Applied Exercise Physiology: Unit 3: Lecture 1 (Cardiac Function During Exercise [HR, SV, and CO])
Terms in this set (135)
Heart Rate (HR):
Stroke Volume (SV):
Ejection Fraction (EF%):
Cardiac Output, Q (CO):
What is the main function of the cardiovascular system?
to transport things!
-has immune functions effects
-has endocrine system effects
How does the blood aid in thermoregulation?
warm blood (due to exercise or core body temp) travels from that area towards the surface of the skin... dissipates into air/activates sweat
What are the structures of the cardiovascular system?
What part of the heart are we focusing on in lecture? Why?
we focus on the left side of the heart
because that's the side that physically pumps the blood to the other tissues of the body (systemic circulation)
In order to get more blood flow to working muscle, what must mechanistically occur?
increased cardiac function
What are the cardiovascular responses to acute exercise?
altered heart rate (HR)
altered stroke volume (SV)
altered cardiac output (CO)
What are the two types of cells in the heart muscle? What are their respective roles?
contractile (myocardial) cells
-muscle cells that contract the muscle (create the tension that turns into the pressure that makes blood flow)
-are pink (in the diagrams from class)
-are what do the depolarizing (affect cardiac excitation-contraction coupling)
-make up the cardiac conduction system
-influence: heart rate & strength of cardiac input
-are yellow (in diagrams from class)
What composes the cardiac conduction system?
What are contractile (myocardial) cells? Where are they located? What do they do?
located in the heart
are muscle cells that contract the muscle (create the tension that turns into the pressure that makes blood flow)
are pink (in the diagrams from class)
What are autorhythmic cells? Where are they located? What do they do?
located in the heart
are what do the depolarizing (affect cardiac excitation-contraction coupling)
make up the cardiac conduction system
influence: heart rate & strength of cardiac input
are yellow (in diagrams from class)
What is the sequence of structures for cardiac excitation-contraction coupling?
Bundle of His
What is the significance of the SA node?
is the "pacemaker" of the cell
depolarizes the most rapidly/is the first structure in the sequence of cardiac excitation-contraction coupling
What occurs during the P wave?
AKA depolarization of the SA node and the AV node
What occurs during the QRS wave?
AKA depolarization down the Bundle of His and into the L&R Bundle Branches and Purkinje Fibers --> ventricles contract
What occurs during the T wave?
AKA the heart depolarizes so it's able to contract again
Which wave depicts the depolarization of the Bundle of His, Bundle Branches, and Purkinje Fibers?
AKA ventricular contraction
Which wave depicts the SA and AV node to contracting?
AKA atrial depolarization
Which wave depicts ventricular repolarization?
Which wave depicts atrial repolarization?
this occurs here, but is overshadowed by the bulk of the action, which involves ventricular contraction
Explain Intrinsic Heart Rate
The SA node controls HR... it intrinsically initiates 100 contractions per minute (AKA 100 BPM) when it lacks any extrinsic control (AKA sympathetic or parasympathetic control)
When the heart is dominantly controlled by the parasympathetic nervous system at rest, how does that affect the intrinsic heart rate?
the parasympathetic nervous system decreases heart rate (which will be explain later).... makes the HR deviate from intrinsic HR (100 BPM) and it in turn changes the HR to 80 BPM at rest
What is our intrinsic heart rate (how many BPM)?
What's higher: intrinsic HR BPM, or resting HR BPM? Why?
Intrinsic HR BPM is higher than resting HR BPM (intrinsic = 80 BPM... resting = 100 BPM)
this is because intrinsic HR is HR lacking an external control
resting HR is controlled by the parasympathetic NS at rest... this slows down HR
How is heart rate modulated?
HR is modulated extrinsically by the autonomic NS (sympathetic and parasympathetic NS)
signals from other parts of the body are integrated at the brain and signal either the PNS or SNS to release their respective catecholamines, which have either inhibitory or stimulatory effects on the heart
The autonomic nervous system controls lead to the secretion of catecholamines (NE, Epi) from the adrenal medulla, therefore affecting the heart
What happens to people's hearts after they've had heart surgery?
they have no autonomic control of their heart --> the nerves innervating the heart have been cut
-healthy peoples HR at rest is lower than people with heart transplants
-healthy peoples HR during exercise = higher than people with heart transplants
this is caused by lack of autonomic control
Extrinsic Control of HR:
This is what modulates HR --> the heart is controlled extrinsically by the autonomic nervous system (sympathetic and parasympathetic nervous system) which either raises or lowers heart rate (depending on external factors)
Explain how the Parasympathetic Nervous System modulates HR
-The body is at rest
-An AP is sent to the cardioinhibitory center in the brain
-A signal is sent along the vagus nerve (the PNS's #1 neuron)
-signal arrives at the SA node, the AV node (AKA the Effectors)
-The SA node and AV node become hyperpolarized (are therefore harder to depolarize, which means the heart beats less --> decreased HR)... AKA
negative chronotropic reffect
(the HR is lower than intrinsic HR [AKA 100 BPM])
What is the main effect of the PNS's control of HR?
the SA node and AV node are hyperpolarized
What is the HR when the body is under parasympathetic control at rest?
Negative chronotropic effect:
when the body's HR is lower than intrinsic HR (AKA below 100 BPM)
when the body experiences bradycardia, it is likely under parasympathetic control
when HR drops below 60 BPM
body is under parasympathetic control
When the body is under parasympathetic control, does it experience a positive or negative chronotropic effect?
negative chronotropic effect
HR drops below intrinsic HR (below 100 BPM)... because SA & AV nodes become hyperpolarized --> are more difficult to make beat --> HR decreases
When the body is under parasympathetic control, does it experience a positive or negative ionotropic effect?
Parasympathetic activity cannot control the contractile force of the heart (inotropic effect = contractile force is altered)
the muscular layer of the heart
located in the medulla oblongata
important in sympathetic control of the heart
located in the medulla oblongata
important in parasympathetic control of the heart
when the body is in a resting state, AP's are sent to the cardioinhibitory center, which then relays signals down the vagus nerve for the release of ACh from the adrenal medulla --> causes HR to slow down
the #1 nerve used in the parasympathetic nervous system... relays inhibitory signals from the brain to the heart, which slows down HR
Effectors: SA node, AV node (hyper polarizes them, so they're harder to excite... leads to decreased HR)
Neurotransmitter: ACh (released from the adrenal medulla)
occurs when the parasympathetic NS is very active
vagal tone = the vagus nerve is highly active... the vagus nerve is the #1 nerve used in the parasympathetic NS to send cardioinhibitory signals
Explain how Sympathetic Nervous System modulates HR
-the body is either exercising or under some other kind of stress
-AP is sent to the brain (cardioacceleratory center)
-signal is sent to the SA & AV nodes, as well as the ventricular pericardium
-SA & AV nodes become more depolarized (so they're easier to depolarize --> the heart can beat more) AKA
positive chronotropic effect
(HR > 100 BPM)
-Ventricular pericardium is stimulated --> increases contractile force (increases the amount of blood pumped per beat) AKA
positive inotropic effect
-uses NE as neurotransmitter
-BPM = 100+
What are the effectors for sympathetic nervous control of the heart?
SA & AV nodes
What is the significance of the SNS innervating the pericardium of the ventricle?
the SNS alters the force of the ventricles --> affects SV (AKA the amount of blood pumped out per beat)
when HR rises above 100 BPM
body is under sympathetic control (body under physical, emotional stress)
When the body is under sympathetic control, does it experience a positive or negative chronotropic effect?
positive chronotropic effect
HR rises intrinsic HR (above 100 BPM)... because SA & AV nodes become depolarized --> are easier to make beat --> HR increases
When the body is under sympathetic control, does it experience a positive or negative ionotropic effect?
positive ionotropic effect
an effector of the cardioacceleratory center is the ventricular pericardium... when NE (norepinephrine) reaches the heart, the ventricular pericardium is stimulated... the force of myocardial contraction increases... more blood can be pumped out per beat (increased SV)
What is the main effect of the SNS's control of HR?
the SA node and AV node are more depolarized
the ventricular pericardium is stimulated
alters HR by affecting the polarization of the SA and AV nodes of the heart
(parasympathetic = hyperpolarization --> decreased HR (HR < 100 BPM)
(sympathetic = depolarization --> increased HR (HR > 100 BPM)
alters the contractile force of the heart (by changing the stimulation of the ventricular pericardium)
(sympathetic = stimulation --> increased SV)
(does not affect the parasympathetic NS [because the PNS does not innervate the pericardium of the ventricles])
BPM < 100 BPM (below intrinsic HR)
BPM > 100 BPM (above intrinsic HR)
At rest, vagal tone is high. This contributes to:
A. positive chronotropic response
C. negative inotropic response
When the body is at rest, what happens with neural control in regard to the heart?
the HR is a balance between sympathetic and parasympathetic inputs
What is the typical resting HR for some who's untrained?
What is the typical resting HR for some who's trained?
Why is there a difference in resting HR for trained individuals vs untrained individuals?
trained individuals have higher vagal tone than untrained individuals
leads to trained individuals having more dominant parasympathetic control over HR
leads to decreased HR at rest
How does training affect vagal tone?
training = increased vagal tone = decreased HR at rest
parasympathetic control becomes more dominant then sympathetic control at rest --> decreased resting HR
Explain why and how the anticipatory response occurs
Anticipatory response = HR rises in anticipation of something (that will cause increased emotional or physical stress)
-feedforward control (idea you're going to do something = feedforward command telling HR to rise)
-less parasympathetic activity = decrease in vagal tone
-more catecholamine release (NE = decreased vagal tone, increased HR)
When we exercise, (parasympathetic/sympathetic) activity increases
increases in intensity = increase in stress = increase in sympathetic activity (NE release) = increased HR
HR increase is _______________________________ to exercise intensity
the higher the exercise intensity, the higher the HR
Steady State HR:
indicates optimal HR for meeting circulatory demands at a given
on a graph, this is represented as a point of plateau
Additional note: if intensity increases, steady state HR increases too
What is the amount of time it takes for HR to catch up to a new exercise intensity?
the highest HR achieved in all-out effort until fatigue (volitional fatigue)
What happens to HR max levels with age?
HR max declines with age (leads to a reduced ability to deliver blood to the skeletal muscle)
How to calculate HR max #1:
HRmax = 220-age
How to calculate HR max #2:
HRmax = 208-(0.7 x age)
know how to calculate HR max for test
What is the application of knowing HR max for exercise physiology?
HRmax (and steady-state HR) are the basic estimate of aerobic fitness
What is the best way to calculate aerobic fitness?
HR and HR Max
What % is the typical end point for HR max tests? Why?
85% HR max is usually the cut off point for testing
allows for a safety cushion
if you'd reach 100% HR max, you'd probably die
Stroke Volume (SV):
the amount (Volume) of blood pumped per ventricular contraction
Typical SV at rest:
the filling phase
blood travels from the atria to the ventricles
End-diastolic Volume (EDV):
the volume of blood that is in the ventricles after it has filled up
AKA: "The greatest amount of blood within the heart at one time"
when the heart is contracting
blood is ejected from the heart to other parts of the body
End-systolic Volume (ESV):
the volume of blood that remains in the ventricle at the end of contraction
(not all of the blood within the heart is ejected when the heart beats)
AKA: "The blood that's left over after the heart beats"
How do you calculate stroke volume (SV)?
SV = EDV-ESV
(filling)-(what left over after contraction)
the percent of the EDV that is pumped per beat
AKA how efficiently the heart pumps blood
How do you calculate EF?
EF = (SV/EDX)x100%
Why is EF used in the clinal setting?
to evaluate cardiac function
can be used to predict mortality
What happens in order to increase Ejection Fraction (EF)?
a change in contractile FORCE (AKA a
positive inotropic response
increased sympathetic activity = NE stimulates ventricular pericardium = positive inotropic response = increased ejection fraction (EF)
how much blood returns to the left side of the heart
AKA: end-diastolic ventricular stretch
the blood that returns from systemic circulation and into the inferior and superior vena cavae --> R heart
the flexibility of the heart
naturally declines with age
In order to increase preload, what must be increased?
increased venous return, ventricular distensibility (AKA increased flexibility of the heart) = increased preload
How does increased venous return affect the heart?
it increases preload (AKA the amount of blood that returns to the left heart)
High venous return = (high/low) preload?
more venous return = more blood to the L heart
High ventricular distensibility = (high/low) preload?
more pliability/flexibility = more blood to the L heart
Why does increased preload = increased SV?
more preload = more blood available in the ventricles = more blood that the blood is able to pump to the rest of the body = more blood is pumped out per beat due to high availability (increased SV)
heart contract with more force (due to positive inotropic effect), so SV increases
Explain the Frank-Starling Mechanism:
increased stretch in the heart = increased contraction strength in the heart
in the heart, when the muscle fibers are stretched, the thick & thin filaments are arranged so tension is increased
positive inotropic effect
heart stretch is due to EDV (my theory: because there's the max. amount of blood the blood can allow in it at the time)... more blood available = more tension is needed to push as much of it out of the heart as it can to get rid of it
the force of contraction the heart is capable of producing
What is a unique feature of Contractility?
contractility of the heart (the amount of force that the heart is able to produce) acts
in other words, the contractility/force of the heart doesn't depend on the amount of blood available in the heart (doesn't depend on Frank-Stratling mechanism)
at the same EDV (volume of blood in the ventricles), we can increase SV by increasing Contractility
Also: contractility is controlled by catecholamine release
What is the mechanism for contractility that leads to increased SV?
-increased sympathetic activity
-increased NE release (Epi also)
-increased Ejection Fraction
positive inotropic effect
the pressure/resistance in the arteries/blood vessels
What is the effect of high afterload on SV?
high afterload = high resistance/pressure --> low SV
the blood from the heart must work against a pressure that is similar to it's own... less blood gets ejected per beat (because there's a lot to press against) = low SV
What is the effect of low afterload on SV?
low afterload = low resistance/pressure --> high SV
the blood from the heart must have to work against a pressure much lower than it's own... a lot of blood can be ejected per beat (because there isn't much to press against = high SV
What is the relationship between exercise intensity and HR?
high exercise intensity = high HR
What is the relationship between exercise intensity and SV?
linear relationship for a while... then it plateaus
at 40-60% of VO2 max, the relationship is linear... then plateau occurs
Mechanisms for SV During Acute Exercise: Preload
Increased preload = Increased SV
Mechanisms for SV During Acute Exercise: Heart Rate
Increased Heart Rate = decreased time allowed for heart to fill with blood = Decreased SV
Mechanisms for SV During Acute Exercise: Contractility
Increased Contractility = Increased SV (due to more sympathetic activation during activity --> more catecholamine release = more contractility (due to more heart muscle stimulation)
Mechanisms for SV During Acute Exercise: Afterload
Decreased Afterload = Increased SV
exclusive to aerobic exercise only!!!!!
-aerobic exercise --> vasodilation of blood vessels (relax) --> decreased total peripheral resistance --> decreased afterload --> increased SV
Why does is the supine position different than the standing position?
standing = blood must work against gravity (less venous return)
What happens to EDV eventually during high intensity exercise?
there's a slight decrease in EDV (the max amount of blood that the heart fills up with) during high intensity activities because the heart pumps so often that it doesn't;t have enough tie to fill up with the amount of blood that it normally does
What are the 3 ways to assist in venous return?
1. one-way venous valves
2. skeletal muscle pump
3. respiratory pump
How do one-way valves help with venous return?
the valves prevent back flow
when the valves close in the veins, it's hard to get blood back to the feet.. instead, the blood flows back to the heart (venous return) (which is what the body wants/needs)
How does the skeletal muscle pump help with venous return?
as muscles contract, they compress the veins in the same anatomical location
muscle compresses veins = high pressure = blood flow back to the heart (venous return)
How does the respriatory muscle pump help with venous return?
the respiratory increases when we exercise (need to breathe more frequently)
inhale = increased volume of thoracic cavity = decreased pressure within the lungs (and vice versa)
high pressure in the veins and low pressure in the lungs = a pressure gradient that essentially "sucks" the blood back to the heart
Cardiac Output (Q):
the total volume of blood pumped per minute
synonymous with "blood flow"
How to calculate Cardiac Output (Q):
Q = HR x SV
What is the average total blood volume (in Liters)?
What is the typical resting CO (Q)?
~5 L/min (so we usually pump all of our blood through our circulation every minute)
What is the relationship between exercise intensity and Cardiac Output (CO, Q)?
increased exercise intensity = increased cardiac output
Typical resting Q? (cardiac output)
Typical untrained Qmax? (cardiac output max)
Typical trained Qmax? (cardiac output max)
What are all of the factors that affect heart rate (HR)?
What are all of the factors that affect stroke volume (SV)?
-duration of contraction
What systems are active in resistance exercise (which therefore alter blood flow)?
-increased SNA --> VC
-increased hormones --> VC
-increased metabolic VD --> VD
-mod endothelial VD --> mod VD
-increased muscle metaboreflex -> VC
What systems are active in aerobic exercise (which therefore alter blood flow)?
-increased endothelial VD --> VD
-mod increased SNA --> mod VC
-mod increased hormones --> mod VC
-mod increased metabolic VD --> mod VD
How does blood flow redistribution happen?
vasoconstriction/vasodilation at the level of the
Explain how VD occurs as the body thermoregulates
as the body temp increases, vasodilation occurs
heat buildup influences glycolysis --> decreased tension production........ heat moves down a gradient form warm muscles --> blood --> skin --> environment....... homeostatic reflex diverts CO to the skin.......... consequences of not enough blood flow to the skin = poor thermoregulation --> increased core body temp (which then limits excitation-contraction coupling... could lead to centra fatigue//central command failure)
Explain how the wide variety of inputs compete for blood flow (Q)
during exercise, there are several inputs that require blood flow.... all of these inputs compete for a limited blood supply (the body can only contain so much blood, after all)
exercise = increased work for respiratory muscles --> less blood is available for skeletal muscles
Explain cardiovascular drift
Main goal of the body: maintain CO (AKA keep CO constant)
over time, we sweat and get hot --> increased core temperature/dehydration = less blood within blood vessels = decreased stroke volume ((this may require changes in cardio function in order to compensate for this))
Overview: sweaty work = increased HR to maintain CO (because of decreased SV from sweat)
SV drifts which leads to a compensatory increase in HR to work to maintain CO
LO: ID the components of the cardiovascular system that change during acute exercise to match VO2 )and oxidative ATP production) to exercise intensity
LO: Review the role of the cardiac conduction system to control heart rate and cardiac contractile force. ID the typical values for resting heart rate.
LO: Describe the expected changes in heart rate during acute exercise
-ID reasonable numbers for exercise HR
-Be able to predict HR max
that match heart rate to exercise intensity
LO: Differentiate between Stroke Volume (SV) and Ejection Fraction (EF%)
-ID three factors that modulate SV at rest
-Explain how each factor influences SV during acute exercise
LO: Review how Cardiac Output is calculated
LO: Propose reasonable values for stroke volume and cardiac output at rest
LO: Describe the expected changes in Strove Volume and Cardiac Output during acute exercise