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KINE 639 - Dr. Green Section 1 Clinical Physiology I, II, III, IV. Definitions, Concepts, and Hemodynamics. Cardiac Anatomy. Aorta. Superior Vena Cava. Left Pulmonary Artery. Left Atrium. Right Pulmonary Veins. Left Pulmonary Veins. Right CA. Left Anterior Descending CA. Right Atrium.

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slide1

KINE 639 - Dr. Green

Section 1

Clinical Physiology I, II, III, IV

slide3

Cardiac Anatomy

Aorta

Superior Vena Cava

Left Pulmonary Artery

Left Atrium

Right Pulmonary Veins

Left Pulmonary Veins

Right CA

Left Anterior Descending CA

Right Atrium

Inferior Vena Cava

Left Ventricle

Right Ventricle

slide4

Cardiac Anatomy

Aorta

Superior Vena Cava

Left Pulmonary Artery

Aortic Valve

Left Atrium

Right Pulmonary Veins

Left Pulmonary Veins

Right Atrium

Tricuspid Valve

Mitral Valve

Inferior Vena Cava

Left Ventricle

Right Ventricle

Notice that the left ventricle contains more electrically active muscle mass than the right ventricle

slide5

Lungs

The Normal Heart and Regional Circulation

Anterior Cutaway View

Pulmonary Semilunar Valve

Aorta

Left Pulmonary Artery

Superior Vena Cava

Left Pulmonary Veins

Left Atrium

Right Pulmonary Artery

Aortic Semilunar

Valve

Bicuspid or Mitral Valve

Right Pulmonary Veins

Tricuspid Valve

Apex

Inferior Vena Cava

Septum

slide6

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

slide7

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%

slide8

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

300

600 - 750

Peak Exercise

Workload or Power (kg meters / min)

slide9

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
slide10

Starlings Law of the Heart and Contractility

Starling’s Law:

The greater the EDV (blood going in the heart), the more blood comes out of the heart

SV

(left ventricular performance)

uContractility

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

slide11

Influences on Myocardial Contractility

u Contractility related to :

Exercise: - ub sympathetic adrenergic nerve output

Catecholamines:-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

slide12

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 ConsumptionVO2 of the heart muscle (myocardium)
        • "estimated" by RPP: HR X SBP
slide13

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 )

slide14

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

slide15

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
slide16

Neurophysiology - Definitions

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

Motor cortex

(control of voluntary muscles)

Central sulcus

Basil nuclei

(planning, organizing, coordinating motor movements)

Sensory cortex

(Sensation & pain)

Essential Knowledge of the Areas of the Brain in Green

Sulcus

Corpus callosum

Gyrus

Choroid Plexus

Broca’s area

(motor, speech

Taste area

Thalamus

Parietal lobe

General interpretive

area

Parietal lobe

Frontal

lobe

Pineal gland

Frontal lobe

Occipital lobe

Occipital

lobe

Visual

area

Reticular

activation

system (sleep wake)

Hypothalamus

Temporal lobe

Pituitary gland

Optic chiasma

Cerebellum

(movement

coordination & balance)

Lateral sulcus

Cerebellum

Pons

Brainstem (control of HR, BP, and respiration)

Medulla oblongata

Auditory

cortex

Vestibular

area

Temporal lobe

Fourth Ventricle

Central canal

slide17

Organization of the Nervous System

Nervous System

Central Nervous System (CNS)

Peripheral Nervous System (PNS)

Spinal Cord

Brain

Motor (efferent) Neurons

Sensor (afferent) Neurons

Autonomic Nervous System

Somatic Nervous System

Voluntary movement

Output to

Skeletal muscles

Involuntary (Reflexes)

Input from

Internal receptors

Output to smooth

muscles and CVS

Sympathetic Motor System

Parasympathetic Motor System

Relaxing responses

Neurotransmitter:

acetylcholine

Cholinegeric nervous system

Flight or Fight responses

Neurotransmitter:

nonadrenaline

Adrenergic nervous system

slide18

Adrenergic Receptors & Associated Responses

  • a1stimulation:
    • Constriction of blood vessels
      • Vascular smooth muscle activation
    • Constriction of lung bronchioles
    • Constriction of bladder muscles
    • u myocardial cardiac contractility
    • Relaxation of GI tract
  • a2stimulation:
    • u central sympathetic outflow
      • u release of E & NE
      • a1 & b1 receptor activation
    • Constriction of lung bronchioles
  • b1stimulation:
    • u in HR
    • u in myocardial contractility
    • u in Renin secretion
      • u fluid retention
  • b2stimulation:
    • Dilation of lung bronchioles
    • Dilation of blood vessels

Agonist – body molecule or drug “stimulator”

Antagonist - body molecule or drug “in-activator”

a2Agonists

b1 & b2Agonists

Agonists in the adrenergic system are primarilyepinephrineandnorepinephrine

Antagonists are many times associated with drugs known as “blockers” i.e.“b-blocker”or“a-blocker”

Responses

slide19

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

slide20

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

development of the driving pressure in the human cardiovascular system
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)

slide22

Arterial Pressures in Maroon

The “Closed” Cardiovascular Hemodynamic System

Venous Pressures in Blue

LV

PO2 = 160

PCO2 = .3

RV

LA

RA

LUNGS

AORTA

(13)

(100)

(3)

(0)

PO2 = 100

PCO2 = 40

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)

high compliance

64% of blood volume

(40)

(2)

CAPILLARYBEDS

ARTERIOLES

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

slide23

Pressure, Flow, and Resistance by Vascular Cross Sectional Area

Veins

Vena Cava

Veins

Vena Cava

Capillaries

Venules

Capillaries

Venules

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

slide24

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?v=yGlFBzaTuoI&feature=related

http://www.youtube.com/watch?v=dYgYcH7R29I&NR=1

slide25

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

slide26

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)

slide27

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 )

slide28

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)

slide29

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 rd venous return r d CVP)

2

7

CENTRAL VENOUS PRESSURE (mmHg)

can also be called CARDIAC PRELOAD

slide30

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

slide31

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

slide32

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
slide33

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)

slide34

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)

slide35

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)

slide37

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

slide38

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
    • dpressure r dreceptor firing r usympatheticsr u HR r u pressure
    • u pressure r ureceptor firing r uparasympatheticsr d HR r d pressure
  • Atrial Stretch receptors: u receptor stretch ru ANP ruNa+excretionru urine output
              • d receptor stretch ruADHrdNa+excretionrd urine output
    • AtrialNatriureticPeptide 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 O2or d CO2r uparasympathetic discharge r d HR
    • dO2 or u CO2r dpH rpressor area stimulation in medulla r uHR

ADH Molecule

slide39

Cardiorespiratory Control

  • Stroke Volume (SV) – regulated by Frank Starling mechanism
    • u venous returnr 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 uSV back to normal
    • Extrinsic hormonal influences
      • Norepinephrine release r u HR and SV
slide40

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 areceptors r u TPR
    • Fight or flight response
  • Q
  • Blood Volume
    • Renin – Angiotensin System
slide41

HYPOTENSION

HYPOVOLEMIA

Renin - Angiotensin System

u H2O reabsorbed

d renal profusion

u sympathetic tone

u ADH (vasopressin)

d stretch in afferent arteriolar JG cells

d NACL delivery to macula densa cells

u messangial cell contraction

uRENIN

d GFR

uangiotensin I

d stretch receptor activation in atria, aorta, and carotid sinuses

uangiotensin 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 ru BP

neg feedback

dRENIN

slide42

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 rdehydration
      • Most liquors have congenerswhich 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
slide43

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 > 104 0 + d BP or u HR r consider IV fluid replacement
slide44

Cardiorespiratory Control

  • Skeletal Muscle Blood Flow – autoregulated – 2mechanisms
  • 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 VDM’s released r u vasodilation
        • u vasodilation u blood flow r VDM’s 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
slide45

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
slide46

Cardiorespiratory Control

  • Respiration: Minute Ventilation (VE) = Tidal Volume X Respiratory Rate
  • GenerallyControlled via central chemoreceptors in the medulla-pons respiratory center
  • Peripheral chemoreceptors
    • u blood CO2 content r receptor activation ru VE
    • dblood O2 content r receptor activation ru VE
  • Central chemoreceptors in the medulla respiratory center – Dominant Influence
    • u blood CO2 & lactate r receptor activation ruVE
    • PaCO2 ru HCO3¯ + H+ r H+ activates receptor ru VE
  • Respiratory control during exercise – no consensus but research suggests:
    • Muscle spindle & proprioceptor activation ru VE at early onset of an exercise bout
    • Respiratory centers (medulla) sends afferent signals to expiratory muscles during exercise
    • u venous returnr atrial receptor activation ru VE ??
    • Intrapulmonary receptor activation ru VE ??
    • Peripheral chemoreceptors may play a role in steady state & high intensity exercise VE ??
  • Minute ventilation mechanistic changes during an u in exercise intensity
    • Low exercise intensity: VEu by both u TV and u RR
    • High exercise intensity: VE u by u RR only
  • Notes:
  • O2 cost of breathing during exercise: 4.5% VO2 (low int.) up to 12.5%VO2 (high int.)
slide48

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 dtime 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)

slide49

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
        • Muscle pump
        • u inspiration r d thoracic pressure
          • Blood flows to an area of reduced pressure
        • u inspiration r u abdominal pressure
          • Contraction of abdominal muscles r squeezing of abdominal veins

??

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

slide50

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
    • d at max exercise to meet exercising muscle demands
    • u during exercise recovery, again for heat dissipation

Acute Responses to Aerobic Exercise

slide51

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
slide52

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, NKC’s, and immunoglobulins
        • More pathogens detected and killed
      • Transient din 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
slide53

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 andDEBTS

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
slide54

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

slide56

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)
  • NCNC
  • 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 VO2at rest or at any submaximal workload
  • Max Workload (measured at peak exercise)
  • NC
  • VO2= HR x SV x AVO2diff
  • some studies show
  • a slight decrease

Effects of Exercise Training on the Components of the Fick Relationship

slide57

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 VEduring submax & max exercise
    • Tidal Volume
      • Rest: NC dVE / VO2during submax exercise
      • Submax exercise: uu significantly
      • Max exercise: u
    • Anaerobic Threshold or OBLA or Ventilatory Threshold
      • Occurs at a higher percentage of VO2 max
      • Pre-training: 50% VO2max Post-training: 80% VO2max
slide58

Mitochondria

    • u number, size and membrane surface area
  • Aerobic Enzymes in Exercising Muscle
    • u Krebs cycle enzymes (succinate dehydrogenase)
    • ub oxidation enzymes (carnitine acyltransferase)
    • u electron transport enzymes (cytochrome oxydase)
  • Fatty Acid & Glycogen Utilization
    • u utilization of boxidative 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
  • u Resistance to Pathological Events
    • Smallerinfarct size and quicker recovery
    • Less of a d in ventricular function during ischemia

Training Adaptations

Death from all causes increases significantly when VO2max falls below

7.9 METS (27.65 ml/kg/min)

Kodama’s Meta Analysis, JAMA, 301, 19, 2009.

slide63

"Average" Values for Sedentary and Trained Individuals

Oxygen Consumption

( liters / minute)

slide64

"Average" Values for Sedentary and Trained Individuals

Oxygen Consumption

( ml / kg / minute)

slide67

"Average" Values for Sedentary and Trained Individuals

Minute Ventilation

( liters / minute)

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