Objectives • Review of anatomy & blood flow

Cardiovascular System

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

• CV regulation & integration • Functional capacity of CV system • Adaptations to exercise

Cardiovascular System

Figure 15.3a

• Composed of blood, the heart, and vasculature within which blood is pumped throughout the body a) Pulmonary Circulation 9 Concerning blood flow to, within and from the lungs

b) Systemic Circulation 9 Concerning blood flow to, within and from the remainder of the body 9 Consists of tissue/organ specific circulation beds (ex: renal, hepatic, skeletal muscle, etc.)

Blood • Water, clotting proteins, transport proteins, lipoproteins, glucose, FA, antibodies, waste products

Figure 15.1

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

55% of whole blood (0.3ml O2)

140 mmHg systolic > 90 mmHg diastolic

• Treatment a) Exercise b) Drug therapy

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Blood Flow Continuum

Blood Pressure (cont.) c) Mean Arterial Pressure – the average force exerted by the blood against the arterial walls during the entire cardiac cycle MAP = Diastolic BP + [0.33(Systolic BP – Diastolic BP)]

• Arteries, arterial BP & arterioles • Capillaries:

EXERCISE

REST

d) Relationship between BP, Cardiac Output & TPR Cardiac Output = MAP / TPR TPR = MAP / Cardiac Output

Blood Flow Continuum • Venous system – serves as blood reservoirs • Skeletal muscle pumps & venous pooling a) Application of an active cool down Figure 15.5C

BF & Pressure in the Systemic

BP Response to Exercise • Resistance exercise: a) Straining compresses vessels b) TPR ↑ c) Sympathetic nervous system activity, cardiac output, and MAP increase in attempt to restore muscle BF

Heavy resistance training intensifies the BP response

Figure 15.7

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BP Response to Exercise (cont.) • Graded Exercise: a) Systolic pressure ↑ with increases in workload b) There is a linear relationship between workload and systolic BP c) Diastolic pressure remains fairly constant

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

BP Response to Exercise (cont.) • Upper Body Exercise a) Resistance to flow is increased with upper body exercise b) Smaller vessels in upper body compress more easily

• Recovery BP a) Following endurance exercise, there is a hypotensive response b) BP temporarily falls below normal resting values

Myocardial O2 Use • At rest, myocardium extracts ~ 70–80% available O2 from the coronary vessels • During exercise flow must increase to meet O2 demand a) Flow may increase 5–7 times

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

Measurement of Myocardial Work • Rate Pressure Product: Systolic BP x HR = RPP

• Myocardial Metabolism – reliant upon energy released from aerobic metabolism a) Myocardium has a significantly higher mitochondrial density compared to skeletal muscle

• Allows the heart to utilize available substrates depending on activity Figure 15.13

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CV Regulation & Integration

Figure 15.14

Intrinsic Regulation

Time sequence (seconds) for electrical impulse transmission

Figure 16.1

Measuring Electrical Activity Electrocardiogram (ECG or EKG)

Measuring Electrical Activity Electrocardiogram (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 9 Accelerate SA node depolarization which increases HR (chronotropic effect) 9 Increases contractility (inotropic effect)

b) Systemically – Stimulation produces vasoconstriction (except coronary vasculature) 9 Release of norepinephrine by adrenergic fibers causes vasoconstriction 9 Vasomotor tone

Extrinsic Regulation (cont.) • Parasympathetic neural input: a) Localized – Stimulation of vagus nerves causes release of the neurohormone acetylcholine which slows sinus discharge & therefore HR 9 Slows sinus discharge & therefore ↓ HR 9 No effect on contractility

Figure 16.3

Central Command

Exercise Anticipation

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

Figure 16.10

Figure 16.6

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Peripheral Input • Chemoreceptors: monitor metabolites, blood gases

Distribution of BF during Exercise

• Mechanoreceptors: monitor movement and pressure • Baroreceptors: monitor blood pressure in arteries a) Aortic arch & carotid sinus

Local Factors within the Muscle

Nitric Oxide

• 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: 9 9 9 9 9 9

↑ blood flow ↑ temperature ↑ CO2 ↑ acidity ↑ adenosine, K+ & Mg2+ ↑ NO

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)

Functional Capacity of the CV System

• Minor role during exercise

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Cardiac Output (Q)

Cardiac Output (Q)

• Q = HR x SV

• Q = HR x SV

• Methods of Measuring Q

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

a) Direct Fick = (VO2ml·min-1/a-vo2 difference) x 100

• Q at rest a) Values vary depending upon: 9 Emotional state (central command via cardioaccelerator nerves & nerves modulating arterial resistance) 9 Posture

b) Average male (70kg) ~ 5L · min-1 c) Average female (56kg) ~ 4L · min-1

•

Untrained vs. Endurance trained characteristics of Q at rest:

•

a) Variation in resting HR Q Untrained: Trained:

5000

mL·min-1

=

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

Rest =

5000 mL·min-1 =

~ 25% lower in females

HR

x

SV

70 b·min-1

x

71 mL·min-1

b·min-1

x

100 mL·min-1

50

9 Subsequently a more gradual rise to meet exercise metabolic demands

b) Variation between groups often observed as intensity ↑

b) Mechanisms:

Maximal Exercise Q = HR

9 Increased vagal tone (parasympathetic) w/decreased sympathetic drive 9 Increased blood volume 9 Increased myocardial contractility and compliance of left ventricle

•

x

SV

Untrained:

22,000 mL =

195 b·min-1 x

113 mL·min-1

Trained:

35,000 mL =

195 b·min-1 x

179 mL·min-1

Mechanisms: a) Enhanced cardiac filling in diastole (preload) & a more forceful ejection caused by an ↑ in end diastolic volume (EDV) 9 Starling’s Law: the greater the stretch, the more forceful the contraction (contractility)

b) Greater systolic emptying 9 greater 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

Blood Flow Distribution @ Rest

• ↓ SV and coinciding a gradual ↑ in HR • Proposed mechanisms: a) Progressive H2O loss and a fluid shift from plasma to tissues 9 Drop in PV decreases central venous cardiac filling pressure

b) Increased core temperature c) Progressive increase in HR with CV drift during exercise ↓ EDV, subsequently reducing SV 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 minute b) Resting oxygen consumption (VO2) ~ 250 to 300mL·min-1 c) Leaves ~ 750mL of oxygen returning to the heart unused

Q & O2 Transport (cont.)

Q & VO2max Association

• Exercise conditions: a) Even during max exercise, Hb saturation remains nearly complete, so each L of blood carries ~ 200mL of O2 9 Ex: a max exercise Q of 16L x 200mLO2·L-1 ~ 3200mL

b) Debate exists as to the real cause of a VO2max plateau 9Q 9 O2 extraction at the tissues 9 O2 delivery

Central Peripheral Figure 17.4

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O2 Extraction: a-vO2 Difference

From Rest to Exercise

• Exercise oxygen consumption increases by: a) Increased cardiac output b) Greater use of the O2 already carried by the blood 9 Expanding a-vO2 difference

VO2 = Q x a-vO2 difference

Figure 17.5

• Factors affecting a-vO2 difference during exercise: a) Central – diversion of blood flow to working tissues b) Peripheral 9 Increased skeletal muscle microcirculation increases extraction 9 Increase in capillary to fiber ratio 9 Cells ability to regenerate ATP aerobically 9 Increased # and size of mitochondria 9 Increased aerobic enzyme concentration

Cardiac Hypertrophy

CV Adaptation/ Response to Training

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 Figure 21.7

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Heart Rate

Figure 21.9

Cardiac Output

Stroke Volume

Figure 21.10

a-v O2 difference

Figure 21.12

Figure 21.11

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 capabilities b) Mitochondrial mass & density increased

• Reduction in BP

Figure 21.6

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