Cardiorespiratory Response to Exercise

Two major adjustments of blood flow during exercise

1. Increased cardiac output

2. Redistribution of blood flow from inactive organs to active muscle

Arteries and arterioles

Carry blood AWAY from the heart

Capillaries

Exchange of O2, CO2, and nutrients with the tissues

Veins and Venues

Carry blood TOWARD the heart

Blood flow of the heart

Right side of the heart

Deoxygenated blood that circulates into the pulmonary system

• Superior/Inferior Vena Cava

• Right atrium

• Tricuspid valve

• Right Ventricle

• Pulmonary valve

• Left pulmonary artery ——> pulmonary circulation

Left side of the heart

Oxygenated blood that flows into the systemic circulation

• Right/Left Pulmonary veins

• Left atrium

• Left AV (mitral) valve

• Left ventricle

• Aortic Valve

• Aorta —→ Systemic circulation

Epicardium

Outer layer of the heart with capillaries that serves as a liubricative outer cover

Myocardium

Cardiac muscle that provides muscular contractions that eject blood from the heart chambers

Endocardium

Serves as protective inner lining of the chambers and valves

Intercalated discs

Permit transmission of electrical impulses that allow ions to cross from one fiber to another via leaky membranes

Functional Synctium

Depolarization of one fiber causes all others to become excited and contract as one unit

Damage to cardiomyocytes during an MI is due to

• Free radical damage (impaired enzyme function)

• Inability to regulate free calcium (activates proteases)

Exercise training protects the heart by:

• Increased cellular antioxidant capacity

• Enhanced mitochondrial resistance to ischemic reperfusion damage

• Improved handling of cellular calcium during calcium mediated damage

Type of exercise that provides protection

• 3-5 days of endurance exercise lasting 40-60 minutes/day

• HIIT

• More recently, resistance training

Systole

• Occurs in both the atria and ventricles

• Contraction phase

• Ejection of blood

• Approximately 2/3 of blood is ejected from ventricles per beat

• Shorter during exercise

Diastole

• Occurs in both atria and ventricles

• Relaxation phase

• Filling with blood

• Shorting during exercise

Pressure changes in Diastole

• Pressure in the ventricles is low

• Fills with blood from the atria

• AV Valves open when ventricular pressure is < atrial p

Pressure changes in Systole

• Pressure in ventricles rises

• Blood ejected in pulmonary and systemic circulation

• Semilunar valves opens when ventricular pressure > aortic p

Heart sounds

• First: Closing of AV Valves

• Second: Closing of aortic and pulmonary valves

Systolic pressure

• First sound

• Pressure generated during ventricular contraction

Diastolic pressure

• Second sound

• Pressure in the arteries during cardiac diastole

Pulse pressure

Difference between systolic and diastolic

Mean Arterial Pressure (MAP)

Average pressure in the arteries

MAP = DBP + 0.33(SBP-DBP)

Primary hypertension

Unknown cause, multifactorial

Secondary hypertension

Result of some other disease process

Determinants of MAP

• Cardiac output

• Total Vascular resistance

Short term regulation of MAP

• Sympathetic nervous system

• Baroreceptors on aorta and carotid arteries

Long term regulation of MAP

Kidneys via control of blood volume

Factors that influence arterial blood pressure

• Increase in blood volume

• HR increase

• SV increase

• Blood viscosity increases

• Peripheral resistance increases

SA Node

Pacemaker of the heart, initiates depolarization

AV Node

Passes depolarization to the ventricles, brief delay allows for ventricular filling

Bundle brances

Connect atria to the left and right ventricle

Purkinje Fibers

Spread waves of depolarization throughout the ventricles

P wave

• First bump on ECG

• Atrial depolarization (blood flows into the ventricle)

QRS Complex

• Ventricular depolarization (contraction) and atrial repolarization

• Atrial repolarization is hidden on an ECG

T-wave

Ventricular repolarization

ECG indication of MI

Depression in ST segement

When does the QRS complex occur

At the beginning of ventricular systole

When does the T wave occur

At the beginning of Ventricular diastole

Cardiac Output

Product of Heart Rate and Stroke Volume

Cardiac Output is dependent on

• Training state

• Gender (larger person has more blood volume)

Parasympathetic Nervous System

• Arises from neurons in the CVCC

• Vagus nerve stimulation

• Slows HR by inhibiting SA and AV node

Sympathetic nervous system

• Via cardiac accelerator nerves

• Nerve endings release Norepinephrine

• Increases HR and forces contraction by stimulating the SA node and ventricles

Increased HR at beginning of exercise is due to

Parasympathetic withdrawal

Parasympathetic regulation

• Increase in BO detected by baroreceptors

• Sent to CVCC

• Para activity increases to slow HR and Q in order to normalize BP

Sympathetic regulation

• Pressure receptors detect an increase in right atrial pressure

• CVCC signals that an increase in venous return has occurred

• To prevent back up of blood, Q must increase

• CVCC sends sympa accelerator nerve impulses to heart to increase HR and force of contraction

Beta-blockers

Compete with catecholamines at beta-adrenergic receptors in the heart

• Reduce heart rate and contractility

• Lower myocardial oxygen demand

• Lowers HR during exercise

Heart Rate Variablity

• Measures finite time points between cardiac cycles

• Balance between sympathetic and parasympathetic nervous systems

Low HRV

• Good predictor of sudden cardiac death

• Risk factor for development of HF, MI, and HTN

Cause of low HRV

• Physical inactivity

• age

• decrease in parasympathetic tone

• Increase in sympathetic tone at rest

End-diastolic Volume (EDV)

Volume of blood in the ventricles at the end of diastole (preload)

Average aortic blood pressure

• Pressure the heart must pump against to eject blood (afterload)

• It is the pressure pushing back on the left ventricle

• High MAP is a barrier to SV

Ventricular contractility is enhanced by

• Circulating catecholamines

• Direct stimulation of the heart by cardiac accelerator nerves

How does an increase in catecholamines increase contractility?

Increases the entry of extracellular calcium to cardiac muscle fiber which increases cross-bridge activation and force production between actin and myosin

Frank-Sterling mechanism

• Greater EDV results in a more forceful contraction

• Due to stretch of the ventricles and lengthening of the cardiac fibers

• Dependent on venous return

Venous return is increased by:

1. VENOConstriction

2. Skeletal muscle pump

3. Respiratory pump

Venoonstriction

SNS stimulation of smooth muscle in the veins that moves blood back toward the heart

Skeletal muscle pump

• Rhythmic skeletal muscle contractions force blood in the extremities toward the heart

• One-way valves in the veins prevent backflow

Respiratory pump

• Changes in thoracic pressure pull blood toward the heart

• Inspiration decreases pressure in thorax and increases pressure in abdominal region, sending blood back to heart

Factors that influence Cardiac Output

Heart Rate

• PNS

• SNS

Stroke Volume

• Contraction Strength

• EDV

• MAP

• Stretch/Frank-Sterling

Plasma

• Liquid portion of blood

• Contains ions, protein, and hormones

Cells (in blood)

RBCs

• Contain hemoglobin to carry O2

WBCs

• Important in preventing infection

Platelets

• Important in clotting

Hematocrit

Percentage of blood composed cells

Blood flow

• Directly proportional to the pressure difference between the left ventricle and the right atrium

• Inversely proportional to resistance

Pressure Proportion

Proportional to the difference between MAP and right atrial pressure

(Driving pressure)

Blow flow is increased by:

Either an increase in blood pressure or a decrease in resistance to flow

Resistance depends on:

• Length of the vessel (doesn’t change)

• Viscosity of the blood

• Radius of the vessel

  • More constriction = more resistance

  • More dilation = less resistance

Sources of vascular resistance

• MAP decreases throughout the systemic circulation

• The largest BP drop occurs across the arterioles

  • Accounts for 70-80% of the decline in MAP

  • Called “resistance vessels”

Increased in O2 delivery is accomplished by

• Increased cardiac output

• Redistribution of blood flow

  • From inactive organs to working skeletal muscle

Max HR in adults

220 - age (years)

Increased SV

• Increases, then plateaus at 40-60%

• No plateau in highly trained subjects d/t better venous return and increased EDV

aVO2 difference

• Amount of O2 that is taken up from 100 mL of blood

• Difference between arterial O2 content vs venous O2 content

• Increases during exercise due to higher O2 uptake in tissues

  • Used for oxidative ATP production

FICK equation

VO2 = Q x aVO2 difference

What does it mean when DBP goes up

That vasoconstriction in the arterioles is increasing

Barrier to vasodilation

Afterload (we want it to decrease)

Venous return when standing

Promotes blood pooling in the legs, lowering venous return, and a lower EDV

Upright exercise and SV

Increases SV due to a larger EDV and venous return, especially at a higher HR

Supine exercise (swim) and SV

Increases SV

Vsiceral organs and inactive tissues during exercise

• SNS Vasoconstriction

• Blood flow reduced to 20-30%

Skeletal muscle during exercise

• Vasodilation d/t autoregulation

• Blood flow increases to meet metabolic demand

• Intensity and motor unit recruitment dictate the demand

• 
  

Vasoactive regulators and factors

• Increase in nitric oxide

• Prostaglandins

• Adenosine

• Endothelium derived hyperpolarization factors

• ATP

Changes in HR and BP depend on:

• Type, intensity, and duration of exercise

• Environment (hot/humid conditions)

Pressure and volume response to exercise

• SV elevated d/t increased EDV and low ESV

• Decrease in Cardiac cycle (faster HR)

• Intraventricular pressure increases d/t elevated afterload

Emotional influence on exercise

• Elevated HR and BP d/t an increase in SNS activity

• Does not increase peak HR or BP during exercise

Changes at the onset of exercise

• Rapid increase in HR, SV, Cardiac output

• They plateau in submaximal exercise below the lactate threshold

Changes during recovery

• Decreased HR, SV, and Q

  • Dependent on duration, intensity, and conditioning

HR and Q during incremental exercise

Increases linearly with increasing work rate until 100% VO2 max is met

BP during incremental exercise

Systolic BP increases, MAP increases linearly, Diastolic BP remains fairy constant

Double Product during incremental exercise

Increases linearly with exercise intensity.

Represents the metabolic demands of the heart

HR x SBP

Double product and CAD

Exercise the subject at the intensity just below their double product

Arm work exercise

• Higher HR due to sympathetic stimulation

• Higher BP due to vasoconstriction of large inactive muscle mass

Recovery from intermittent exercise is dependent on

• Fitness level

• Temperature/humidity

• Duration and intensity

HR response following heavy intensity intermittent exercise

Causes a cumulative HR between efforts resulting in near maximal HR and delays complete recovery

Prolonged exercise results in

• Maintained cardiac output

• Gradual decrease in SV

  • Decreased venous return

• Gradual increase in HR

  • “Cardiovascular drift”

Factors that increase Cardiac Output

• Cardiac Rate

• Stroke Volume

• SNS

• Improved venous return

• Deeper breathing

Factors that increase blood flow to muscles

• Metabolic vasodilation

• SNS constriction in visceral organs

• Skeletal muscle activity

• Venoconstriction

Central Command Theory

The initial signal to “drive” CV system comes from higher brain centers (CVCC or medulla)

• Due to centrally generated motor systems

Heart mechanoreceptors

Respond to stretches in the walls of: carotid sinus, atria, ventricles, and pulmonary vessels