Cardiovascular Dynamics During

ExerciseChapters 15 & 16

IntroductionAt rest: O2 supply = O2 demand

Exercise: O2 demand increases

To the muscles

To the heart

To the skin

Maintain flow to the brain

How does the heart increase O2 supply to meet the O2 demand?

Cardiac OutputQ = heart rate times stroke volume

Cardiac OutputBlood flow per minute.

At rest Q = 5-6 liters/min

Q increases linearly with the demand for more O2

Indicator of oxygen supply

How does cardiac output increase?

Increase heart rate

Increase stroke volume

Heart RateResting heart rate

Anxiety

Dehydration

Temperature

Digestion

Over-training

The most important factor for increasing Q during acute exercise.

Heart RateWhat causes HR to increase during exercise?

Decrease parasympathetic (vagal) stimulation

Increase sympathetic stimulation

Heart RateSteady state exercise

Why does heart rate level off during steady state exercise?

Heart Rate

Increases with intensity and levels off at maximal effort.

– HRmax = 220 – age

– (± 12)

Stroke Volume

Volume pumped per beat of the heart

Influenced by preload and afterload

Stroke VolumeIncreases until about 25-50% of maximum

After that it may plateau (untrained) or continue to increase (trained)

Decrease at maximum effort?

Stroke VolumeHow does stroke volume increase during exercise?

Increase preload (EDV)

– Increase venous return

• Muscle pump, etc.

Decrease afterload

– Vasodilation

• Metabolic control and sympathetic stimulation

Increase contractility (ESV)

– Increase sympathetic stimulation

Frank-Starling Mechanism

Frank-Starling mechanism: the ability of the heart to alter the force of contraction is dependent on changes in preload.

As the myocardial fibers are stretched, the force of contraction is increased.

Because the length of the fiber is determined primarily by the volume of blood in the ventricle, EDV is the primary determinant of preload

This graph depicts the Frank-Starling mechanism of compensation in CHF.

The black curves represent ventricular function in a normal subject and the colored curve is with left ventricular dysfunction.

Line N to A represents the initial reduction in cardiac output due to CHF.

Line A to B represents the Frank-Starling mechanism of compensation; an increase in left ventricular end-diastolic pressure needed to maintain cardiac output.

Stroke Volume

Stroke Volume

Increased sympathetic stimulation

Increased sympathetic stimulation

Vasodilation from

‘autoregulation’

Vasodilation from

‘autoregulation’

Cardiovascular driftCaused by a decrease in venous return

Cardiac output is maintained by…..?

Cardiovascular Drift

Stroke Volume

SV greater in trained

Most significant effect of training

Result

• An increase in cardiac output…

• Increase HR

• Increase SV

• …results in an increase in O2 supply

Hemodynamics

Blood Vessels

Arteries

Arterioles

Capillaries

Venules

Veins

Physical Characteristics of Blood

• Plasma

Liquid portion of blood

Contains ions, proteins, hormones

• Cells

Red blood cells

Contain hemoglobin to carry oxygen

White blood cells

Platelets

Important in blood clotting

The Blood

Arterial blood carries 20 ml of oxygen per 100 ml of blood

HematocritPercent of blood composed of cells

The Blood

• Arterial blood: 97-98% saturated with O2

• Venous blood

– Rest – 75%

– Exercise – 25%

Blood PressureExpressed as systolic/diastolic

Normal is 120/80 mmHg

High is ≥140/90 mmHg

Systolic pressure (top number)

Pressure generated during ventricular contraction (systole)

Diastolic pressure

Pressure in the arteries during cardiac relaxation (diastole)

Blood Pressure

• Pulse pressure

Difference between systolic and diastolic

• Mean arterial pressure (MAP)

Average pressure in the arteries

Pulse Pressure = Systolic - Diastolic

MAP = Diastolic + 1/3(pulse pressure)

Mean Arterial Pressure

• Blood pressure of 120/80 mm Hg

• MAP = 80 mm Hg + .33(120-80)

• = 80 mm Hg + 13

• = 93 mm Hg

Hemodynamics

• Based on interrelationships between:

– Pressure

– Resistance

Hemodynamics: Pressure

Blood flows from high → low pressure

Proportional to the difference between MAP and right atrial pressure (ΔP)

Blood Flow Through the Systemic Circuit

Hemodynamics: Resistance

Resistance depends upon:

Length of the vessel

Viscosity of the blood

Radius of the vessel

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

Resistance = Length x viscosity

Radius4

Hemodynamics: Blood Flow

Directly proportional to the pressure difference between the two ends of the system

Inversely proportional to resistance

Flow = Δ PressureResistance

Sources of Vascular Resistance

MAP decreases throughout the systemic circulation

Largest drop occurs across the arterioles

Arterioles are called “resistance vessels”

Pressure Changes Across the Systemic Circulation

Pressure Changes During

the Cardiac Cycle

Factors That Influence Arterial Blood Pressure

Cardiovascular Control

How can the blood vessels increase blood flow?

Vasodilation to increase blood flow to muscles and skin

Waste products (metabolic or local control)

Sympathetic stimulation (cholinergic)

Vasoconstriction to maintain blood pressure

Sympathetic stimulation (adrenergic)

Maximum muscle blood flow is limited by the ability to maintain blood pressure

Vasodilation

Vasoconstriction

Blood Vessels

Oxygen Extraction

Measured as a-v O2 difference

• a = O2 in arteries (20 ml/100 ml of blood)

• v = O2 in veins (15 ml/100 ml of blood)

• (a-v)O2 = 5 ml/100 ml of blood

a-v O2 differenceNo change in O2 content in the blood

Remains at 20 ml/100 ml of blood

Decrease in O2 inside the muscle

Greater pressure difference between the blood and the muscles

Oxygen moves from a HIGH pressure area (blood) to a LOW pressure area (muscle)

Therefore, more O2 is extracted from the blood

High pressure to a Low pressure

High pressure to a Lower pressure

20 ml or P02 98 20 ml or P02 98

PO2 = 40 PO2 = 20

RESTING EXERCISE

15 ml extracted5 ml extracted

Lower PO2 due to an increase in O2

consumption (VO2) during exercise

Oxygen Consumption

VO2

liters per minute

milliliters per kilogram per minute

VO2 = oxygen supply x oxygen extraction

VO2 = Q x a-v O2 difference

VO2 = HR x SV x a-v O2 difference

Oxygen ConsumptionAn increase in oxygen supply leads to an increase in oxygen consumption

Increase in cardiac output

With help from HR and SV

Increase in (a-v)O2

More O2 is supplied and extracted

Therefore, more O2 can be used by the muscle fibers (mito)

Oxygen Consumption

Q and a-v O2 difference each account for 50% of the increase in VO2 during exercise

Near maximal exercise, Q accounts for 75% of the increase in VO2

Oxygen Consumption

VO2 increases with intensity

VO2 = rate of blood flow times the O2 extracted from a given amount of blood

VO2 = cardiac output x a-vO2 difference

VO2 can increase by

A greater blood flow

Taking more oxygen out of every 100 ml of blood

What limits aerobic exercise?

Lack of oxygen supply?

If so, wouldn’t the muscles be more anaerobic?

And, wouldn’t the heart also be more anaerobic?

But an anaerobic heart produces angina

Maybe the central nervous system protects the heart from ischemia by causing muscle fatigue before the heart becomes ‘anaerobic’?