KINE 639 - Dr. Green

1
KINE 639 - Dr. Green Section 1 Clinical
Physiology I, II, III, IV
2
Definitions, Concepts, and Hemodynamics
3
Cardiac Anatomy
Aorta
Left Pulmonary Artery
Superior Vena Cava
Left Atrium
Right Pulmonary Veins
Left Pulmonary Veins
Right CA
Left Anterior Descending CA
Right Atrium
Inferior Vena Cava
Left Ventricle
Right Ventricle
4
Cardiac Anatomy
Aorta
Superior Vena Cava
Left Pulmonary Artery
Aortic Valve
Left Atrium
Right Pulmonary Veins
Left Pulmonary Veins
Right Atrium
Mitral Valve
Tricuspid Valve
Inferior Vena Cava
Left Ventricle
Right Ventricle
Notice that the left ventricle contains more
electrically active muscle mass than the right
ventricle
5
The Normal Heart and Regional Circulation
Anterior Cutaway View
6
The Normal Heart - Coronary Artery Anatomy
Left Main CA
Layers of the Arterial Wall
Circumflex
Adventitia
Media
Intima
Right CA
Marginal Branch
Left Anterior Descending CA
7
Left Ventricular Volumes - Definitions
End Diastolic Volume (EDV) Volume at the end of
diastole (end of ventricular filling). In a
healthy heart this is directly proportional to
venous return End Systolic Volume (ESV) Volume
at the end of systole (end of ventricular
contraction) Stroke Volume (SV) EDV -
ESV Ejection Fraction (EF) SV EDV
NOTE Resting Ejection Fraction (EF) is the best
indicator of both heart performance and heart
disease prognosis
Left ventricular norm for EF at Rest
approximately 62 Left Ventricular norms for Max
Exercise approximately 80
8
Changes in Left Ventricular Volumes with Exercise
of Increasing Intensity
EDV
120
110
100
90
Left Ventricular Volume (ml)
80
70
SV
EDV - ESV SV
60
50
40
30
20
ESV
10
Rest
600 - 750
300
Peak Exercise
Workload or Power (kg meters / min)
9
Definitions

• Cardiac Output (Q) HR X SV
• Cardiac Index Q / body surface area
• Preload (EDV) volume of the left ventricle at
  the end of diastole
  dependent on venous return compliance
  (stretchability) of ventricle
• Afterload resistance to ventricular emptying
  during systole or the
  amount of pressure the left ventricle must
  generate to squeeze blood into the aorta. In a
  a healthy heart this is synonymous with Aortic
  Pressure Mean Arterial Pressure (MAP)
• Frank Starling Law of the Heart the heart will
  contract with greater force as preload (EDV)
  is increased r more blood in more blood out
• Myocardial Contractility the squeezing
  contractile force that the heart can develop at
  a given preload
• Regulated by
• Sympathetic nerve activity (most influential)
• Catecholamines (epinephrine norepinephrine)
• Amount of contractile mass
• Drugs

10
Starlings Law of the Heart and Contractility
Starlings Law The greater the EDV (blood
going in the heart), the more blood comes out of
the heart
SV (left ventricular performance)
u Contractility
Normal Contractility
SV at Preload X - u contractility
SV at Preload X Normal cont.
SV at Preload X - d contractility
d Contractility (heart failure)
The State of Myocardial Contractility determines
the amount of blood (SV) that comes out of the
heart at a given preload
Preload (venous return or EDV)
Preload X
11
Influences on Myocardial Contractility
u Contractility related to Exercise - u b
sympathetic adrenergic nerve output Catecholamine
s - Epinephrine Norepinephrine Excitement or
Fear - Fight or flight mechanism Drugs -
Digitalis Sympathomimetics d Contractility
related to Loss of contractile mass - Most
likely due to heart attack Myocardial muscle
disease - Cardiomyopathy Drugs - Anesthetics,
Barbiturates
12
Definitions

• Arteriovenous Oxygen Difference (AVO2D) the
  difference in oxygen content between arterial
  and venous blood
• measured in ml - ml O2 / 100 ml blood
• Oxygen Consumption (VO2) - the rate at which
  oxygen can be used in energy production and
  metabolism
• absolute measures L O2 / min , ml O2 / min
• relative measures ml O2 / kg body wt. / min
• Fick equation VO2 Q X AVO2D
• Maximum Oxygen Consumption (VO2max) maximum rate
  at which a person can take in and utilize oxygen
  to create usable energy
• defined as plateau of consumption rate increase
• often estimated with VO2peak
• Myocardial Oxygen Consumption VO2 of the heart
  muscle (myocardium)
• "estimated" by RPP HR X SBP

13
Definitions

• Systolic Blood Pressure (SBP) pressure measured
  in brachial artery during systole (ventricular
  emptying and ventricular contraction period)
• Diastolic Blood Pressure (DBP) pressure measured
  in brachial artery during diastole (ventricular
  filling and ventricular relaxation)
• Mean Arterial Pressure (MAP) "average" pressure
  throughout the cardiac cycle against the walls
  of the proximal systemic arteries (aorta)
• estimated as .33(SBP - DBP) DBP
• Total Peripheral Resistance (TPR) - the sum of
  all forces that oppose blood flow
• Length of vasculature (L)
• Blood viscosity (V)
• Vessel radius (r)

TPR ( 8 ) ( V ) ( L ) ( p ) ( r
4 )
14
Cardiovascular Hemodynamic Basics
Pressure (MAP) P aorta P
vena cava Resistance (TPR)
(8) (V) (L)
(?) (r 4)
Flow (Q)
(?) (Pa Pv) (r 4) (8) (V) (L)
Flow (Q)
Normally Resting Q is about 5 - 6 liters / minute
V viscosity of fluid (blood) flowing through
the pipe L length of pipe (blood vessel) r
radius of the pipe (blood vessel) Pa aortic
pressure Pv venous pressure
15
Respiratory Physiology - Definitions

• Minute Ventilation (VE) amount of air passing
  through the lungs in one minute
• Dyspnea - breathing difficulty
• Respiratory Exchange Ratio - amount of CO2
  expired by the lungs divided by the amount of O2
  extracted from the air in the lungs (VCO2 / VO2
  ). RER .7 r 100 fat 0
  carb RER .85 r 50 fat 50 carb RER
  1.0 r 0 fat 100 carb

16
Neurophysiology - Definitions

• Afferent - sensory nerves - going toward spinal
  column
• Efferent - effector nerves - going away from
  spinal column

Essential Knowledge of the Areas of the Brain in
Green
17
Organization of the Nervous System
Nervous System
Central Nervous System (CNS)
Peripheral Nervous System (PNS)
Brain
Spinal Cord
Motor (efferent) Neurons
Sensor (afferent) Neurons
Autonomic Nervous System
Somatic Nervous System
Voluntary movement
Input from Internal receptors
Output to Skeletal muscles
Output to smooth muscles and CVS
Involuntary (Reflexes)
Sympathetic Motor System
Parasympathetic Motor System
Relaxing responses
Neurotransmitter acetylcholine
Cholinegeric nervous system
Neurotransmitter nonadrenaline
Flight or Fight responses
Adrenergic nervous system
18
Adrenergic Receptors Associated Responses

• a1 stimulation
• Constriction of blood vessels
• Vascular smooth muscle activation
• Constriction of lung bronchioles
• Constriction of bladder muscles
• u myocardial cardiac contractility
• Relaxation of GI tract
• a2 stimulation
• u central sympathetic outflow
• u release of E NE
• a1 b1 receptor activation
• Constriction of lung bronchioles
• b1 stimulation
• u in HR
• u in myocardial contractility
• u in Renin secretion
• u fluid retention
• b2 stimulation
• Dilation of lung bronchioles

Agonist body molecule or drug
stimulator Antagonist - body molecule or drug
in-activator
a2 Agonists
b1 b2 Agonists
Agonists in the adrenergic system are
primarily epinephrine and
norepinephrine Antagonists are many times
associated with drugs known as blockers
i.e.b-blocker or a-blocker
Responses
19
Brain
Lungs
Arteries (Stiff
Inflexible Pipes)
Veins
(Flexible Compliant Pipes)
Intima
Intima
Valve
Elastin
Elastin
Media
Media
Liver
Stomach
Externa
Externa
Pancreas
Serosa
Intestines
Kidneys
The Systemic Circulation
Arterioles and Pre-capillary Sphincters
Skin
Muscle
20
Microcirculatory Anatomy a Capillary Bed
Arteriole
Smooth Muscle
Pre-capillary Sphincters (closed in this
illustration)
Anastomosis (Shunt)
Capillary Bed
Metarteriole
Capillary in Cardiac Muscle (arrows)
Venule
21
Development of the Driving Pressure in the Human
Cardiovascular System
100
Arterial
100
Pressure
Normal Resting Pressure Driving the Blood from
Left Ventricle to Vena Cava 100 - 0 100
mmHg
(mm Hg)
26
Mean Circulatory Filling Pressure
7
7
0
7
6
7
0
Central
0
Venous
Pressure
(mm Hg)
1
5
0
Normal Resting Cardiac Output
Cardiac Output (Q)
(Liters / min)
22
Arterial Pressures in Maroon
The Closed Cardiovascular Hemodynamic System
Venous Pressures in Blue
LV
PO2 160 PCO2 .3
RV
LA
RA
LUNGS
AORTA
(100)
(13)
(0)
PO2 100 PCO2 40
(3)
9 of blood volume
(7)
SYSTEMIC ARTERIES
Ohms Law Flow (Q) upstream pressure
downstream pressure
resistance
(92)
low compliance 13 of blood volume
VEINS (CAPACITANCE VESSELS)
(20)
(40)
high compliance 64 of blood volume
(2)
ARTERIOLES
CAPILLARYBEDS
PO2 40 PCO2 46
7 of blood volume
Systemic Circulation 100 mmHg 0 mmHg
100 ml / sec 6 liters / min Flow (Q)
1 mmHg sec / ml
23
Pressure, Flow, and Resistance by Vascular Cross
Sectional Area
Capillaries
Venules
Veins
Vena Cava
Capillaries
Venules
Veins
Vena Cava
Arterioles
Arterioles
Arteries
Arteries
Aorta
Aorta
Cross Sectional Area
100 mmHg
Flow Velocity
0 mmHg
100 mmHg
Relative Resistance to Flow
Mean Arterial Pressure
0 mmHg
24
MV is an Atrio-Ventricular Valve (AV) and is
bi-cuspid
Aortic valve is a semilunar valve
The Cardiac Cycle
Aortic Valve opens
Aortic Valve closes
SYSTOLE
120
Aortic Pressure (mmHg)
80
Left Ventricular Pressure (mmHg)
MV closes
MV opens
Atrial Contraction
Passive Ventricular Filling
Left Atrial Pressure (mmHg)
0
120
Left Ventricular Volume (ml)
0
0 .2
Time (sec)
http//www.youtube.com/watch?vyGlFBzaTuoIfeature
related
http//www.youtube.com/watch?vdYgYcH7R29INR1
25
Using Ventricular Pressure Curves as Indices of
Contractility Cardiac Function
dP/dt change in pressure per unit of time
dP/dt
dP/dt
Normal Heart Failure
120
Pressure
Note elevation in end diastolic pressure
indicating the build up of pressure in the heart
due to failure
0
Time
26
Cardiac Vascular Function Curves
Cardiac Function Curve
- illustrates
Q
what happens to Q when Pv changes.
5
CARDIAC
OUTPUT
(Liters / min)
operating point for the cardiovascular system
2
Pv
CENTRAL VENOUS PRESSURE (mmHg)
CARDIAC PRELOAD (mmHg)
RIGHT ATRIAL PRESSURE (mmHg)
27
Cardiac Function Curve - Q is the dependent
variable (in effect, Q is controlled by venous
return TPR)
Sympathetic Stimulation ( Exercise)
Normal Curve
CARDIAC
u Intrapleural Pressure ( Pressure in the chest
cavity ) To maintain same Q, CVP must u
OUTPUT
(Liters / min)
5
u TPR r u afterload
Parasympathetic Stimulation or Heart Failure
2
7
CENTRAL VENOUS PRESSURE (mmHg)
( can also be thought of as CARDIAC PRELOAD or
RIGHT ATRIAL PRESSURE )
28
Cardiac Vascular Function Curves
Cardiac Function Curve
- illustrates
Q
what happens to Q when Pv (venous
5
return - preload) changes.
CARDIAC
OUTPUT
operating point for the cardiovascular system
(Liters / min)
Vascular Function Curve
- illustrates what
happens to Pv when Q changes.
2
7
Pv
CENTRAL VENOUS PRESSURE (mmHg)
CARDIAC PRELOAD (mmHg)
RIGHT ATRIAL PRESSURE (mmHg)
29
Vascular Function Curve - central venous pressure
is dependent variable (in effect, CVP and venous
return are controlled by Q)
Sympathetic Stimulation Exercise r
venoconstriction r u total active vascular
volume ( Transfusion u blood Volume )
CARDIAC
OUTPUT
Normal Curve
(Liters / min)
5
Decreased Arteriolar Resistance d TPR ( Exercise
) ( Peripheral Vasodilation )
Increased Arteriolar Resistance ( Peripheral
Vasoconstriction) (u TPR r d venous
return r d CVP)
2
7
CENTRAL VENOUS PRESSURE (mmHg)
can also be called CARDIAC PRELOAD
30
Changes in Cardiac Vascular Function Curves
with Exercise
During Exercise, an u in sympathetic output will
cause 1. venoconstriction (VF curve shifted
rightward) 2. d TPR r vasodilation (VF curve
rotated upward) (caused primarily by
vasodilator metabolites) 3. u HR contractility
(cardiac curve shifted upward)
8 - 13
CARDIAC
OUTPUT
(Liters / min)
5
7
2
11
CENTRAL VENOUS PRESSURE (mmHg)
can also be called CARDIAC PRELOAD
31
Changes in Cardiac Vascular Function Curves
with Acute Compensated Heart Failure
CARDIAC
OUTPUT
1
3
(Liters / min)
Q 5 Liters / min
2
CENTRAL VENOUS PRESSURE (mmHg)
can also be called CARDIAC PRELOAD
1. Normal point of operating system normal
cardiac output 2 Pump begins to fail r Q falls
below normal resting levels 3. Renin-angiotensin
system activated r fluid retained r u MCFP r u Q
32
Changes in Cardiac Vascular Function Curves
with De-compensated Heart Failure
CARDIAC
OUTPUT
1
3
Q 5 Liters / min
(Liters / min)
4
2
5
Cause of peripheral edema
CENTRAL VENOUS PRESSURE (mmHg)
can also be called CARDIAC PRELOAD

• 1. Normal point of operating system normal
  cardiac output
• 2. Pump begins to fail r Q falls below normal
  resting levels
• Renin-angiotensin system activated r fluid
  retained r u MCFP r u Q
• Pump decline continues and Q falls once again
• More fluid is retained to try and compensate, but
  now Q is below a level where normal fluid
  balances can be maintained r r pattern continues

33
Left Ventricular Pressure Volume Loop
Aortic Valve Closes ESV ESP
Aortic Valve Opens
120
Left Ventricular Pressure (mmHg)
SV
Isovolumic contraction
Mitral Valve Closes EDV EDP
6
Slope of dashed line ventricular contractility
40
140
Mitral Valve Opens Ventricular Filling Begins
Volume (ml)
34
Effects of an Increase in Preload on Left
Ventricular Pressure Volume Loop
u Ejection Pressure
120
Left Ventricular Pressure (mmHg)
u SV
u EDV u EDP
6
40
140
Volume (ml)
35
Effects of an Increase in Afterload on Left
Ventricular Pressure Volume Loop
u ESV u ESP
120
Left Ventricular Pressure (mmHg)
d SV
6
40
140
Volume (ml)
36
Mechanism of Control of Cardiovascular and
Respiratory Systems
37
atrial stretch / pressure receptors located in
right left atria, junction of right atria and
vena cava, and junction of left atria and
pulmonary veins
Sites of Cardiorespiratory Control
38
Cardiorespiratory Control

• Heart Rate Neurohormone (neurotransmitter) and
  CNS (medulla) regulation
• Parasympathetic vagus control (Neurotransmitter
  Acetylcholine)
• Vagal control is dominant at rest influence
  is withdrawn when exercise begins
• Sympathetic cardioacceleration
  (Neurotransmitters EPINEPHRINE NOREPINEPHRINE)
• Baroreceptor influences
• Sympathetic discharge indirectly proportional to
  firing rate
• Parasympathetic discharge is directly
  proportional to firing rate
• d pressure r d receptor firing r u sympathetics r
  u HR r u pressure
• u pressure r u receptor firing r u
  parasympathetics r d HR r d pressure
• Atrial Stretch receptors u receptor stretch r
  u ANP r u Naexcretion r u urine output
• d receptor stretch r u ADH r d Naexcretion r d
  urine output
• Atrial Natriuretic Peptide released by myocytes
  in the atria r u urine flow r d BP
• Aniti-Diuretic-Hormone (vasopressin) released by
  pituitary r d urine flow r u BP
• Chemoreceptor influences
• Main function protect brain from poor perfusion
• u O2 or d CO2 r u parasympathetic discharge r
  d HR
• d O2 or u CO2 r d pH r pressor area
  stimulation in medulla r u HR

ADH Molecule
39
Cardiorespiratory Control

• Stroke Volume (SV) regulated by Frank Starling
  mechanism
• u venous return r u EDV r u stroke volume
• Cardiac Output (Q) main determinant body O2
  needs
• Autoregulated by two distinct mechanisms
• Intrinsic changes in preload, afterload, and SV
• u afterload r initial d in Q r u EDV (preload) r
  u SV back to normal
• Extrinsic hormonal influences
• Norepinephrine release r u HR and SV

40
Cardiorespiratory Control

• Blood Pressure influenced by 4 major factors
  (some interrelated)
• Total peripheral resistance
• Baroreceptor (BR) and CNS Influences
• u BP r u BR firing rate r vasodilation r d BP
• d BP r d BR firing rate r u sympathetics r u
  BP
• Chemoreceptor influences
• dO2, u CO2, d pH r CNS stim. r
  vasoconstriction
• Circulating catecholamine influences
• E and NE have varying effects on TPR
• E and NE usually activate a receptors r u TPR
• Fight or flight response
• Q
• Blood Volume
• Renin Angiotensin System

41
HYPOTENSION HYPOVOLEMIA
Renin - Angiotensin System
u H2O reabsorbed
d renal profusion
u sympathetic tone
u ADH (vasopressin)
d NACL delivery to macula densa cells
d stretch in afferent arteriolar JG cells
u messangial cell contraction
u RENIN
d GFR
u angiotensin I
d stretch receptor activation in atria, aorta,
and carotid sinuses
u angiotensin II
u BLOOD PRESSURE via vasoconstriction
(angiotensin II is a potent vasoconstrictor)
u aldosterone
neg feedback
u Na re-absorption (and K excretion)
Controls Body Fluid Balance and Associated
Regulation Mechanisms and Pathways
u thirst (thirst is more strongly regulated by
osmotic receptors in the hypothalamus)
u ECF volume r u BP
neg feedback
d RENIN
42
Dehydration

• Dehydration the loss of body water and
  associated electrolytes
• Causes
• Gastroenteritis (viral / bacterial infection r
  vomiting diarrhea) - most common
• Diseases yellow fever, cholera,
• Excessive alcohol consumption
• The excess fluid is flushed out by the kidneys
  u water usage r dehydration
• Most liquors have congeners which are toxic to
  body r removal necessary
• The clearer better quality your liquor (vodka
  gin) the less congeners
• more distillation cycles r better quality
• When you drink, head vessels dilate.constriction
  next morning r headache
• Congener removal done by liver d liver glucose
  r hypoglycemia lethargy
• Prolonged exercise without fluid replacement
  (heat exhaustion heat stroke risk)
• Diabetes hyperglycemia r u glucose excretion r
  u water loss r dehydration
• Shock blood loss due to some hypotensive state
  caused by injury or disease
• Gastrointestinal blood loss bleeding from
  ulcers or colorectal cancer

43
Dehydration

• Signs Symptoms of dehydration
• Dry mouth, dry swollen tongue, rapid heart rate
  (possible chest palpitations)
• Lethargy (sluggishness), confusion
• Poor skin turgor (a pinch of skin does not
  spring back into position)
• Good test for ailing elderly folks
• Elevated BUN (renal function test) NH4
  metabolized in liver excreted by kidneys
• Elevated creatinine r d GFR (kidney clearance of
  waste products)
• Increased blood viscosity
• Headache
• Fluid loss r low blood pressure r dizziness upon
  standing up
• A high urinary specific gravity (comparison of
  density to water 1 gram / cm 2)
• Treating Dehydration
• Sip small amounts of water
• Drink carbohydrate / electrolyte solutions
  Gatorade, Pedialyte, etc.
• If core body temperature gt 104 0 d BP or u HR
  r consider IV fluid replacement

44
Cardiorespiratory Control

• Skeletal Muscle Blood Flow autoregulated 2
  mechanisms
• Mechanism 1 Vasodilator Metabolites
• Usually overrides adrenergic neurohormone
  control
• Mediated by vasodilator metabolite (VDM) buildup
  removal
• Adenosine (ATP by-product), CO2, H,
  prostaglandins
• Exercise Example (negative feedback control)
• Muscle exercises r VDMs released r u
  vasodilation
• u vasodilation u blood flow r VDMs removed r
  vasoconstriction
• Mechanism 2 Myogenic response
• Involves stretch activated Ca channels
  (negative feedback control)
• u blood flow r vessel stretch r Ca channel
  activation
• u Ca in smooth muscle r vasoconstriction
  r d flow

45
Cardiorespiratory Control

• Systemic Blood Flow During Exercise
• Autonomic influences
• Sympathetic outflow circulating catecholamines
• a activation r vasoconstriction in non -
  exercising tissue
• Redistribution of blood flow during maximal
  exercise
• - NC in brain blood flow - 500 ml/min u to
  heart
• - 11,300 ml/min u to muscle - 400 ml/min u to
  skin
• - 500 ml/min d to kidneys - 800 ml/min d to
  viscera
• - 200 ml/min d to various other parts of the body

46
Cardiorespiratory Control

• Respiration Minute Ventilation (VE) Tidal
  Volume X Respiratory Rate
• Generally Controlled via central chemoreceptors
  in the medulla-pons respiratory center
• Peripheral chemoreceptors
• u blood CO2 content r receptor activation r u
  VE
• d blood O2 content r receptor activation r u VE
• Central chemoreceptors in the medulla
  respiratory center Dominant Influence
• u blood CO2 lactate r receptor activation r
  u VE
• PaCO2 r u HCO3 H r H activates
  receptor r u VE
• Respiratory control during exercise no
  consensus but research suggests
• Muscle spindle proprioceptor activation r u VE
  at early onset of an exercise bout
• Respiratory centers (medulla) sends afferent
  signals to expiratory muscles during exercise
• u venous return r atrial receptor activation r
  u VE ??
• Intrapulmonary receptor activation r u VE ??
• Peripheral chemoreceptors may play a role in
  steady state high intensity exercise VE ??
• Minute ventilation mechanistic changes during an
  u in exercise intensity

47
Acute Cardiorespiratory Responses to Endurance
Exercise
48
Acute Responses to Aerobic Exercise

• Oxygen Consumption (VO2)
• u VO2 in direct proportion to u workload (power
  requirement of exercise)
• Expressed in both relative and absolute terms
• Relative ml O2/kg/min Absolute ml/min or
  L/min
• Average VO2max for 40 year old male 37 ml/kg/min
• Oxygen consumption linked to caloric expenditure
  (1 liter of O2 consumed 5 kcal)
• Heart Rate
• u up to 3 times resting value at peak exercise
  (mainly due to d time spent in diastole)

180 160 140 100
Heart Rate
HR VO2 relationship is linear until about 90
VO2max
1.0 2.0 3.0
Oxygen Uptake (L / min)
50 150 250
Workloads (Watts)
49
Acute Responses to Aerobic Exercise

• Stroke Volume
• u up to 1.5 resting value at peak exercise
• Increase levels off at 40 - 50 VO2 max ??
• u in venous return r u EDV (Starling mechanism)
• d ESV eluding to an u in myocardial
  contractility
• u ejection fraction rest 58 max
  exercise 83
• Cardiac Output (Q)
• u up to 4 times resting value at peak exercise
  (u is rapid at onset, then levels off)
• u Q r u venous return
• Venous return mediated by and related to
• Sympathetic venoconstriction

??
120 110 70
120 110 70
Stroke Volume (ml/beat)
Recent Findings
All Older Studies
25 50 75 100
25 50 75
Percentage of VO2 max
Percentage of VO2 max
50

• Arteriovenous oxygen difference
• Difference in O2 between arterial and mixed
  venous blood
• Illustrated by the oxyhemoglobin desaturation
  curve
• u approximately 3 fold from rest to max exercise
• At rest, about 25 of arterial O2 is extracted
• At peak exercise about 75 - 85 of arterial O2
  is extracted
• Blood Pressures and Resistance to Flow
• SBP u - failure to u signifies heart failure
• DBP slight u or slight d or NC
• MAP slight u
• TPR d - mainly due to vasodilation in
  exercising muscle
• Coronary (Myocardial) Blood Flow
• 4.5 of Q goes to myocardium at rest and at peak
  exercise
• This increase is due to u MAP and CA
  vasodilation
• Blood Flow to the Skin
• u as exercise duration u to allow for heat
  dissipation

Acute Responses to Aerobic Exercise
51
Acute Responses to Aerobic Exercise

• Minute Ventilation
• Resting average 6 Liters/min
• Peak exercise average 175 Liters/min (29
  fold increase from rest to max)
• Respiratory rate resting 12-18 peak
  exercise 45-60
• Tidal volume resting .5 liters peak
  exercise 2.25 Liters
• Plasma Volume
• Blood plasma u in the interstitium of exercising
  muscle
• Fluid shift results in a 5 d in plasma volume
• This is termed Hemoconcentration
• Blood viscosity increases

52
Acute Responses to Aerobic Exercise

• Immune system
• During moderate / vigorous exercise, the
  following changes occur in immune activity
• Transient u in the re-circulation of
  neutrophils, NKCs, and immunoglobulins
• More pathogens detected and killed
• Transient d in stress hormones (cortisol) and
  inflammatory mediators (cytokines)
• Cortisol and cytokines suppress the immune
  system
• Immune function returns to normal in a few
  hours, but exercise improves surveillance
• 25 - 50 reduction in sick days with upper
  respiratory infections (colds, flu, etc.)
• Opposite effect occurs with prolonged heavy
  exercise
• Example after marathon, immune function d 2 - 6
  fold depending on time of year

53
Oxygen Debt and Deficit
Note upward Drift in VO2
Oxygen Deficit
Oxygen Debt (EPEOC)
Steady State VO2
VO2
Untrained or people with
certain cardiorespiratory
diseases will have larger
DEFICITS and DEBTS
Rest
EXERCISE TIME AT CONSTANT WORKLOAD
Termination of bout
Onset of bout

• Oxygen Deficit due to
• Delay in time for aerobic ATP production to
  supply energy
• Oxygen Debt due to
• Resynthesis of high energy phoshosphates (CP,
  ATP)
• Replace oxygen stores
• Lactate conversion to glucose (gluconeogenesis)
• u HR, respiration, catecholamines, body
  temperature

54
OBLA
Respiratory Compensation (hyperventilation)
Desaturation in CHF COPD patients
Desaturation in Elite Athletes
No Change in VE VCO2
Ventilatory and Metabolic Changes During Exercise
Increasing workload
55
Training Adaptations to Chronic Endurance Exercise
56

• Resting
• NC NC
• VO2 HR x SV x
  AVO2diff
• due to due to
• u time in diastole
  u preload
• d afterload (small)
• u ventricle size
• u blood volume
• Submax Workload (measured at same pre-training
  workload)
• NC NC
• VO2 HR x SV x
  AVO2diff
• note a slight d in afterload (mentioned above)
• accompanied by a d in HR translates into a
  reduction
• myocardial VO2 at rest or at any submaximal
  workload
• Max Workload (measured at peak exercise)

Effects of Exercise Training on the Components of
the Fick Relationship
57
Training Adaptations

• Mean Arterial Pressure
• Small d at rest or during exercise
• Systolic and Diastolic Blood Pressure
• Small d(6 10 mmHg) at rest
• Larger d (10 12 mmHg) at submaximal workload
• Exercise first line of therapy for borderline
  hypertensives
• Some studies report a mean d of about 9 mmHg
• Total Peripheral Resistance and Afterload
• u capillarization (more parallel circuits) r d
  Transit time for blood
• d TPR r d Afterload
• Respiratory Variables
• Respiratory Rate
• Rest NC
• Submax exercise d slightly
• Air remains in lungs longer
• More O2 extracted (about 2)
• Max exercise u u VE during submax max
  exercise
• Tidal Volume
• Rest NC d VE / VO2 during submax exercise

58

• Mitochondria
• u number, size and membrane surface area
• Aerobic Enzymes in Exercising Muscle
• u Krebs cycle enzymes (succinate dehydrogenase)
• u b oxidation enzymes (carnitine
  acyltransferase)
• u electron transport enzymes (cytochrome
  oxydase)
• Fatty Acid Glycogen Utilization
• u utilization of b oxidative pathways to produce
  ATP
• Called the glycogen sparring effect
• d RER for any given submaximal workload
• u muscle glycogen stores (with high carbohydrate
  diet)
• No Appreciable Change in Resting Metabolic Rate
• Exception training induced u in lean muscle
  mass
• d Platelet Aggregation
• u Fibrinolytic Activity
• d Circulating Catecholamines
• u vagal tone r d risk of arrhythmia

Training Adaptations
Death from all causes increases significantly
when VO2max falls below 7.9 METS (27.65
ml/kg/min) Kodamas Meta Analysis, JAMA, 301,
19, 2009.
59
"Average" Values for Sedentary and Trained
Individuals
Heart Rate ( beats / minute )
60
"Average" Values for Sedentary and Trained
Individuals
Stroke Volume ( ml / beat )
61
"Average" Values for Sedentary and Trained
Individuals
Cardiac Output ( liters / minute)
62
"Average" Values for Sedentary and Trained
Individuals
A-V O2 Difference ( ml)
63
"Average" Values for Sedentary and Trained
Individuals
Oxygen Consumption ( liters / minute)
64
"Average" Values for Sedentary and Trained
Individuals
Oxygen Consumption ( ml / kg / minute)
65
"Average" Values for Sedentary and Trained
Individuals
Systolic Blood Pressure ( mm Hg)
66
"Average" Values for Sedentary and Trained
Individuals
Diastolic Blood Pressure ( mm Hg)
67
"Average" Values for Sedentary and Trained
Individuals
Minute Ventilation ( liters / minute)