Module 1: Clinical Exercise Physiology and Electrophysiology

Why is understanding CV anatomy, physiology, and underlying principles of the ECG important?

It’s one of the most vital organs and helps transfer oxygen and oxygenate blood, heart pumps oxygenated and nutritious blood, heart is muscle itself so it needs oxygen and nutrients to stay healthy and work, when there is an issue in the heart getting oxygen and nutrients the whole body also gets compromised (can have a heart attack)

ACSM certifications: health-related fitness/preventative

-Group Ex instructor

-Personal trainer

-Ex physiologist

ACSM Certifications: clinical

Clinical Ex Physiologist: like personal trainer but for people that have diseases, highly controlled supervised setting.

Competencies include extensive knowledge of:

-functional anatomy

-exercise physiology

-pathophysiology

-electrocardiography

-behavior/physiology

-gerontology

-GXT in the clinical setting

Graded exercise test (GXT)

A test that evaluates an individual’s physiological response to staged increases in exercise intensity, exercise (stress) placed on body shows abnormality but at rest you’ll probably not see it

Reasons for GXT Fitness

-determination of functional capacity

-determination of appropriate exercise intensities, energy expenditures

-determination of exercise program effectiveness

Reasons for GXT Clinical

-determination of functional capacity

-determination of appropriate exercise intensities, energy expenditures

-determination of exercise program effectiveness

-diagnosing CAD in patients with chest pain

-evaluating disease severity in patient with CAD or stable angina

-determine the severity of silent ischemia in patients with multiple risk factors

-evaluation of other cardiac abnormalities/pathologies

-assess the efficacy of drug treatment

Typical measurements during GXT

ECG, heart rate, blood pressure, perceived exertion, angina pain, work rate/intensity, time, gas exchange (VO2 consumption and RER which indicates substrate use anaerobic metabolism)

CV supports like and exercise

Exercise stresses the CV, electrophysiology allows the heart to meet the demands GXT assesses function of heart under increase stress/demand

Structure of the heart

Four chambers and four sets of valves (two atrioventricular and two semilunar), control blood flow throughout the heart and out of the heart

The chambers:

Atria and the ventricles, the atrioventricular valves (tricuspid and bicuspid (mitral) valves, the semilunar valves (pulmonary and aortic valves)

What happens to the cardiac muscle during training?

The heart adapts to exercise

Ventricular remodeling

Primary exercise adaptations to myocardium occur in ventricles (left), LV myocardium may increase (cardiac hypertrophy), lumen of LV may increase (increase in chamber volume)

Increase in chambers size = greater stroke volume (more blood pumped out)

Ventricular hypertrophy = bigger muscle allows for more forceful contractions

Type of adaptations depends on the type of training

Increase endurance exercise = increase heart rate = increase blood volume circulation = increase stretch stress of LV = increase LV diameter due to the increase of blood volume for increased period of time

Increase in exercise = increase in blood pressure = increase in force needed by LV to push blood out = increase in LV hypertrophy

Concentric vs eccentric hypertrophy

Both can have increase thickness and increase in size it just depends on the type of exercise and which type of training is more dominant, hypertrophy but in different ways

Eccentric hypertrophy

Increase in LV size or volume, volume overload, chamber dilation, increase in myocyte length » increase in myocyte width, no fibrosis, no cardiac dysfunction, increase in series

Concentric hypertrophy

Pressure overload, without chamber dilation, increase in myocyte witdth » increase in myocyte length, no fibrosis, no cardiac dysfunction, increase in thickness, increase in parallel

The athlete’s heart

Increased heart mass, normal cardiac function, reversible, normal cell pattern

Endurance athlete (Eg. runner, swimmer)

-thickening of LV walls

-LV dilation

Strength athlete (e.g weightlifter, wrestler)

-thickening of LV walls, mild LV dilation

Combination athlete (eg. rower, canoeist)

-gross thickening of LV walls, LV dilation

The failing heart

Increased heart mass, reduced cardiac function, irreversible, cell death and fibrosis, increased mortality, disorganized cell pattern

Hypertension (due to high bp):

-thickening of LV walls

-no dilation in early stages of disease

Dilated cardiomyopathy, heart failure:

-thinning of LV walls

-significant LV dilation

Hypertrophic cardiomyopathy (born with it):

-gross thickening of LV walls

-no dilation/decrease in LV chamber size

Sudden cardiac death

Causes under 35 years old: inherited conditions such as HCM or arrhythmias, prevalence of HCM (about 8% of athletic population) in general population is 1 in 200 (initial presenting symptom may be SCD), congenital abnormalities accounted for about 11% of SCD cases, 25% of cases had a structurally normal heart (implicating that arrhythmias may be a leading cause), ARVC in other countries accounted for about 25% of SCD cases

Causes over 35 years old: coronary artery disease, main cause is atherosclerotic CAD

Most impacted populations are males, African Americans, and basketball players

Hypertrophic cardiomyopathy

Asymmetrical LV hypertrophy, disruption of myocyte organization and impulse propagation, predispose to arrhythmias, sarcomere disorganization, myosin mutations, fibrosis, LV outflow obstruction

May live without detection/diagnosis (sudden cardiac death may be the initial manifestation)

~30% of SCD athletes reported chest pain, shortness of breath, performance decline, palpitations, pre-syncope, syncope

Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)

Pathological features: substitution of right ventricular myocardium tissue with fibrous and fatty tissue

Molecular genetic features: mutations of desmosomal proteins (important for cell adhesion)

Pathophysiological features: intercalated disk remodeling with abnormalities/loss of desmosomes (disruption of junctions between cells w/ myocyte disruption and cell death)

Signs and symptoms: clinically overt (may have minimal or no structural abnormalities), sudden cardiac death may be initial manifestation, most common symptoms include heart palpitations and effort induces syncope

Prognosis: depends on the severity of the arrhythmia and dysfunction, major risk factors are unexplained syncope, non-sustained ventricular tachycardia during monitoring/exercise testing, and severe systolic dysfunction

Treatment options: treatments work to alleviate symptoms but do not work to prevent the progression of disease: restriction from sport, beta-blockers prevention of arrhythmias and reduction of right ventricular wall stress, antiarrhythmic drug therapy, catheter ablation, defibrillator therapy, cardiac transplantation

Distribution of cardiac output during rest and exercise

In CAD with exercise it’ll be a problem cuz more blood will have a heard time going through the heart

With heavy exercise cardiac output is 25 L/min, heart will have 4-5% of that blood flow and muscle will have 70-85% since it has the highest metabolic demand so it’ll get the most blood

With rest cardiac output is 5 L/min, the heart will have 4-5% of that blood flow and the muscle will get 15-20%, it may seem that the heart gets the same amount but its not cuz same percentage but different cuz the overall amount increases so the heart during rest still gets less amount than when exercising

myocardial blood supply

Blood flows through coronary vessels occur during diastole, during period of lower pressure during relaxation, compression of vessels occur during ventricular contraction (systole), main coronary arteries branch off aorta, heart gets majority of its blood during diastole vs the body gets blood during systole

Right coronary artery

Surface, large, epicardial, supplies right side of heart, divides into marginal and posterior interventricular artieres

Left (main) coronary artery

Surface, large, epicardial, supplies left side of heart, divides into circumflex and anterior descending arteries

Right coronary artery

Divides into marginal and posterior interventricular arteries

Feeds:

-right atrium

-right ventricle

-inferior wall of left ventricle

-posterior wall of left ventricle

-1/3 interventricular septum

Supplies SA node in of 50% population, supplies AV node in of 90% population

Left coronary artery

Divides into anterior descending artery and circumflex artery

Anterior descending artery:

-anterior-lateral surface of left ventricle

-2/3 interventricular septum

-“widowmaker” (blockage; location and amount of muscle it feeds)

Circumflex artery (CX)

-left atrium

-lateral surface of left ventricle

-supplies SA node in 40-50% of population

-supplies AV node in 10% population

Widowmaker

95% blockage at the beginning of the left anterior descending artery, now blood supply to this whole area is compromised and if not treated the front wall of the heart dies with often disastrous consequences

Coronary artery circulation

Effects of compression are greatest in the endocardium, most distal from main blood supply, most susceptible to ischemia, highly efficient rate of O2 extraction (~70%)

Effect of atherosclerosis on flow

Poiseuille’s law: flow is affected greatly by radius of vessel

Increase radius = increase flow exponentially

Decrease radius = decrease flow exponentially

F = r^4

Cardiac cycle

All events (mechanical and electrical) that occur during one heartbeat

Diastole: relaxation phase, chambers fill with blood, twice as long as systole

Systole: contraction phase ventricles contract, expel blood into aorta and pulmonary arteries

Rest heart rate = 75 beat /min, systole : 0.3 sec (38%), diastole: 0.5 sec (62%), total cycle time = 0.8 sec

Heavy exercise heart rate = 180 beats/min, systole : 0.2 sec (61%), diastole 0.13 sec (39%), total cycle time 0.33 sec

Diastole dripped way more than systole so during exercise diastole is decreased

Coronary blood flow during the cardiac cycle

Most of coronary blood flow happens in diastole, so during exercise, the drop in time in diastole challenges the heart’s ability to deliver blood through the coronary artery. Also there’s more blood that needs to move through there at a shorter amount of time

CAD: EKG to detect CAD with exercise, if there’s a blockage it may cause ischemia due to increase of flow and decrease of time in diastole but with decreased radius

Myocardial ischemia

Temporary lack of adequate coronary blood flow relative to myocardial oxygen demands; often manifested as angina pectoris (chest pain)

Myocardial infarction

Vessel occlusion resulting in injury/necrosis (death) of myocardial tissue

Stable angina

Predictable chest pain, regular, expected when stress is added and increase in cardiac demand, no change in size and not rupturing

Unstable angina

Unpredictable chest pain from myocardial ischemia, just happens out of nowhere, when the plaque ruptures, can clot

Atherosclerosis

Previous view: plumbing problem, liquid build up on the surface of artery walls

Current view: response to injury, inflammation and responses, promotes buildup of plaque, causes plaque ruptures leading to blood clots, happens in the wall of the vessel (in the endothelium) instead of on it

Lumen vs endothelium: vast majority of CAD occurs without luminal narrowing (stenosis), angiogram images lumen, no stenosis = no ischemia so EKG won’t detect it

Many patients first manifestation of CAD is not angina, MI or death, minimal stenosis, lipid panel, EKG, Ca2+ score, CT angiogram, catheterization and angiogram

Atherosclerotic plaque has a core containing lipids and debris from dead cells (esterified cholesterol and cholesterol crystals), fibrous cap containing smooth muscle cells and collagen fibers stabilizes the plaque.

Immune cells including macrophages, T cells and mast cells populate the plaque, and are frequently in an activated state, produce cytokines, proteases, pro-thrombotic molecules and vasoactive substances which can affect plaque inflammation and vascular function, calcification occurs, until complications occur, an intact endothelium covers the plaque.

When plaque ruptures and a thrombus occur, the size of the lumen does not matter, patient will have an acute MI, unstable angina, sudden cardiac death, size of the lumen is not good predictor of which patients will experience these complications

Thrombus

Conglomeration of fibrin and platelets, often containing red and white blood cells

CAD and GXT

EKG does not detect plaque buildup, it detects ischemia

Why is exercise good model for detecting CAD when stenosis present? Heart gets blood during diastole, during exercise diastole time decreases and cardiac output increases, so if there’s stenosis it would cause ischemia

Myocardium

Cardiac muscle: striated, short, fat, branched, interconnected cells, the connective tissue endomysium acts as both tendon and insertion, intercalated discs anchor cardiac cells together and allow free passage of ions, heart muscle behaves as a function syncytium (functionally it acts like one single thing)

Cardiac muscle fibers are interconnected end to end, at intercalated disks, little neural innervation, cell-to-cell (electrogenic coupling) (leaky membranes, ions cross from cell to cell)

Allows for performance as function syncytium

Uninucleated, only one fiber type, similar to type I, high capillary density, high number of mitochondria (highly aerobic and fatigue resistant)

Desmosomes

Transmembrane proteins that hold cells together

Gap junctions

Intracellular channels that rapidly conduct action potentials

Autorhythmic (pacemaker cells)

Generate spontaneous intrinsic AP (SA node, AV node, bundle of his, purkinje fibers), SA node prime pacemaker (highest intrinsic rhythmicity), create electrical conduction system, specialized tract of tissues (facilitate AP through heart from pacemaker), transit AP rapidly (vary in size, excitability, myofibrilar content, voltage-gated channels)

Contractile

Do not generate spontaneous intrinsic AP, receives AP from neighboring cells (which received AP from a pacemaker cell through tract of conduction system), primary function to contract

Lactate as fuel

Lactate from skeletal muscle transported into blood to myocardium (and type I skeletal muscle muscle)

Monocarboxylate transporters (MCT)

MCT1: mitochondria and sarcoplasm in SM and myocardium (lactate uptake and oxidation, correlated with oxidative capacity)

MCT4: sarcolemmal in SM (greater expression in type II, lactate efflux)

Type II produces more lactate cuz it’s more anaerobic, heart is a big user of lactate as a fuel (use lactate as substrate to generate ATP), type I fibers and heart have transporters that uptake lactate

Increase in intensity = increase in lactate, lactate can be used as a fuel source via oxidative phosphorylation but type II are not aerobic so won’t use oxi phos so MCT (lactate shuttles) send lactate out of muscle cells, goes into circulation, and goes to other muscle tissue and heart

Intracellular lactate shuttle

Lactate from glycolysis is transported into mitochondria (MCT1), mitochondrial LDH oxidized lactate to pyruvate (proceeds to oxi phos)

Lactate exists cell, enters circulation (MCT4), cardiac myocardial uptake (transported to mitochondria, MCT1, mitochondrial LDH oxidizes lactate to pyruvate (proceeds to oxi phos) glycogen or gluconeogenesis in liver)

Myocardium vs skeletal muscle

Skeletal muscle cells:

-large, long, unbranded, multinucleated

-intermittent, voluntary contractions

-Ca2+ released from SR

Myocardial cells

-small, short, branched, one nucleus

-continuous, involuntary rhythmic contractions

-Ca2+ induced Ca2+ release (Ca2+ from ECF stimulates SR Ca2+ release)

Cardiac conduction system

Intrinsic and extrinsic control

-“pacemaking” cardiac cells, spontaneously depolarize

-autonomic nervous system, sympathetic and parasympathetic innervation