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Chapter 9
Outline
Organization of the
Circulatory System
Structure of the Heart
Pulmonary and Systemic
Circuits
Heart: Myocardium
and Cardiac Cycle
Myocardium
Cardiac Cycle
Arterial Blood Pressure
Factors That Influence
Arterial Blood Pressure
Electrical Activity of the
Heart
Cardiac Output
Regulation of Heart Rate
Heart Rate Variability
Regulation of Stroke
Volume
Hemodynamics
Physical Characteristics
of Blood
Relationships Among
Pressure, Resistance,
and Flow
Sources of Vascular
Resistance
Changes in Oxygen
Delivery to Muscle
During Exercise
Changes in Cardiac
Output During Exercise
Changes in Arterial-Mixed
Venous O2 Content
During Exercise
Redistribution of Blood
Flow During Exercise
Regulation of Local Blood
Flow During Exercise
Circulatory Responses
to Exercise
Emotional Influence
Transition From Rest to
Exercise
Recovery From Exercise
Incremental Exercise
Arm Versus Leg Exercise
Intermittent Exercise
Prolonged Exercise
Regulation of
Cardiovascular
Adjustments to
Exercise
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Chapter 9
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Chapter 9
Capillaries
Exchange of O2, CO2, and nutrients with tissues
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Chapter 9
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Chapter 9
Systemic circuit
Left side of the heart
Pumps oxygenated blood to the whole body via arteries
Returns deoxygenated blood to the right side of the heart via
veins
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Chapter 9
Pulmonary and
Systemic Circulations
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Chapter 9
Myocardium
The heart wall
Epicardium
Myocardium
Endocardium
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Chapter 9
Coronary vessels
Characteristics
Function
Epicardium
Serous membrane
(visceral
including blood
pericardium) capillaries, lymph
capillaries, and nerve
fibers
Serves as
lubricative
outer covering
Myocardium
Provides muscular
contractions that
eject blood from
the heart chambers
Endocardium
Serves as
protective inner
lining of the
chambers and
valves
Fibrous pericardium
Serous pericardium
Pericardial cavity
Figure 9.3 The heart wall is composed of three distinct layers: (1) epicardium, (2) myocardium, and (3) endocardium.
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Chapter 9
Cardiac muscle
TABLE 9.1
Structural Comparison
Contractile proteins: actin
and myosin
Shape of muscle fibers
Nuclei
Z-discs
Striated
Cellular junctions
Connective tissue
Heart Muscle
Present
Present
Elongatedno branching
Functional Comparison
Energy production
Calcium source (for contraction)
Neural control
Regeneration potential
Skeletal Muscle
Aerobic (primarily)
Sarcoplasmic reticulum and
extracellular calcium
Involuntary
Noneno satellite cells present
Multiple
Present
Yes
No junctional complexes
Epimysium, perimysium, and
endomysium
Aerobic and anaerobic
Sarcoplasmic reticulum
Voluntary
Some possibilities via satellite cells
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Chapter 9
Diastole
Relaxation phase
Filling with blood
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Chapter 9
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Chapter 9
Diastole
0.3 second
0.5 second
Systole
Diastole
0.2 second
0.13 second
CONFIRMIN
Rest
Heart rate = 75 beats/min
Heavy exercise
Heart rate = 180 beats/min
Illustration of cardiac cycle at rest and during exercise. Notice that increases in heart rate during e
ved primarily through a decrease in the time spent in diastole; however, at high heart rates, the len
nt in systole also decreases.
Time (seconds)
A healthy 21-year-old female might have an
resting heart rate of 75 beats per minute. This
0
0.2
0.4
120
hat the total cardiac cycle lasts 0.8 second,
second spent in diastole and the remaining
100
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nd dedicated toCopyright
systole
(17) (see Fig. 9.5). If
0.6
Chapter 9
Systole
Pressure in ventricles rises
Blood ejected in pulmonary and systemic circulation
Semilunar valves open when ventricular P > aortic P
Heart sounds
First: closing of AV valves
Second: closing of aortic and pulmonary valves
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Chapter
.13
second
during exercise are achieved primarily through a decrease in the time spent in diastole;
ength of time spent in systole also decreases.
120
0.2
0.4
0.6
0.8
100
Pressure (mm Hg)
Time (seconds)
80
Ventricle
60
40
20
0
Volume (ml)
Systole
Diastole
120
80
40
1st
2nd
Heart sounds
Chapter 9
Bundle Branches
To left and right ventricle
Purkinje fibers
Throughout ventricles
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Chapter 9
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Chapter 9
Electrocardiogram (ECG)
Records the electrical activity of the heart
P wave
Atrial depolarization
QRS complex
Ventricular depolarization and atrial repolarization
T wave
Ventricular repolarization
CONFIRMING
PAGES
Heart: Myocardium
and Cardiac
Cycle
Chapter 9
Normal Electrocardiogram
0.8 second
Millivolts
+1
PQ
segment
ST
segment
T wave
P wave
0
Q
PR
S
interval
QT
interval
QRS interval
Atria
contract
Ventricles
contract
Atria
contract
Ventricles
contract
Chapter 9
Atherosclerosis
Fatty plaque that narrows coronary arteries
Reduces blood flow to myocardium
Myocardial ischemia
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Chapter 9
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Chapter 9
Key
Wave of
depolarization
Wave of
repolarization
P
Q
Copyright
2015 McGraw-Hill
Education. Allbetween
rights reserved.
No reproduction
or distribution
the prior written
consent
McGraw-Hill
Figure 9.12
An illustration
of the relationship
the hearts
electrical
events andwithout
the recording
of the
ECG.ofPanels
12 Education.
Chapter 9
onship between the hearts electrical events and the recording of the ECG. Panels 12
formation of the P wave. Panels 34 illustrate ventricular depolarization and formals 56 illustrate repolarization of the ventricles and formation of the T wave.
Time (seconds)
0.2
0.4
120
100
0.6
0.8
Intraventricular
pressure rises
as ventricles
contract
80
60
Intraventricular
pressure falls
as ventricles
relax
40
20
0
Systole
Diastole
ECG R
P
Q
AV valves
close
P
Q
S
S1
S2
Semilunar
valves close
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Chapter 9
Systolic pressure
Pressure generated during ventricular contraction
Diastolic pressure
Pressure in the arteries during cardiac relaxation
Pulse pressure
Difference between systolic and diastolic
Chapter 9
Short-term regulation
Sympathetic nervous system
Baroreceptors in aorta and carotid arteries
Increase in BP = decreased SNS activity
Decrease in BP = increased SNS activity
Long-term regulation
Kidneys
Via control of blood volume
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Chapter 9
Short-term regulation:
Baroreceptors in aorta and carotid arteries
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Chapter 9
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Chapter 9
In Summary
Blood pressure can be increased by one or all of the following factors:
a. Increase in blood volume
b. Increase in heart rate
c. Increased blood viscosity
d. Increase in stroke volume
e. Increased peripheral resistance
The pacemaker of the heart is the SA node.
A recording of the electrical activity of the heart during the cardiac
cycle is called the electrocardiogram (ECG).
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Cardiac Output
Chapter 9
Cardiac Output
The amount of blood pumped by the heart each
minute
Product of heart rate and stroke volume
Heart rate
Number of beats per minute
Stroke volume
Amount of blood ejected in each beat
Q = HR x SV
Cardiac Output
Chapter 9
Subject
CONFIRMING PAG
Typical Resting and Maximal Exercise Values for Stroke Volume (SV), Heart Rate
) for College-Age Untrained Subjects and Trained
(HR), and Cardiac Output (Q
Endurance Athletes (Body Weights: Male 5 70 kg; Female 5 50 kg)
?
SV
HR
Q
(ml/beat)
(beats/min)
(l/min)
Rest
Untrained male
Untrained female
Trained male
Trained female
Max Exercise
Untrained male
Untrained female
Trained male
Trained female
72
75
50
55
3
3
3
3
70
60
100
80
5
5
5
5
200
200
190
190
3
3
3
3
110
90
180
125
5
5
5
5
5.00
4.50
5.00
4.40
22.0
18.0
34.2
23.8
Note that values are rounded off. Data from references 3, 22, and 68.
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Carotid
baroreceptors
Cardiac Output
Chapter 9
Chapter 9
Cardiac Output
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Cardiac Output
Chapter 9
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Cardiac Output
Chapter 9
End-Diastolic Volume
Frank-Starling mechanism
Greater EDV results in a more forceful contraction
Due to stretch of ventricles
Respiratory pump
Changes in thoracic pressure pull blood toward heart
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FIRST PAGES
Cardiac Output
Chapter 9
ath
a
an
8).
ales
olm
in
200
Stroke volume (ml)
ed
he
100
Normal
resting
value
200
300
400
Cardiac Output
Chapter 9
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Chapter 9
Cardiac Output
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Cardiac Output
Chapter 9
Cardiac
output
Cardiac rate
Stroke volume
Contraction
strength
Parasympathetic
nerves
Sympathetic
nerves
End-diastolic
volume (EDV)
Mean arterial
pressure
Stretch
FrankStarling
18
Factors that regulate cardiac output. Variables that stimulate cardiac output are shown by solid arr
tors that reduce cardiac output are shown by dotted arrows.
MODYNAMICS
Blood sample
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Cardiac Output
Chapter 9
In Summary
Cardiac output is the product of heart rate and stroke volume (Q = HR
x SV). Figure 9.18 summarizes those variables that influence cardiac
output during exercise.
The pacemaker of the heart is the SA node. SA node activity is
modified by the parasympathetic nervous system (slows HR) and the
sympathetic nervous system (increases HR).
Heart rate increases at the beginning of exercise due to a withdrawal
of parasympathetic tone. At higher work rates, the increase in heart
rate is achieved via an increased sympathetic outflow to the SA node.
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Cardiac Output
Chapter 9
In Summary
Stroke volume is regulated by: (1) end-diastolic volume, (2) afterload
(i.e., aortic blood pressure), and (3) the strength of ventricular
contraction.
Venous return increases during exercise due to (1) venoconstriction,
(2) the muscle pump, and (3) the respiratory pump.
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Hemodynamics
Chapter 9
Cells
Red blood cells
Contain hemoglobin to carry oxygen
Platelets
Important in blood clotting
Hematocrit
Percentage of blood composed of cells
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Hemodynamics
Chapter 9
Components of Blood
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Hemodynamics
Chapter 9
Pressure
Proportional to the difference between MAP and right atrial
pressure ( Pressure)
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Chapter 9
Hemodynamics
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Hemodynamics
Chapter 9
Hemodynamics
Resistance depends upon:
Length of the vessel
Viscosity of the blood
Radius of the vessel
Length x Viscosity
Resistance =
Radius4
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Hemodynamics
Chapter 9
Capillaries Venules
Large
veins
Blood pressure
(mm Hg)
Precapillary sphincters
120
Left
Large
ventricle arteries
Arterioles
80
Stroke volume
(ml beat1)
100
80
60
40
140
120
100
80
0
Resistance vessels
Exchange
vessels
Capacitance
vessels
ardiac output
(! min1)
20
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25
20
15
10
Hemodynamics
Chapter 9
In Summary
Blood is composed of two principle components, plasma and cells.
Blood flow through the vascular system is directly proportional to the
pressure at the two ends of the system, and inversely proportional to
resistance.
The most important factor determining resistance to blood flow is the
radius of the blood vessel.
The greatest vascular resistance to blood flow is offered in the
arterioles.
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Chapter 9
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D Pressure
Blood flow 5 _____________________________
Resistance
200
160
During intense exercise, the metabolic need for oxygen in skeletal muscle increases many times over the
resting value. To meet this rise in oxygen demand,
blood flow to the contracting muscle must increase.
As mentioned earlier, increased oxygen delivery to
exercising skeletal muscle is accomplished via two
mechanisms: (1) an increased cardiac output and (2)
a redistribution of blood flow from inactive organs to
the working skeletal muscle.
50
75
100
2 max
~40% VO
140
120
100
80
25
50
75
100
25
50
75
100
25
50
75
100
25
50
75
100
25
Cardiac output
(. min1)
Heart rate
(beats min1)
CHANGES IN OXYGEN
DELIVERY TO MUSCLE
DURING EXERCISE
Diastolic
80
20
15
10
5
200
150
100
Arteriovenous
O2 difference
(ml 100ml1)
Mean
120
Length 3 Viscosity
Resistance 5 ____________________________________________________
Radius4
The greatest vascular resistance to blood flow is
Systolic
240
25
Stroke volume
(ml beat1)
Changes in
Cardiovascular
Variables During
Exercise
IN SUMMARY
Blood is composed of two principal components: plasma and cells.
Blood flow through the vascular system is directly proportional to the pressure at the two
ends of the system and inversely proportional
to resistance:
Blood pressure
(mm Hg)
Chapter 9
50
18
12
6
2 max
Percent VO
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prior written consent of McGraw-Hill Education.
Chapter 9
Increased SV
Increase, then plateau at 4060% VO2 max
No plateau in highly trained subjects
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Chapter 9
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Chapter 9
Fick equation
Relationship between cardiac output (Q), a-vO2 difference, and
VO2
VO2 = Q x avO2 difference
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Chapter 9
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Chapter 9
At the beginning o
muscle vasodilation tha
1,400
metabolic control (41). T
1,200
tion is termed autoreg
1,000
be the most importan
800
flow to muscle during e
bolic rate of skeletal m
600
local changes such as
400
increases in CO2 tension
Rest
adenosine concentratio
(increase in acidity) (se
100
local changes work toge
arterioles feeding the co
80
Vasodilation reduces t
60
therefore increases bloo
changes, blood delivery
40
during heavy exercise m
above that during rest (4
20
tion is combined with r
in skeletal muscle. At res
0
25
50
75
100
illaries in skeletal musc
2 max
Percent VO
however, during intens
FigureEducation.
9.23 All
Changes
splanchnic
capillaries
in contracting
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rights reserved.in
No muscle
reproduction orand
distribution
without the priorblood
written consent of McGraw-Hill
Education.
Chapter 9
CONFIRMING PAGES
25 /min.
100%
35%
45%
24%
0.51%
34%
8085%
Heavy exercise
~20 /min.
Heavy
exercise
Rest
~0.75 /min.
Rest
100%
2025%
45%
20%
35%
15%
45%
1520%
Cardiac output
= 5 /min.
5 /min.
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Figure 9.24 Distribution of cardiac output during rest and maximal exercise. At rest, the cardiac output is 5 ,/min.
Chapter 9
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Chapter 9
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Chapter 9
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Chapter 9
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Chapter 9
Important in autoregulation
With other local factors
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Chapter 9
In Summary
Oxygen delivery to exercising skeletal muscle increases due to (1) an
increased cardiac output and (2) a redistribution of blood flow from
inactive organs to the contracting skeletal muscle.
Cardiac output increases as a linear function of oxygen uptake during
exercise. During exercise in the upright position, stroke volume
reaches a plateau at approximately 4060% of VO2max; therefore, at
work rates above 4060% VO2max, the rise in cardiac output is due
to increases in heart rate alone.
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Chapter 9
In Summary
During exercise, blood flow to contracting muscle is increased, and
blood flow to less-active tissues is reduced.
Regulation of muscle blood flow during exercise is primarily regulated
by local factors (called autoregulation). Autoregulation refers to
intrinsic control of blood flow by changes in local metabolites (e.g.,
oxygen tension, pH, potassium, adenosine, and nitric oxide) around
arterioles.
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Chapter 9
Environmental condition
Hot/humid vs. cool
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Stroke volume
(ml beat1)
Exercise
15
Recovery
10
5
120
100
80
140
Heart rate
(beats min1)
PONSES
Cardiac output
( min1)
120
100
80
60
0
10
20
emotionally charged
Rest
Exercise
Recovery
heart rates and blood
Exercise and recovery time (min)
e same work in a Copyright
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Chapter 9
During recovery
Decrease in HR, SV, and cardiac output toward resting
Depends on:
Duration and intensity of exercise
Training state of subject
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Chapter 9
Incremental Exercise
Heart rate and cardiac output
Increases linearly with increasing work rate
Reaches plateau at 100% VO2 max
Blood pressure
Mean arterial pressure increases linearly
Systolic BP increases
Diastolic BP remains fairly constant
and systolic blood pressure that occurs during exercise results in an increased workload on the heart.
The increased metabolic demand placed on the heart
during exercise can be estimated by examining the
double product. The double product (also known
TABLE 9.3
Changes in the Double Product (i.e., Heart Rate 3 Systolic Blood Pressure)
During an Incremental Exercise Test in a Healthy 21-Year-Old Female Subject
Note that the double product is a dimensionless term that reflects the relative changes in the workload placed on the
heart during exercise and other forms of stress.
Heart Rate
(beats ? min21)
Condition
Rest
Exercise
25% V~ O2 max
50% V~ O2 max
75% V~ O2 max
100% V~ O2 max
www.mhhe.com/powers9e
85-214.indd 209
Systolic Blood
Pressure (mm Hg)
Double Product
75
110
8,250
100
140
170
200
130
160
180
210
13,000
22,400
30,600
42,000
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209
24
Chapter 9
Blood pressure
Due to vasoconstriction of large inactive muscle mass
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Chapter 9
180
160
Arm
exercise
140
Leg
exercise
120
100
Heart rate
(beats min1)
Heart Rate
160
Arm
exercise
140
120
Leg
exercise
100
0
Stroke volume
(ml beat1)
|
1.0
|
1.5
|
2.0
Heart rate
(beats min1)
Blood pressure
(mm Hg)
200
Cardiac output
( min1)
180
160
140
120
Changes in
Chapter 9
Intermittent Exercise
Recovery of heart rate and blood pressure between
bouts depend on:
Fitness level
Temperature and humidity
Duration and intensity of exercise
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Chapter 9
Prolonged Exercise
Cardiac output is maintained
Gradual decrease in stroke volume
Due to dehydration and reduced plasma volume
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Chapter 9
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Chapter 9
In Summary
The changes in heart rate and blood pressure that occur during
exercise are a function of the type and intensity of exercise
performed, the duration of exercise, and the environmental
conditions.
The increased metabolic demand placed on the heart during exercise
can be estimated by examining the double product.
At the same level of oxygen consumption, heart rate and blood
pressure are greater during arm exercise than during leg exercise.
The increase in heart rate that occurs during prolonged exercise is
called cardiovascular drift.
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during
Chapter 9
ring
ar drift.
eginning
after the
here is a
which is
mulation
a vasodiand a re-
CARDIAC
OUTPUT
Cardiac
rate
Sympathoadrenal
system
BLOOD FLOW TO
SKELETAL MUSCLES
Stroke
volume
Improved
venous
return
Metabolic
vasodilation
in muscles
Sympathetic
vasoconstriction
in viscera
Skeletal
muscle
activity
Deeper
breathing
Figure 9.28
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Chapter 9
Muscle mechanoreceptors
Sensitive to force and speed of muscular movement
Baroreceptors
Sensitive to changes in arterial blood pressure
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Chapter 9
Central command
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Chapter 9
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CONFIRMING
PAGES to Exercise
Regulation of Cardiovascular
Adjustments
Chapter 9
r exercise) are
r motor signals,
cardiovascular
cardiovascular
mechanorecepmechanorecep(baroreceptors)
the aortic arch
ensitive to intassium, lactic
r brain centers
ses to exercise
to the cardiogata) has been
Central
command
(higher brain
centers)
CV
control center
Baroreceptors
Heart
Blood vessels
Skeletal muscle
muscle spinChemoreceptors
Mechanoreceptors
ve to the force
ese receptors,
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nformation to Copyright Figure
9.29 A summary of cardiovascular control during
Chapter 9
In Summary
The central command theory of cardiovascular control during
exercise proposes that the initial signal to drive the cardiovascular
system at the beginning of exercise comes from higher brain centers.
Although central command is the primary drive to increase heart rate
during exercise, the cardiovascular response to exercise is fine-tuned
by feedback from muscle chemoreceptors, muscle
mechanoreceptors, and arterial baroreceptors to the cardiovascular
control center.
Copyright 2015 McGraw-Hill Education. All rights reserved. No reproduction or distribution without the prior written consent of McGraw-Hill Education.
Chapter 9
Copyright 2015 McGraw-Hill Education. All rights reserved. No reproduction or distribution without the prior written consent of McGraw-Hill Education.
Chapter 9
CLINICAL
APPLICATIONS
9.1
Endurance Exercise Protects Against
Cardiac
g Protects
the Injury
Heart During Heart Attack
100
Percentage of cardiac injury during
a myocardial infarction
80
FIGURE 9.4
60
40
20
0
Untrained
Trained
durance exerc
the heart again
during a heart
that during a m
infarction (i.e.,
exercise-traine
als suffer signi
cardiac injury
untrained indi
from reference
Copyright 2015 McGraw-Hill Education. All rights reserved. No reproduction or distribution without the prior written consent of McGraw-Hill Education.