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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