Cardiovascular Dynamics During Exercise Chapters 15 & 16

Introduction At 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 Output Q = heart rate times stroke volume

Cardiac Output Blood 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 Rate Resting heart rate Anxiety Dehydration Temperature Digestion Over-training The most important factor for increasing Q during acute exercise.

Heart Rate What causes HR to increase during exercise? Decrease parasympathetic (vagal) stimulation Increase sympathetic stimulation

Heart Rate Steady 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 Volume Increases until about 25-50% of maximum After that it may plateau (untrained) or continue to increase (trained) Decrease at maximum effort?

Stroke Volume How 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 Vasodilation from ‘autoregulation’

Cardiovascular drift Caused 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

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

Percent of blood composed of cells Hematocrit Percent of blood composed of cells

The Blood Arterial blood: 97-98% saturated with O2 Venous blood Rest – 75% Exercise – 25%

Blood Pressure Expressed 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 = Systolic - Diastolic 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 Pressure Resistance

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

High pressure to a Low pressure High pressure to a Lower pressure a-v O2 difference No 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

Lower PO2 due to an increase in O2 consumption (VO2) during exercise RESTING EXERCISE 20 ml or P02 98 20 ml or P02 98 5 ml extracted 15 ml extracted PO2 = 40 PO2 = 20 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 Consumption An 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’?