of coronary blood flow = heart attack (MI)
coronary arteries of the heart
Right coronary artery, left main coronary artery, circumflex artery, left anterior descending artery
epicardium function
serves as lubricative outer covering
myocardium function
provides muscular contractions that eject blood from the heart chambers
endocardium function
serves as protective inner lining of the chambers and valves
cardiac muscle connections
connected by intercalated discs
- rapid transmission of electrical signals from cell to cell
- heart muscle forms a functional syncytium: unit where they all squeeze together
cardiac muscle type
all one fiber type, similar to type I muscle fibers
- more mitochondria than skeletal muscle
- heavily reliant on aerobic metabolism
cardiac muscle regeneration properties
no satellite cells so limited ability to heal/ regenerate after injury
comparison of muscle tissue and skeletal muscle in contractile proteins, nuclei, and cellular junctions
both skeletal and heart muscles have contractile proteins (actin and myosin)
heart muscle has a singular nucleus while skeletal muscle shave multiple nuclei
heart muscles have intercalated discs, but skeletal muscles have no cellular junctions
main structure of the heart
Four chambers, but two “pumps”
- Left and right side of the heart
- Separated by interventricular septum
One-way valves prevent backflow of blood
- Left ventricular thickness > right ventricle
But holds the same volume of blood
ventricle sizes
Larger mass of myocardium of the left ventricle and septum are needed to pump blood throughout the body, which is under relatively higher pressures
physiological adaptations for heart
Results from specific exercise stimulus
Concentric vs. eccentric hypertrophy
pathological heart adaptations
Results from disease state (i.e., hypertension)
Associated with loss of myocytes and increased collagen causing fibrosis of the heart
ventricular cardiac cycle
Repeating pattern of contraction & relaxation of heart
- Systole – contraction phase
Ejection of blood
- Diastole – relaxation phase
–Filling with blood
At rest – diastolic time is longer than systolic time
Exercise – duration of both are shorter
- Greater reduction in diastole
cardiac cycle: ventricular systole
Isovolumetric ventricular contraction
- pressure rises
- ↑ Pressure → AV valves close (heart sound 1, “lub”)
- Pressure builds, but not yet sufficient to overcome pressure in the arteries so no outflow (volume stays the same)
Ventricular ejection
- Pressure in ventricle exceeds aorta & semilunar valves open
- Blood flows out of the ventricles
- At end, blood in ventricle = end-systolic volume (ESV)
cardiac cycle: ventricular diastole
Isovolumetric ventricular relaxation
- Semilunar valves close (heart sound 2, “dub”)
- Ventricular pressure drops with no outflow (volume stays same)
Ventricular filling
- Pressure in ventricles drops below atrial pressure
- Atrioventricular (AV) valves open
- Blood flows from atria to ventricles
~70% blood is passive; ~30% is active
- At end, blood in ventricle = end-diastolic volume (EDV)
what are the sounds of the heart?
s1: closing of AV valves
S2: closing of semilunar valves
isovolumetric contraction
same amount of blood but building pressure
ejection phase
building pressure but volume drops
pressure-volume loop
volume of blood that heart gets rid of with one contraction
arterial blood pressure
expressed as systolic/ diastolic
- normal is less than 120/80
systolic pressure
pressure generated during ventricular contraction
diastolic pressure
pressure in the arteries during cardiac relaxation
Mean arterial pressure (MAP)
average weighted pressure in arteries: on average what is the pressure in arteries and blood vessels
Mean arterial blood pressure equation
2/3DBP + 1/3SBP
importance of MAP
average MAP is used to determine proper spread of oxygen to body and kidneys
hypertension
Persistently elevated BP above 130/80 mmHg
- Primary (essential) hypertension
–Cause unknown (multifactorial)
–90% cases of hypertension
Secondary hypertension
-Result of some other disease process
hypertension risk factors
Left ventricular hypertrophy: muscle gets thicker
Atherosclerosis and heart attack: damage to walls
Kidney damage: damage to blood vessels in kidney
Stroke
determinates of mean arterial pressure (MAP)
Cardiac output - amount of blood pumped by the heart each minute
Total vascular resistance - sum of resistance to blood flow provided by all systemic vessels
MAP = cardiac output (Q) x total vascular resistance
Cardiac output
Average ~5 L (more specific values next slide)
Product of heart rate (HR) & stroke volume (SV)
-Heart rate – number of beats per minute
-Stroke volume – amount of blood ejected per beat
Dependent on training state and sex
Q=HR X SV
Blood pressure increase
anything that increases HR, SV, blood volume, or peripheral resistance will cause an increase in BP
typical Hr/Sv values
max heart rate doesn’t change w/ exercise
resting heart rate decrease and strove volume increase w/ exercise
exercise increases max cardiac output
intrinsic control
cardiac control that originates from within the heart
- pacemaker activity
-generates its own electrical signal
- no external stimulation
extrinsic control
cardiac control by factors originating outside the heart
- autonomic nervous system: para sympathetic and sympathetic
- endocrine control: epinephrine and norepinephrine (catocolings)
intrinsic control: spontaneous rhythmicity
special heart cells generate and spread electrical signal
pacemaker cells have an unstable membrane potential called a pacemaker potential
- not a resting membrane potential because it never “rests” like skeletal muscle cells
- contain unique “funny channels or I channels
- combined effect of NA, K, and Ca reach depolarization threshold and AP occurs
sinoatrial node (SA node)
pacemaker, initiates depolarization (contraction)
stimulates right and left atrial contraction
atrioventricular node (AV node)
passes depolarization to ventricles
brief delay to allow for ventricular filling
AV bundle/bundle branches
travels along interventricular septum
connects atria to left and right ventricle
Purkinje fibers
spread wave of depolarization throughout ventricles
stimulates right and left ventricular contraction
depolarization of cardiac muscle
Spreads through heart via conduction from cardiomyocyte to cardiomyocyte
- Gap junctions are electrical connections between adjacent cells
–They consist of a linkage between specialized ion channels on the adjacent cell membranes
–They are a component of larger structures called intercalated disks
-Allows heart to function as a “syncytium”
–Contrasts with skeletal muscle, where every fiber needs nerve innervation
extrinsic control of HR - parasympathetic
Innervation via vagus nerve (cranial nerve X)
Carries impulses to SA, AV nodes
-Releases Ach and hyperpolarizes (neg.) cells
–Slower spontaneous depolarization
-Decreases HR (chronotropic suppression)
Decreases HR below intrinsic HR
Influence referred to as parasympathetic tone
extrinsic control of HR - sympathetic
Innervation via cardiac accelerator nerves
Carries impulses to SA, AV nodes, & myocardium
-Releases NE and facilitates depolarization
-Increases HR (chronotropic enhancement)
-Increases force of contraction (inotropic enhancement)
Increases HR above intrinsic HR
Determines HR during physical, emotional stress
Maximum HR: ~250 beats/min
control of exercise heart rate
When you start to exercise it starts as a withdraw of parasympathetic than sympathetic kicks in to increase HR the rest of the way
electrocardiogram
recording of heart’s electrical activity
- 12 lead ECG is clinical standard: for different views of heart
- Provides different electrical views of heart
- Not a measure of a single AP; represents the sum of multiple APs in many myocardial cells
what are the two major components of an ECG?
Waves – parts of the trace that go above or below the baseline value
Segments – sections of baseline between waves
QRS complex
ventricular depolarization
- Signal spreads from AV bundle → Purkinje fibers
- Represents ventricular contraction
P wave
atrial depolarization
- Electrical signal travels SA → AV node
- Represents atrial contraction
T wave
ventricular repolarization
RR interval
gives HR
electriocardiogram and contractions
doesn’t actually tell you that the heart is actually contracting but it does say electricity is moving through the heart -> can expect it can, but can’t always assume
QR
ventricle depolarization and atria repolarization
Diagnostic use of ECG
ECG recorded during incremental exercise
- known as a stress test
- physician can observe changes in patient’s ECG
How is blood pressure controled?
Acutely maintained by autonomic reflexes
Baroreceptors
Located in carotid and aorta
Sensitive to changes in arterial pressure (“baro-”)
Afferent signals from baroreceptor to brain
Efferent signals from brain to heart, vessels
Adjustment of arterial pressure back to normal
stop shaking
baroreceptors
Located in carotid and aorta
Sensitive to changes in arterial pressure (“baro-”)
Afferent signals from baroreceptor to brain
Efferent signals from brain to heart, vessels
Adjustment of arterial pressure back to normal
Baroreflex Scenario
Drop in blood pressure
Reduction in baroreceptor activity signaling
Afferent signal to medulla oblongata (brain stem)
Cardiovascular control center (CVCC)
↓ vagal tone (parasympathetic)
↑ sympathetic activity
Mean arterial pressure (MAP) equation
Cardiac Output (Q) x Total Vascular Resistance
Cardiac output (Q)
Heart Rate (HR) x Stroke Volume (SV)
stroke volume (SV)
amount of blood ejected per beat
Regulation of stroke volume:
Preload
EDV: end-diastolic volume
Quantityof blood in the ventricles at the end of diastole
afterload
Pressure in the systemic arteries, aortic valve
Reflects the pressure the heart must pump against to eject blood
Contractility
Strength of ventricular contraction
Influenced by direct SNS stimulation, circulating catecholamines
regulation of stroke volume: preload
Dependent on venous return
Frank-Starling mechanism
Greater EDV = more forceful contraction
Creates more stretch within the ventricles
effects preload for regulation of stroke volume
Venous return increased by:
Venoconstriction via sympathetic nervous system
Skeletal muscle pump
Respiratory pump
Body position
important for preload regulation of stroke volume
preload, stroke volume, and frank-sterling mechanism relationship
greater preload = greater stroke volume = greater frank-sterling mechanism = greater cardiac output
characteristics of veins
Less smooth muscle and very elastic
Venous system “stores” much of the body’s blood volume (approximately 2/3 of total)
SNS activity results in venoconstriction of the venous system (veins and venules)
Venoconstriction results in blood within this “reservoir” being sent back to heart and arterial circulation
skeletal muscle pump
Rhythmic mechanical compression with skeletal muscle contraction
One-way valves in veins prevent the backflow of blood
respiratory pump
During inspiration:
↓ Thoracic (chest) pressure
↑ Abdominal pressure
Gradient promotes blood flow towards heart
Quiet breathing (rest) aids in venous return, but effect is enhanced with exercise:
Greater respiratory rate (more frequent breaths)
Greater depth (deeper breathing)
increased preload caused by
Venus return and plasma value and results in increased stroke volume
increased afterload caused by
resistance in system: blood pressure in aorta and decreases stroke volume
increased contractility caused by
sympathetic nervous system stimulation, increased preload and increases stroke volume
hemodynamics
Blood flow through the circulatory system results from pressure differences between the two ends of the system
Physical regulation of blood flow to tissues involves interrelationships between pressure, flow, and resistance
Blood flow control is important for regulating nutrient delivery to, and waste removal from tissues
Greater flow when more delivery and removal is needed; less flow when less is needed
blood flow
Directly proportional to the pressure difference between the two ends of circulatory system (P1 – P2)
Inversely proportional to resistance
𝐁𝐥𝐨𝐨𝐝 𝐟𝐥𝐨𝐰=(∆ 𝐏𝐫𝐞𝐬𝐬𝐮𝐫𝐞)/𝐑𝐞𝐬𝐢𝐬𝐭𝐚𝐧𝐜𝐞
pressure
Driving pressure across circulatory system is ~100 mmHg
Force that drives flow – provided by contraction
resistance depends on
Length of the vessel
Viscosity of the blood
Radius of the vessel
Resistance =(𝐋𝐞𝐧𝐠𝐭𝐡 𝐱 𝐕𝐢𝐬𝐜𝐨𝐬𝐢𝐭𝐲)/(𝐑𝐚𝐝𝐢𝐮𝐬𝟒 )
easiest way to affect flow
change R
Greatest vascular resistance occurs in arterioles
Vasoconstriction or vasodilation – extrinsic control
arteriola diameter is controlled by
tonic release of norepinephrine
increased norepinephrine releases a receptors
constricts blood vessels
decreased norepinephrine releases a receptors
dilates blood vessels
what vessel has the biggest impute from SNS and so allows for biggest drop in texture?
Arterioles
Resistance Vessels: Arterioles
Richly innervated by the sympathetic nervous system
Thick layer of smooth muscle relative to lumen
Constriction/dilation of arterioles is key for regulation of pressure and flow
components of blood
Plasma
Liquid portion of blood
Contains, ions, proteins, and hormones
Cells
Red blood cells – contain hemoglobin
White blood cells – prevent infection
Platelets – blood clotting
Hematocrit – percentage of blood composed of cells
Blood Viscosity
Thickness of blood (due to red blood cells)
Several times more viscous than water
Viscosity ↑ as hematocrit ↑
Plasma volume must ↑ as red blood cell ↑
Occurs in athletes with training or acclimatization
Hematocrit and viscosity remain stable
Exercise in heat may result in ↑ viscosity
oxygen delivery during exercise
Metabolic need for oxygen in skeletal muscle is significantly greater than for resting
Increased O2 delivery accomplished by:
Increased cardiac output (Q)
Rest: ~5 L/min
Exercise: ~ 25 L/min
Redistribution of blood flow
no
fick principle
states oxygen consumption (VO2) of a tissue is dependent on:
Blood flow to that tissue
Amount of O2 extracted from the blood by the tissue
VO2 = Q x a-vO2 difference
SV X HR peripheral factor
central factors
Cardiac Output: Stroke Volume
Increases in proportion with intensity up to approximately 40-60% of VO2max
Beyond this, it plateaus (no further change)
At high HRs, time for ventricular filling ↓
Possible exception: elite endurance athletes
Influence of EDV and ESV on SV
Changes in EDV and ESV both contribute to increases in SV
Stroke Volume and Body Position
Body position has a major influence on SV
True at rest and during exercise
Related to the effect of gravity on venous return
Gravity promotes blood pooling in legs, lowering venous return, lower EDV (less Frank-Starling effect)
Upright exercise results in increased SV
Due to larger EDV, increased venous return
Increase in EDV and SV at high HR
Supine exercise (for example, swim) results in small increases in SV
Due to resting SV being relatively high while supine
effects of vasoconstriction
increase resistance = length X viscosity/ decrease radius ^4
decrease blood flow = change in pressure/ increase resistance
Cardiac Output: Heart Rate
Increases in proportion to exercise intensity (linear)
Maximal HR (HRmax): highest HR achieved in all-out effort to volitional fatigue
Highly reproducible
Decreases with age
Age-predicted HRmax
HRmax = 220 − age in years
HRmax = 208 − (0.7 × age in years)
Additional Influence on Heart Rate
Elevated heart rate (and BP) in emotional environment
Mediated by increase in SNS
Can increase pre-exercise values, but not maximal values
Anticipatory response
HR increase above resting just before start of exercise
Decrease vagal tone (parasympathetic)
Arterial-Mixed Venous O2 Content
Acute exercise ↑ O2 extraction from blood
Nearly triples from rest to maximal exercise
a-vO2 diff increases because:
Greater O2 extraction by active muscle due to an ↑ in amount of O2 used for oxidative production of ATP
Redistribution of blood to active tissues
- arterial doesn’t change concentration of oxygen venus system changes
Which factor matters most for increasing SV?
after SV reaches a plateau then HR is main factor that effects VO2 max
Redistribution of Blood Flow During Exercise
Increased blood flow to working skeletal muscle
At rest, 15-20% of cardiac output to muscle
During maximal exercise, increases to 80-85%
Decreased blood flow to less active organs
Liver, kidneys, gastrointestinal tract
Redistribution depends on metabolic rate
Dictated by exercise intensity
blood flow during exercise
increases VO2 max/ intensity and more blood flows to muscles then kidneys during exercise
blood flow through the body during exercise
blood flow to brain decreases but more blood is delivered so it ends up still beign more blood to brain
regulation of local blood flow
Arterioles in skeletal muscle have relatively high vascular resistance at rest (adrenergic sympathetic stimulation)
During exercise
- Decrease in vascular resistance
- ”Recruitment” of capillaries in skeletal muscle
Autoregulation
intrinsic ability of local tissues to regulate blood flow to match the metabolic rate
- Greater need = greater flow
- Local vasodilation triggered by metabolic and endothelial products
flow is proportional to demand
increasing workload = increasing blood flow
Metabolic mechanisms (vasoactive agents) of skeletal muscle vasodilation
increase O2 demand (decrease O2)
build up of local metabolic by-products: increase co2, K, H, and lactic acid
endothelial mechanisms
increase blood flow causes shear stress on endothelium as more blood hits walls of blood vessels
secretes vasodilators - nitric oxide (vasodilates), prostaglandins, endothelial-derived hyperpolarizing factor (EDHF)
skeletal muscle vasodilation
metabolic regulation and endothelium-mediated vasodilation work hand in hand
functional sympatholysis
Vasoactive molecules released from active skeletal muscle inhibit sympathetic vasoconstriction
Reduce vascular responsiveness to 𝘢-adrenergic receptor activation
Ex. Endothelium-derived hyperpolarization factor (EDHF) promotes hyperpolarization of smooth muscle cells in arterioles, making it more difficult to constrict
no shaking
increasing exercise does what to mean arterial presure
linearily incrases
What part of blood pressure changes during exercise?
diastolic blood pressure doesn’t change but systolic blood pressure does
resistance training
Transient large increases in SBP, DBP, and MAP
Up to 480/350 mmHg in central arteries
Cause – transient collapse occlusion of vessel in contracting muscle
More common when using Valsalva maneuver
arm vs. leg exercise
At the same oxygen uptake, arm work results in higher:
Heart rate – greater sympathetic stimulation
Blood pressure – vasoconstriction of large inactive muscle mass
Recovery of heart rate and blood pressure between bouts during intermittent exercise depend on:
Fitness level
Temperature and humidity
Duration and intensity of exercise
Heavy-intensity intermittent exercise
Near maximal HR values are possible
HR recovery response for intermittent exercise
HR decreases slower at end of training interval
high intensity/prolonged exercise increases HR more and more and leads to longer recovery of HR
Prolonged Exercise
Cardiac output is maintained
Gradual decrease in stroke volume
- Due to dehydration and reduced plasma volume
Gradual increase in HR during prolonged exercise
- Particularly apparent in heat
- Known as cardiovascular drift
cardiovascular drift
gradual increase in HR during prolonged exercise due to lower stroke volume
constant cardiac output in prolonged exercise
Stroke volume decreases so HR increases
pulmonary ventilation
movement of air in and out of the lungs
mechanical process
pulmonary respiration
exchange of gages in the lungs
movement of oxygen into the blood
movement of carbon dioxide out of the blood
processes involved in the respiratory system
four continuous and simultaneously occurring steps
- ventilation: movement of air from the atmosphere to the alveoli of the lungs
- alveolar gas exchange: movement of gases between the alveoli and the blood
-circulation: transport of gases in blood to body cells/tissues
-systemic gas exchange: movement of gases between blood and cells of the body
conducting zone
functional division
- anatomic ‘dead space”
-passageway for air but no gas exchange
-purpose: filter, warm, and humidify air, and transport it to the respiratory zone
respiratory zone
functional division
- gas exchange between alveoli and capillary blood
- very large surface area for gas diffusing
- surfactant: reduces surface tension and prevents alveoli from collapsing
inspiration
Starts with contraction and downward movement of the diaphragm:
Increase in volume of the thorax
Decrease in intrathoracic pressure
Air moves from high pressure (atmosphere) to low pressure (lungs)
muscles involved in inspiration
External intercostals: elevate and laterally expand ribs
“Accessory muscles” include sternocleidomastoid, scalenes, pectorals (anything that attaches to the trunk, shoulder complex, ribs, sternum and makes the thorax bigger)
Abdominals: not an inspiratory muscle, but stabilize the abdomen as intra-abdominal pressure increases and help the diaphragm to work more efficiently
please stop shaking
expiration
Passive at rest
Inspiratory muscles relax, all structures return to their starting point
Lungs have elastic recoil
Decrease in volume of thorax
Air moves from high pressure (lungs) to low pressure (atmosphere)
Active expiration:
Abdominals
Internal intercostals
pressures in intraabdominal and intrathoracic during inhalation
intraabdominal pressure increases and intrathoracic pressure decreases
Respiratory muscle strength
Measured by assessing the pressure generated during maximal inspiration or maximal expiration
For most healthy people:
Force necessary for ordinary breathing is a small fraction of maximal force
Work of breathing is low and respiratory muscles do not fatigue
Increased workload on respiratory muscles during exercise
Fatigue can occur with very heavy exercise, prolonged moderate exercise
Respiratory muscles can adapt to training just like other skeletal muscle
ventilation during exercise
Ventilation increases proportional to metabolic needs of the active muscle
Ve= F X Vt
ventilation increases even before exercise depending on moderation of exercise
heavy exercise reaches stead state
exercise hyperventilation (hyperpnea)
at low-moderate intensities, mostly tidal volume increases
at high exercise intensity, breathing frequency increases
Arterial PO2 and PCO2 of ventilation during exercise
remains relatively constant
- slight change during transition
Rest to work immediate ventilation changes
increase in ventilation
before muscle contractions
anticipatory or feedforward component
motor cortex association
rest to work secondary ventilation changes
slower, gradual increase towards steady-state value
work to rest: delayed decrease in ventilation
recovery may take several minutes
regulated by blood pH, CO2, body temperature
prolonged exercise in heat
Ve drifts upward due to increased body temperature
arterial PCO2 remains constant
incremental exercise
linear increase in ventilation but after 75% inflection occurs and we need a huge increase in ventilation and PH drops
lactate threshold
exercise intensity above which lactate accumulates in blood when difference in production and clearance of it, can do blood tests but invasive measure
Ventilatory threshold
the breakpoint at which Ve and Co2 output begin to increase exponentially with increasing intensity
- identified as an inflection on the plot of E vs. exercise intensity
Ve increases disproportionately to increase in )2 consumption
rise in Ve caused by rapid increase in PCO2 from production of “non-metabolic CO2
- bicarbonate buffering of acid in blood
increase in blood lactate likely key stimulus for ventilatory threshold
ventilation and lactate threshold
ventilation threshold and lactate threshold happens around same time
exercise induced hypoxemia
developed by some elite endurance-trained athletes exercising at high intensities
possible explanations for exercise-induced hypoxemia
ventilation-perfusion mismatch
diffusion limitation due to how quickly blood moves through lungs
similar to response observed in exercising patients with severe lung disease
control of ventilation
respiratory control center located in medulla oblongata
Control of ventilation: inspiratory region
contains cells that intrinsically fire and control basic rhythm
pacemaker cell - prebotxinger complex (prebotc)
innervates diaphragm and external intercostals
Control of ventilation: expiratory region
no active during normal, quiet breathing (passive)
during exercise, retrotrapezoid nucleus/parafacial respiratory group (RTN/pFRG) innervates rectus abdominus and internal intercostals
Control of ventilation: pontine respiratory center
located in pons (brainstem)
interacts with both PreBotC and RTN/pFRG to fine-tune and regulate breathing during exercise
central command theory
CV control center: medulla oblongata in brain stem
inputs of central command theory
central (motor cortex in brain) - rapid response to exercise; parallel coactivation of CVCC but not very accurate
peripheral: shower responses and fine tuning of responses
- chemoreceptors in muscle
- mechanoreceptors in muscle
- baroreceptors in arteries
pulmonary function tests
look at volume and flow rate
- average title volume - 500 or half a liter
expiratory reserve volume
total air you can blow out
residual volume
air left in lungs: never completely empty
vital capacity
total lung capacity you can move in and out
inspiratory- reserve volume
max amount you can take in
Alveolar ventilation
Amount of fresh air that makes it to alveoli
- not al inspired air participates in gas exchange (anatomic dead space)
alveolar ventilation is the volume of inspired air that reaches the alveoli each minute
Va = Vt -Vd
increasing total volume with be more effective then increasing breath for total ventilation as the dead space is fixed
Dalton’s Law
when a mixture of gases are present, each individual gas exerts a partial pressure, proportional to the fraction of the mix it represents
the partial pressure of which two parts of lung influences difusion?
alveolar air and pulmonary arteries
Fick’s Law
movement of gases across a membrane
impacted by..
- tissues surface area
thickness of tissue
diffusion coefficient of the gas
driving pressure (magnitude of the pressure gradient
rate of diffusion of gases
proportional to surface area and driving pressure
inversely proportional to tissue thickness
diffusion coefficient remain constant but CO2 has greater ease of diffusion than O2
How exercise changes pressure gradient in lungs
pressure in pulmonary arteries changes as more oxygen is being used leading to a more rapid diffusion
perfusion
blood flow in lungs
perfusion principles
At rest: more blood flow to dependent (lower) areas
Due to gravity – therefore, this depends on body position!
Upright: best perfusion in base of lung, worst perfusion in apex (top)
Supine: best perfusion in posterior lung, worst perfusion in anterior lung
During exercise: perfusion is more evenly distributed across lung fields
Matching Ventilation and Perfusion
Goal: maximize the interaction of oxygen-rich air in alveoli and oxygen-depleted blood in pulmonary capillaries
Ventilation/Perfusion ratio (V/Q):
Indicates matching of blood flow to alveolar ventilation
Ideal = 1.0 or slightly higher
physiological dead space
apex: reliteively high ventilation, low perfusion V/g is greater than 1
alveolus compressing blood flow
shunt
base: relatively low ventilation, high perfusion V/Q is way less than one
too much blood flow but smushing alveolus
mid-lower lung fields
best matching V/G = 1
pressure of both makes good gas exchange
ventilation and perfusion during exercise
light to moderate intensity: improves V/Q ration
very heavy exercise may worsen V/Q mismatch
pulmonary capillary transit time
Time required for blood to move through the length of the capillary
i.e. the time when gas exchange can take place
As you move from rest to exercise, heart rate and cardiac output increase
More/faster blood flow through pulmonary circulation
Transit time decreases
Shorter transit time is partially offset because more flow is distributed across all pulmonary capillaries during exercise
How is O2 transported in blood?
Carrier molecule = Hemoglobin (Hb)
Protein in red blood cells
About 99% of oxygen in blood is bound to hemoglobin, <1% dissolves
Main determinant of how much oxygen blood can carry
When leaving pulmonary capillaries, hemoglobin is almost always fully loaded (98-100% saturated) with oxygen
Each hemoglobin can bind 4 O2 molecules
Cooperativity
once the first O2 binds, the other binding sites have increased affinity and more easily bind O2
oxygen- hemoglobin binding and dissociation
Deoxyhemoglobin + O2 Oxyhemoglobin
Direction of the reaction depends on:
Affinity between Hb and O2
PO2 in the blood
At the lung: high PO2 favors binding of O2 to Hb
At the tissues: low PO2 favors dissociation (release of O2 to tissues)
Factors that change the dissociation curve
Decrease in pH (more acidity): lowers Hb-O2 affinity
Increase in temperature: lowers Hb-O2 affinity
- both of these things happen during exercise which allows oxygen to offload at tissues
oxygen in muscles transport
Carrier molecule in muscle cells: Myoglobin (Mb)
Shuttles O2 from the cell membrane to the mitochondria
Myoglobin has a greater affinity for O2 than hemoglobin
Remains bound to O2 even at very low PO2
Allows Mb to store O2 as a reserve for muscle
O2-Mb dissociation curve shaped differently than O2-Hb curve
Loading portion: PO2 = 20 mm Hg
Releasing portion: PO2 = 1-2 mmHg
myglobin vs. Hemoglobin
myoglobin’s unloading portion, only happens when PO2 is very low and really needed so while hemoglobin is already unbinding, myoglobin still wants it
Transport of CO2 in blood
CO2 is transported for removal in three ways:
Dissolved in plasma (10%)
Bound to hemoglobin (20%)
Bicarbonate (70%)
CO2 + H2O H2CO3 H+ + HCO3
relationship between pH, CO2 and ventilation
pulmonary ventilation removes H from blood by the HCO3 reaction
* increased ventilation results in increased exhalation of Co2
- reduces pCO2 in blood
- reduces H+ concentration
- increases pH
decreased ventilation results in increased retention of CO2
- increases pCO2 in blood
- increases H+ concentration
- decreases pH
Neural input
signals from higher brain centers
afferent input from stretch receptors, mechanoreceptors and muscle chemoreceptors
humoral input
blood-borne stimuli reach specific chemoreceptors
Neural input to respiratory control center: higher brain centers
Impulses from motor cortex (central command)
Neural signal passes through medulla and “spill over” causes increase in VE: causes increase in ventilation before exercise has started
Neural input to respiratory control center: stretch receptors (mechanoreceptors) in lungs
located in walls of bronchi and bronchioles
hering-beuer reflex: excessive stress causes inhibitory effects that inhibit inspiration
Neural input to respiratory control center: muscle mechanoreceptors
muscle spindles, GTOs, joint pressure receptors
Neural input to respiratory control center: muscle chemoreceptors
respond to changes in K and H inside and around muscle
- not humoral-mediated
Humoral input to respiratory control center: Central chemoreceptors
located in medulla oblongata
stimulated by increase CO2 or H in cerebrospinal fluid
increases ventilation
humoral input to respiratory control center: peripheral chemoreceptors
located in aortic and carotid bodies
sensitive to increase in PCO2, H, and decrease in PO2 (carotid only)
What part of the systemic system has the highest amount of oxygen?
pulmonary veins since just came from lungs
Humoral responses: PCO2 and PO2
not sensitive to changes in oxygen (except when reaching hypoxic threshold) but highly sensitive to changes in CO2
Carotid body (peripheral chemoreceptors) stimulus
PCO2
pH
PO2
Chemoreceptors stimuli located in meulla oblongata (central chemoreceptors)
PCO2
Aortic body (peripheral chemoreceptor) stimulus
PCO2
pH
Muscle mechanoreceptors stimulus
muscle contractile activity
muscle chemoreceptors (muscle meta baroreceptors) stimulus
pH
potassium
Ventilatory control during exercise: submaximal exercise
linear increase in ventilation
primary drive - increase in ventilation comes from higher brain centers (control command)
fine-tuned by
humoral chemoreceptors and neural feedback from muscle
ventilary control during exercise: heavy exercise
nonlinear (steeper) rise in Ve may result from:
increase in blood H that stimulates carotid bodies
increase in K, body temperature and body catecholamines may also contribute
What fine-tunes ventialtion during exercise
peripheral chemoreceptors
chemoreceptors
What is the primary drive to increase ventilation during exercise?
higher brain centers
Training effect on Ventilatory response
trained person has 20-30% less ventilation at the same work rate due to more efficant metabolism due to higher blood volume, more hemoglobin and prodce less CO2
Endurance training effects key take aways
Endurance training does not affect lung structure or pulmonary function (diffusion capacity)
Structural capacity of normal lung is overbuilt and can adequately maintain CO2/O2 homeostasis during exercise
*Pulmonary system is not usually the limiting factor in prolonged exercise (young/healthy subjects)
Exercise training does result in decreased VE at fixed submaximal workload
Adaptations due to increased aerobic capacity of skeletal muscle, decreased H+ production, decreased afferent feedback stimulating ventilation
Respiratory muscles in exercise
Diaphragm is highly oxidative and fatigue-resistant
Respiratory muscles can fatigue and may limit performance at very heavy work rates
Respiratory muscle training can have a small positive influence on performance
Highly trained endurance athletes show decreased fatiguability of respiratory muscles, even without respiratory muscle training
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