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Cardiovascular Cardiovascular SystemSystem

Objectives• Review of anatomy & blood flow

• Systemic and localized (within the heart) blood flow & blood pressurea) Rest, exercise & recovery

• CV regulation & integration

• Functional capacity of CV system

• Adaptations to exercise

Cardiovascular System• Composed of blood, the heart, and vasculature

within which blood is pumped throughout the body

a) Pulmonary CirculationConcerning blood flow to, within and from the lungs

b) Systemic CirculationConcerning blood flow to, within and from the remainder of the body

Consists of tissue/organ specific circulation beds (ex: renal, hepatic, skeletal muscle, etc.)

Figure 15.3a

Figure 15.1

Blood• Water, clotting

proteins, transport proteins, lipoproteins, glucose, FA, antibodies, waste products

• Plasma – the liquid component of blood & all of it’s non-cellular content

55% of whole blood (0.3ml O2)

<1% of whole blood

Hematocrit: 45% of whole blood (19.7ml O2, 15g Hb)

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• Blood volume ~ 5 L, but varies with:a) Body sizeb) Endurance trainingc) Exposure to extreme environments

• % distribution at rest

Hemodynamics – BF & Resistance• Pressure

a) Blood flows from high → low pressure

• Resistancea) Length of the vesselb) Viscosity of the bloodc) Radius of the vessel

A small change in vessel diameter can have a dramatic impact on resistance!

Resistance =Length x viscosity

Radius4

Figure 15.4

Blood Pressure• Arterial blood pressure – reflects the combined

effects of arterial blood flow per minute & the resistance offered by the peripheral vasculature

a) Systolic BPEstimate of the work of the heart and the force that blood exerts on the arterial wall during ventricular systole

b) Diastolic BPIndicates the ease with which blood flows from the arterioles into the capillaries

Peripheral resistance

BP = Cardiac Output x Total Peripheral Resistance

Arterial BP Classifications Hypertension• Chronically elevated arterial BP

> 140 mmHg systolic> 90 mmHg diastolic

• Treatmenta) Exerciseb) Drug therapy

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Blood Pressure (cont.)

c) Mean Arterial Pressure – the average force exerted by the blood against the arterial walls during the entire cardiac cycle

d) Relationship between BP, Cardiac Output & TPR

MAP = Diastolic BP + [0.33(Systolic BP – Diastolic BP)]

Cardiac Output = MAP / TPR

TPR = MAP / Cardiac Output

Blood Flow Continuum• Arteries, arterial BP & arterioles

• Capillaries:

REST

EXERCISE

Figure 15.5C

Blood Flow Continuum• Venous system –

serves as blood reservoirs

• Skeletal muscle pumps & venous poolinga) Application of an

active cool down

Figure 15.7

BF & Pressure in the Systemic BP Response to Exercise• Resistance exercise:

a) Straining compresses vesselsb) TPR ↑c) Sympathetic nervous system activity, cardiac output,

and MAP increase in attempt to restore muscle BF

Heavy resistance training intensifies the BP response

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BP Response to Exercise (cont.)

• Graded Exercise:a) Systolic pressure ↑

with increases in workload

b) There is a linear relationshipbetween workload and systolic BP

c) Diastolic pressure remains fairly constant

BP Response to Exercise (cont.)

• Upper Body Exercisea) Resistance to flow is increased with upper body

exerciseb) Smaller vessels in upper body compress more easily

• Recovery BPa) Following endurance exercise, there is a hypotensive

responseb) BP temporarily falls below normal resting values

The Heart’s Blood Supply• Coronary circulation:

a) Right and left coronary arteries branch off the upper ascending aorta

b) RCA supplies predominantly the right atrium and ventricle

c) LCA supplies the left atrium and ventricle and a small portion of the right ventricle

Myocardial O2 Use• At rest, myocardium extracts ~ 70–80% available

O2 from the coronary vessels

• During exercise flow must increase to meet O2demanda) Flow may increase 5–7 times

• Vasodilation of the coronary vessels ↑ due to:a) Adenosine (byproduct of ATP breakdown)b) Hypoxiac) Sympathetic nervous system hormones

Figure 15.13

Measurement of Myocardial Work• Rate Pressure Product:

• Myocardial Metabolism – reliant upon energy released from aerobic metabolisma) Myocardium has a significantly higher

mitochondrial density compared to skeletal muscle

• Allows the heart to utilize available substrates depending on activity

Systolic BP x HR = RPP

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Figure 15.14

CV Regulation & Integration

Intrinsic Regulation

Figure 16.1

Time sequence (seconds) for electrical impulse transmission

Measuring Electrical ActivityElectrocardiogram (ECG or EKG)

Measuring Electrical ActivityElectrocardiogram (ECG or EKG)

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Extrinsic Regulation• Elicit changes in HR rapidly through nerves that

directly supply the heart & chemical messengers that circulate in blood

• Sympathetic & Parasympathetic Neural Input

Extrinsic Regulation (cont.)• Sympathetic neural input:

a) Localized – Stimulation of cardioaccelerator nerves causes the release of the catecholamines epinephrine& norepinephrine

Accelerate SA node depolarization which increases HR (chronotropic effect)Increases contractility (inotropic effect)

b) Systemically – Stimulation produces vasoconstriction (except coronary vasculature)

Release of norepinephrine by adrenergic fibers causes vasoconstrictionVasomotor tone

Figure 16.3

Extrinsic Regulation (cont.)

• Parasympathetic neural input:a) Localized – Stimulation of vagus nerves causes

release of the neurohormone acetylcholine which slows sinus discharge & therefore HR

Slows sinus discharge & therefore ↓ HRNo effect on contractility

Central Command

Figure 16.10

Rapid adjustments (feed-forward mechanisms) with the onset of exercise

Exercise Anticipation

Figure 16.6

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Peripheral Input• Chemoreceptors: monitor metabolites, blood

gases

• Mechanoreceptors: monitor movement and pressure

• Baroreceptors: monitor blood pressure in arteriesa) Aortic arch & carotid sinus

Distribution of BF during Exercise

Local Factors within the Muscle• Autoregulatory mechanisms allow for ↑ blood

flow, ↑ blood volume with only a small increase in velocity, and ↑ effective surface area for gas & nutrient exchange

a) Vasodilation induced by:↑ blood flow↑ temperature↑ CO2↑ acidity↑ adenosine, K+ & Mg2+

↑ NO

Nitric Oxide

Figure 16.7

Hormonal Factors• Adrenal medulla releases:

a) Larger amounts of epinephrine and smaller amounts of norepinephrine

b)Cause vasoconstriction (except in coronary & skeletal muscle)

• Minor role during exercise

Functional Capacity of the CV System

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Cardiac Output (Q)• Q = HR x SV

• Methods of Measuring Q a) Direct Fick = (VO2ml·min-1/a-vo2 difference) x 100

Cardiac Output (Q)• Q = HR x SV

• Methods of Measuring Q a) Direct Fick = (VO2ml·min-1/a-vo2 difference) x 100b) Indicator dilutionc) CO2 rebreathing

• Q at resta) Values vary depending upon:

Emotional state (central command via cardioacceleratornerves & nerves modulating arterial resistance)Posture

b) Average male (70kg) ~ 5L · min-1

c) Average female (56kg) ~ 4L · min-1~ 25% lower in females

• Untrained vs. Endurance trained characteristics of Q at rest:a) Variation in resting HR

b) Mechanisms:Increased vagal tone (parasympathetic) w/decreased sympathetic driveIncreased blood volumeIncreased myocardial contractility and compliance of left ventricle

100 mL·min-150 b·min-1 x5000 mL·min-1 =Trained:

71 mL·min-170 b·min-1 x5000 mL·min-1 =Untrained:

SVHR xQ =Rest

• Untrained (UT) vs. Endurance trained (ET) characteristics of Q during exercise:a) Both UT & ET Q ↑ rapidly with onset of exercise

Subsequently a more gradual rise to meet exercise metabolic demands

b) Variation between groups often observed as intensity ↑

179 mL·min-1195 b·min-1 x35,000 mL =Trained:

113 mL·min-1195 b·min-1 x22,000 mL =Untrained:

SVHR xQ =Maximal Exercise

• Mechanisms:

a) Enhanced cardiac filling in diastole (preload) & a more forceful ejection caused by an ↑ in end diastolic volume (EDV)

Starling’s Law: the greater the stretch, the more forceful the contraction (contractility)

b) Greater systolic emptyinggreater systolic ejection overcomes exercise-induced arterial blood pressures (afterload)

c) Expanded blood volume & reduced peripheral resistance in tissues in ET individuals

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CV Drift w/ Prolonged Exercise• ↓ SV and coinciding a gradual ↑ in HR

• Proposed mechanisms:a) Progressive H2O loss and a fluid shift from plasma to

tissuesDrop in PV decreases central venous cardiac filling pressure

b) Increased core temperaturec) Progressive increase in HR with CV drift during

exercise ↓ EDV, subsequently reducing SV

Blood Flow Distribution @ Rest

Figure 17.3

Blood Flow Distribution & Exercise

1. Hormonal vascular regulation

2. Local metabolic conditions

Q & O2 Transport• Arterial blood carries ~ 200mL of O2 per L of

blood

• Resting conditions:a) If Q @ rest ~ 5L·min-1, then 1000mL of O2 would be

available to the body each minuteb) Resting oxygen consumption (VO2) ~ 250 to

300mL·min-1

c) Leaves ~ 750mL of oxygen returning to the heart unused

Q & O2 Transport (cont.)

• Exercise conditions:a) Even during max exercise, Hb saturation remains

nearly complete, so each L of blood carries ~ 200mL of O2

Ex: a max exercise Q of 16L x 200mLO2·L-1 ~ 3200mL

b) Debate exists as to the real cause of a VO2max plateau

QO2 extraction at the tissuesO2 delivery

Central

Peripheral

Q & VO2max Association

Figure 17.4

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O2 Extraction: a-vO2 Difference• Exercise oxygen consumption increases by:

a) Increased cardiac outputb) Greater use of the O2 already carried by the blood

Expanding a-vO2 difference

VO2 = Q x a-vO2 difference

From Rest to Exercise

Figure 17.5

• Factors affecting a-vO2 difference during exercise:a) Central – diversion of blood flow to working tissuesb) Peripheral

Increased skeletal muscle microcirculation increases extractionIncrease in capillary to fiber ratioCells ability to regenerate ATP aerobicallyIncreased # and size of mitochondriaIncreased aerobic enzyme concentration

CV Adaptation/ Response to Training

Cardiac Hypertrophy

Figure 21.7

Plasma Volume Expansion• Up to 20% increase in PV (without changes in

[RBC]) after 3 to 6 aerobic exercise sessions

• Mechanisms:a) Directly related to increased synthesis and retention

of plasma albumin

• Increased PV:a) Increases EDV, SV, O2 transport, & temperature

regulation during exercise

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Figure 21.9

Heart Rate

Figure 21.10

Stroke Volume

Figure 21.11

Cardiac Output

Figure 21.12

a-v O2 difference

Blood Flow Distribution• BF shunting toward Type I fibers (oxidative)

during submaximal exercise

• Better distribution from non-active areas

• Enlarged cross-sectional area of arteries, veins & capillary beds

• Myocardial BF:a) Increased perfusion capabilitiesb) Mitochondrial mass & density increased

• Reduction in BPFigure 21.6