Ex Phys Masters Comprehensive

Front 1

3 critical roles of NO in vascular health

Back 1

1. Mediation of vasodilation

2. Inhibition of platelet aggregation

3. Inhibition of SMC proliferation

Front 2

Atherosclerosis progression (4 steps)

Back 2

1. Endothelium damage

2. Decreased NO causes platelets to aggregate

3. Platelets release PDGF, causing VSM proliferation

4. Plaque accumulates cholesterol and oxidized LDL

Front 3

How do statins work?

Back 3

Inhibit HMG-CoA reductase in liver which is the rate-limiting step in cholesterol synthesis

Front 4

How does training affect DL patients?

Back 4

Modest improvements seen in lipid profile

Main reason to exercise is an improvement in other risk factors (obesity, EDD)

Front 5

Progression of systolic heart failure (5 steps)

Back 5

1. SNS activated to compensate for impaired LV contractility

2. Increased SNA aggravates ischemia and promotes LV remodeling

3. LV enlarges (dilates)

4. Heart can't maintain Q

5. Heart failure worsens (decompensation)

Front 6

Symptoms of CHF (7)

Back 6

1. Fatigue

2. Dyspnea

3. Rapid/irregular heartbeat

4. Exercise intolerance

5. Persistent coughing (lung congestion)

6. Edema in ankles, legs, feet, abdomen

7. Sudden weight gain (fluid retention)

May exhibit ALL or NONE

Front 7

Weber classifications of CHF

Back 7

A - >20 ml/kg/min peak VO2

B - 16-20 ml/kg/min peak VO2

C - 10-16 ml/kg/min peak VO2 (50% likely to die within 3 years)

D - <10 ml/kg/min peak VO2

Front 8

4 complications from CHF

Back 8

1. Kidney damage from decreased BF

2. Heart valve problems from an enlarged heart and increased BP

3. Liver damage from fluid buildup and increased pressure

4. Heart attack/stroke from an increased incidence of blood clots

Front 9

By what mechanism does digitalis work?

Back 9

Inhibits Na/K ATPase

Increase in intracellular Na activates Na/Ca exchanger which brings in Ca and increased contractility

Front 10

What causes exercise intolerance in CHF patients?

Back 10

1. Impaired ability to increase Q

2. Impaired ability to redirect Q to active muscle

CHF is more than a pump failure - it is a systemic disease

Front 11

How does training affect CHF patients?

Back 11

Increase EDD

Increase peak VO2

Increase peak Q (central adaptation)

Increase ability to reduce resistance (peripheral adaptation)

Front 12

5 complications from HT

Back 12

1. Heart attack from hardened arteries

2. Aneurism from weakened/bulging arteries

3. HF from chronic overload of the heart

4. Artery damage from endothelial dysfunction and atherosclerosis

5. Vision loss from thickened, narrowed, torn blood vessels in the eyes

Front 13

By what mechanism do thiazide diuretics work?

Back 13

Inhibit NaCl transporter in DCT

This increases urine excretion, decreases BV and Q

Front 14

By what mechanism do beta blockers work?

Back 14

Prevent NE from binding B1

This decreases HR and contractility, thus decreasing Q

Only blocks B1 since these are more common, and this preserves the B2 receptors of the bronchioles

Front 15

By what mechanism do ACE inhibitors work?

Back 15

Cause dilation by inhibiting AngII formation, which decreases SVR

Front 16

How does acute exercise affect HT?

Back 16

Moderate exercise can decrease BP for up to 13 hours due to a sustained decrease in SVR (PEH)

Front 17

Mechanism for PEH

Back 17

There is an increase in bioavailability of NO up to 2 hours post-exercise, which leads to pretty much FS:

1. NO inhibits release of NE

2. NO decreasesd alpha receptor responsiveness to NE

3. NO acts directly on VSM to cause vasodilation

Front 18

By what mechanism does aspirin work to help alleviated PAD?

Back 18

Inhibits COX and reduces TA2 synthesis

"Activated" platelets make TA2 which promotes platelet clumping and vasoconstriction

Front 19

By what mechanism does Cilostazol work?

Back 19

Inhibits phosphodiesterase III, preventing breakdown of cAMP

Promotes dilation and improves BF

Front 20

How does training affect PAD?

Back 20

1. Improves endothelial function

2. Decreases inflammation

3. Stimulates angiogenesis

4. Improves muscle metabolism

5. Enhances BF

Front 21

How does acute exercise affect T2D?

Back 21

Insulin sensitivity increases one hour post-exercise

Beneficial effects last 12-24 hours

Front 22

How does training affect T2D?

Back 22

Increase GLUT-4 which increases insulin sensitivity

Improve endothelial function

Increase peak VO2

Increase insulin-stimulated glucose uptake

Front 23

Progression of CAD

Back 23

1. Injury to EC initiates atherosclerosis

2. VSM cells proliferate

3. Plaques form

Front 24

3 ways exercise helps increase myocardial perfusion

Back 24

1. Regression of plaques/stenosis

2. Formation of collaterals

3. Enhanced endothelial function

Front 25

How does training affect CAD patients?

Back 25

Increase CBF

Increase VO2 peak

Increase myocardial perfusion

Front 26

Timeline for improvement of myocardial perfusion with training in CAD

Back 26

Short term: increase endothelial function

Intermediate term: angiogenesis

Long term: regression of lesions and collateral formation

Front 27

Deconditioning cycle seen in COPD

Back 27

1. Ventilatory deconditioning (drop in PaO2)

2. CV deconditioning (decreased VO2 max)

3. Muscular deconditioning (atrophy)

Each leads to increased anxiety and decreased physical activity, leading to a worsening of each condition

Front 28

How does training affect COPD patients?

Back 28

Increase VO2 max

Increase walk time

Even small improvements increase quality of life

Front 29

3 major CV adjustments to exercise

Back 29

1. Increase Q

2. Redistribute Q

3. Increase venous return

Front 30

Parasympathetic control of the heart

Back 30

1. ACh binds to M2 receptors

2. Activation of inhibitory protein (Gi)

3. AC activity decreases

4. cAMP reduction

5. HR and conduction velocity decline

Front 31

Sympathetic control of the heart

Back 31

1. NE binds B receptors

2. Activation of stimulatory protein (Gs)

3. AC activity increases

4. Enhanced cAMP production

5. Increased Ca2+ entry

6. Increased HR and contractility

Front 32

Importance of cAMP in HR control

Back 32

Regulates activity of PK-A, which phosphorylates Ca2+ channel

Critical in excitation-contraction coupling

Front 33

4 major properties of arteries

Back 33

1. Thick walls withstand high pressure

2. Large lumens provide low resistance to BF

3. Thick walls prevent gas exchange

4. Elastic fibers propel blood forward

Front 34

4 properties to aid exchange in capillaries

Back 34

1. No SMC

2. Discontinuous endothelium

3. Large surface area

4. Large CSA to decrease BF velocity

Front 35

Fick equation

Back 35

VO2 = Q(a-vO2 diff)

VO2 = HRxSV(a-vO2 diff)

Front 36

Mediation of increased Q during exercise

Back 36

Low intensity: increased SV and HR

>50% VO2 max: increased HR

SV is a limiting factor

Front 37

Experimental evidence of autonomic control of HR during exercise

Back 37

Atropine blocks M2 receptors and prevents HR increase at low intensity exercise

Propanolol block B1 receptors and prevents HR increase at high intensity exercise

Decreased PNA increases HR to 100, further increase mediated by SNA

Front 38

Frank-Starling mechanism

Back 38

SV increases as preload increases

Increased number of cross bridges

Increased sensitivity of myofilaments to Ca

Increased venous return stretches the ventricle

Front 39

3 mechanisms for increased a-vO2 difference

Back 39

1. Muscle fiber recruitment

2. Increased O2 extraction from noncontracting tissue

3. Capillary recruitment (maybe) - increased volume in exchange zone

Front 40

4 mechanisms for venous return

Back 40

1. Increased pressure gradient from aorta to RA

2. NE stimulates alpha1 receptors

3. Skeletal muscle pump

4. Respiratory pump

Front 41

How can SVR decrease if MSNA increases during exercise?

Back 41

Functional sympatholysis!

1. Presynaptic inhibition: vasodilators act on SN reducing NE release

2. Postsynaptic inhibition: dilators make alpha receptor less responsive to NE

3. Dilators act directly on VSM to override constrictor effects

Allows BF to increase while protecting BP

Front 42

What is the main limiting factor for VO2max?

Back 42

Q via SV

Front 43

Mean arterial pressure equation

Back 43

MAP = DBP + 1/3 (SBP-DBP)

Front 44

BP response to isometric exercise

Back 44

BP increases out of proportion to metabolic demand

Front 45

What is the pressor response?

Back 45

CVS attempt to deliver BF despite inability to reduce SVR

Arterioles stay compressed

SBP increases due to increased Q

DBP increases due to increased HR and either an unchanged or increased SVR

Reduced SV due to no dynamic pump to aid venous return

Front 46

SNA response to isometric exercise

Back 46

SNS not activated during contractions <15% max

MSNA increases as a function of time and intensity

Front 47

MBF during isometric exercise

Back 47

MBF increases with increased workload

BF supply matches metabolic demand up to ~15% MVC

>20% MVC BF does not meet demand

Front 48

Central command: mechanism

Back 48

Signal for CV adjustment originates in brain (intent to exercise)

AP from motor cortex activate muscle and CV center simultaneously

CV center adjusts PNA/SNA balance

Feed-forward mechanism for rapid CV adjustment

Proportional muscle and CVS activation

Front 49

Exercise pressor response: mechanism

Back 49

Signal for CV adjustment originate in active muscle

Feedback carried to CV center by group III and IV afferent fibers

Provide local sensor to monitor metabolic and contractile state of muscle

Front 50

Arterial baroreflex: mechanism

Back 50

Signal for CV adjustment is a pressure error

Baroreceptors are free nerve endings in the aortic and carotid sinuses

Send feedback via vagus and sinus nerves

Adjust SNA/PNA to keep BP constant

Front 51

BR response to hypotensive stimulus

Back 51

Decreased receptor firing rate decreases PNA and increases SNA

Increases HR and SVR to restore BP

Front 52

BR response to hypertensive stimulus

Back 52

Increased receptor firing rate increases PNA and decreases SNA

Decreases HR and SVR to restore BP

Front 53

Integrative model for CV control during exercise (draw it out too)

Back 53

1. CC initiates vagal withdrawal and resets baroreflex OP

2. BR resetting creates pressure error - activates SNS

3. EPR monitors local conditions in muscle and increases SNA as needed

Front 54

VO2, Q, and MBF increases during exercise

Back 54

VO2: 10-25 fold

Q: 4-8 fold

MBF: 100 fold

Front 55

Mechanism for the dynamic muscle pump

Back 55

At rest MBF and venous outflow are low

Suring contraction venous outflow increases and arterial inflow is blocked

Relaxation venous pressure drops, pulling blood into muscle

Rapid mechanism for increase in MBF at onset of exercise

Front 56

How does adenosine help control MBF during exercise?

Back 56

Ado released from muscle activates AC

Intracellular Ca decreases in VSM

VSM relaxes

Front 57

How does potassium help control MBF during exercise?

Back 57

K+ released from muscle during contraction

Increased K+ in interstitial fluid causes VSM to hyperpolarize (relax)

RAPID mechanism for dilation at onset of exercise

Front 58

What is conducted vasodilation?

Back 58

ACh from neuromuscular junction "spills over" onto arterioles

Dilation conducted upstream

Mechanism to direct BF to active fibers

Front 59

VO2 adaptations to training: absolute and relative

Back 59

Endurance training increases VO2max 10-40%

Absolute: NO CHANGE

Relative: INCREASE

Front 60

Q adaptation to training: absolute and relative

Back 60

Qmax increases

Absolute: NO CHANGE

Relative: INCREASE

Front 61

HR adaptation to training: absolute and relative

Back 61

Absolute: NO CHANGE

Relative: DECREASE

Front 62

3 mechanisms for training bradycardia

Back 62

1. increased vagal nerve activity to SA node

2. Decreased SNA to SA node

3. Decreased sensitivity of B1 receptors in SA node

Front 63

When does lactate threshold occur?

Back 63

When clearance rates fail to meet production rates

Front 64

How does training affect blood lactate?

Back 64

Increases lactate clearance by enhancing lactate removal by oxidation and gluconeogenesis

Front 65

At what relative intensity does blood lactate concentration begin to rise?

Back 65

~60% VO2max

Front 66

SNA adaptation to training: relative and absolute

Back 66

Absolute: DECREASE FEEDBACK

Relative: NO CHANGE

SNA onset still 45-50% max VO2

Front 67

SV adaptation to training: relative and absolute

Back 67

Absolute: INCREASE

Relative: INCREASE

Front 68

A-VO2 diff after training: absolute and relative

Back 68

Absolute: NO CHANGE

Relative: INCREASE

Front 69

4 reasons for increased a-vO2 diff after training

Back 69

1. Increased capillary density

2. Increased mitochondrial volume

3. Increased oxidative enzyme activity

4. Increased recruitment of muscle fibers due to increased max power

Front 70

Timeline of EDD adaptations to training

Back 70

Short term: Increased in arteries

Intermediate: Arteriogenesis

Long term: Increased in arterioles and angiogenesis

Front 71

Adaptations to passive heating

Back 71

Increased skin BF

Decreased Central BV

Increased Q - can double, up to 60% to skin

Decreased SNA to arterioles in skin

NO-mediated dilation of arterioles in skin

Activation of sympathetic cholinergic nerves

Front 72

Adaptations to exercise in heat

Back 72

Decreased venous return results in decreased SV

Increased HR to attempt to maintain BP

Decreased Q due to decreased SV

Decreased MAP

Decreased skin and muscle BF - skin quits first

Fatigue`

Front 73

4 properties of the conducting zone that make it good for bulk gas flow

Back 73

1. Large lumens for low resistance

2. Thick walls prevent gas exchange

3. SMC innervation by PNS & SNS

4. SMC with M & B receptors

Front 74

Bronchiole initial response to exercise

Back 74

PNS dominant at rest - ACh keeps airway constricted

Mild exercise causes vagal withdrawal - dilation

Heavy exercise causes SNS activation which further decreases airway resistance

Front 75

Tidal volume

Back 75

Volume of air moved in and out of lungs during a single breath

Front 76

Oxygen requirements of ventilatory muscles

Back 76

1-2% at rest

10% at max for untrained

15-16% at max for elite

May "steal" BF from skeletal muscle

Front 77

Ventilatory response to exercise (2 stages)

Back 77

Hyperpnea: breathing increases in proportion to metabolic demand

Hyperventilation: breathing increases out of proportion to metabolic demand

Front 78

Relationship between ventilatory threshold and lactate threshold

Back 78

Tvent tends to coincide with Tlac, but Tvet occurs in patients with McArdle's who physiologically cannot experience a Tlac, so they are not reliant upon one another

Front 79

Possible mechanisms for ventilatory threshold

Back 79

Potassium may stimulate group IV fibers

Potassium and NE may stimulate carotid chemoreceptors (sense decreased PaO2)

Increased CO2 flow to lungs may stimulate chemoreceptors (nobody has found CR in lungs)

Front 80

PO2 of blood:

Entering pulmonary capillaries

Leaving pulmonary capillaries

Back 80

Entering: 40 mmHg

Leaving: 100 mmHg

Front 81

3 reasons PaO2

Back 81

1. Diffusion is not 100% efficient

2. Some blood bypasses ventilated areas of the lungs

3. Small amount of venous blood drains directly into LV via Thebesian veins

Front 82

Explain cooperative binding of O2 to Hb

Back 82

At high PO2, Hb binds O2 at lungs

At low PO2, Hb releases O2 at muscle

Active muscle causes Hb to release ~75% O2

Front 83

Bohr effect and 3 contributors

Back 83

Rightward shift of the O2 dissociation curve - facilitates release of O2 to muscle

1. increased temperature

2. decreased pH

3. increased PCO2

Front 84

How is a-vO2 maintained during exercise in healthy populations?

Back 84

Increased VA maintains O2 diffusion gradient

Capillary recruitment decreases diffusion distance

Transit time of 0.25 sec for RBC in capillaries is sufficient for saturation

Front 85

Removing CO2 during heavy exercise helps maintain...

Back 85

pH

Front 86

3 forms of CO2 transport

Back 86

1. 5% dissolved in plasma

2. 25% bound to Hb

3. 70% bicarbonate (HCO3-)

Front 87

Haldane effect

Back 87

Affinity of Hb for CO2 depends on PO2

Increased PO2 leads to a decreased affinity for CO2

Facilitates release of CO2 to lungs

Front 88

Lactate buffering

Back 88

The hydrogen ion in lactic acid is buffered by HCO3 to produce H2CO3

This can then be broken down into H2O and CO2 for clearance by the lungs

Front 89

Arterial CO2 content is inversely related to...

Back 89

Pulmonary minute volume (MVV)