Ch 19 - circulatory system: heart

Pulmonary circuit

• right side of the heart

• carries deoxygenated blood to lungs for gas exchange and back to the heart

• Oxygen-poor blood arrives from inferior and superior venae cavae

• Blood sent to lungs via pulmonary trunk

Systemic circuit

• left side of the heart

• supplies oxygenated blood to all tissues of the body and returns it to heart

• oxygenated blood arrives from lungs via pulmonary veins

• Blood sent to all organs of the body via aorta

position, size, and shape of heart

• located in mediastinum, between lungs

• base: wide, superior portion of heart, large vessels attach here

• apex: tapered inferior end, tilts to the left

• at any age, heart is size of a fist

Pericardium

• double-walled sac that encloses the heart

• Allows heart to beat without friction, provides room to expand,

  yet resists excessive expansion

• Anchored to diaphragm inferiorly and sternum anteriorly

layers of pericardium

• fibrous: outer wall, not attached to heart

• serious pericardium:

  • parietal - lines fibrous pericardium

  • visceral (epicardium) - covers heart surface

• Pericardial cavity—space between parietal and visceral layers of

  serous pericardium

• Pericarditis—painful inflammation of the membranes

heart wall has ___ layers

3; epicardium, myocardium, endocardium

Epicardium

• visceral layer of serous pericardium

• Serous membrane covering heart

• Adipose in thick layer in some places

• Coronary blood vessels travel through this layer

Endocardium

• Smooth inner lining of heart and blood vessels

• Covers the valve surfaces and is continuous with endothelium

  of blood vessels

Myocardium

• Layer of cardiac muscle proportional to workload

  • Muscle spirals around heart which produces wringing motion, vortex of the heart

• Fibrous skeleton of the heart: framework of collagenous

  and elastic fibers

• Provides structural support and attachment for cardiac muscle and

  anchor for valve tissue

• Electrical insulation between atria and ventricles; important in timing

  and coordination of contractile activity

right and left atria

• Two superior chambers

  • Receive blood returning to heart

  • Auricles (seen on surface) enlarge chamber

right and left ventricles

• two inferior chambers

• pump blood into arteries

chambers and sulcus

• coronary sulcus - separates atria and ventricles

• interventricular sulcus - overlies the interventricular septum that divides the right ventricle from the left

• sulci contain coronary arteries

interatrial and interventricular septum

• wall that separates atria

• muscular wall that separates ventricles

pectinate muscles

internal ridges of myocardium in right atrium and both auricles

trabeculae carneae

internal ridges in both ventricles; may prevent ventricle walls from sticking together after contraction

Atrioventricular (AV) valves

• control blood flow between atria and ventricles

• right AV valve has 3 cusps (tricuspid valve)

• left AV valve has 2 cusps (mitral valve, formerly “bicuspid”)

• chordae tendineae: cords connect AV vales to papillary muscles on floor of ventricles

  • prevents AV vales from involution (prevent flipping by anchoring; think umbrella)

Semilunar valves

• control flow into great arteries; open and

  close because of blood flow and pressure

• Pulmonary semilunar valve: in opening between right

  ventricle and pulmonary trunk

• Aortic semilunar valve: in opening between left ventricle

  and aorta

ventricles relax

• Pressure drops inside the ventricles

• Semilunar valves close as blood attempts to back up into the ventricles from the vessels

• AV valves open

• Blood flows from atria to ventricles

ventricles contract

• AV valves close as blood attempts to back up into the atria

• Pressure rises inside of the ventricles

• Semilunar valves open and blood flows into great vessels

coronary circulation

• 5% of blood pumped by hart is pumped into the heart itself through the coronary circulation to sustain its strenuous workload

• need abundant O2 and nutrients

• 250 mL blood/min.

• blood supply to the heart muscle (myocardium)

left coronary artery (LCA)

• branches off the ascending aorta

• anterior interventricular branch (left anterior descending or LAD)

  • supplies blood to both ventricles and anterior 2/3 of interventricular septum

• arterial supply - blood from aorta to all tissues and organs

circumflex branch

• passes around left side of heart in coronary sulcus

• gives off left marginal branch and then ends on the posterior side of the heart

• supplies left atrium and posterior wall of left ventricle

• arterial supply - blood from aorta to all tissues and organs

right coronary artery (RCA)

• branches off ascending aorta

• supplies right atrium and sinoatrial node (pacemaker)

• right marginal branch: supplies lateral aspect of right atrium and ventricle

• posterior interventricular branch: supplies posterior walls of ventricles

• arterial supply - blood from aorta to all tissues and organs

arterial supply flow through coronary arteries is ___ when heart relaxes

• greatest

• Contraction of the myocardium compresses the coronary

  arteries and obstructs blood flow

• Opening of the aortic valve flap during ventricular systole

  covers the openings of the coronary arteries blocking

  blood flow into them

• During ventricular diastole, blood in the aorta surges back

  toward the heart and into the openings of the coronary

  arteries

angina pectoris

• chest pain from partial obstruction of coronary blood flow

• pain caused by ischemia of cardiac muscle

• obstruction partially blocks blood flow

• myocardium shifts to anaerobic fermentation, producing lactate, thus stimulate pain

myocardial infarction (MI)

• sudden death of a patch of myocardium resulting from long-term obstruction of coronary circulation

• Atheroma (blood clot or fatty deposit) often obstructs coronary arteries or their branches

• Cardiac muscle downstream of the blockage dies

• Heavy pressure or squeezing pain radiating into the left arm

• Some painless heart attacks may disrupt electrical conduction pathways, leading to fibrillation and cardiac arrest

  • Silent heart attacks occur in diabetics and the elderly

veinous drainage

• 5% to 10% of coronary blood drains directly into heart

  chambers (mostly right ventricle) by way of the small cardiac

  veins

• Most coronary blood returns to right atrium by way of the

  coronary sinus which has three main inputs: great cardiac,

  posterior interventricular, and left marginal veins

great cardiac vein

• travels alongside anterior interventricular artery

• collects blood from anterior portion of heart

• empties into coronary sinus

middle cardiac vein (posterior interventricular)

• found in posterior sulcus

• collects blood from posterior portion of heart

• drains into coronary sinus

coronary sinus

• large transverse vein in coronary sulcus on posterior side of heart

• collects blood and empties into right atrium

cardiomyocytes

• striated, short, thick, branched cells, one central nucleus surrounded by light-staining mass of glycogen

• repair of damage of cardiac muscle is almost entirely by fibrosis (scarring)

intercalated discs

• join cardiomyocytes end to end with three features: interdigitating folds, mechanical junctions, and electrical junctions

• Interdigitating folds: folds interlock with each other, and increase surface area of contact

mechanical junctions

• tightly join cardiomyocytes

• Fascia adherens—broad band in which the actin of the thin myofilaments is anchored to the plasma membrane

• Desmosomes—mechanical linkages that prevent

  contracting cardiomyocytes from being pulled apart from

  each other

metabolism of cardiac muscle

• depends mostly almost exclusively on aerobic respiration to make ATP

  • rich in myoglobin (O2 storage) and glycogen (fat stroage)

  • huge mitochondria: fills 25% of cell

• adaptable to different organic fuels

  • more vulnerable to oxygen deficiency than lack of specific fuel

• fatigue resistant because it makes use of anaerobic fermentation or oxygen debt mechanisms; doesn’t fatigue for a lifetime

conduction system

• coordinate heartbeat

• composed of an internal pacemaker and nerve-like conduction pathways through myocardium

• generates and conducts rhythmic electrical signals

conduction system order

• sinuatrial (SA) node: modified cardiomyocytes

  • pacemaker initiates each heartbeat and determines heart rate

  • pacemaker in right atrium near base of super vena cava

• signals spread through atria

atrioventricular (AV) node

• located near right AV valve at lower end of interatrial septum

• electrical gateway to the ventricles

• fibrous skeleton - insulator prevents currents from getting to ventricles by any other route

atrioventricular (AV) bundle (bundle of His)

• bundle of forks into right and left bundle branches

• branches pass through interventricular septum toward apex

• subendothelial conducting networks

  • nerve-like process spread throughout ventricular myocardium

  • cardiomyocytes then pass signal from cells to cells though gap junctions

foremen ovale vs fossa ovalis

• opening in the interatrial septum

• ovale: present in fetal heart

• ovalis: present in adults (closed opening)

systole vs diastole

• contraction of heart

• relaxation of heart

• usually refers to the action of the ventricles

sinus rhythm

• normal heartbeat triggered by SA node

• adult at rest 70 to 90 bpm (vagal tone)

ectopic focus

• a region of spontaneous firing other than SA node

• may govern heart rhythm if SA node is damaged

• nodal rhythm - if SA node is damaged, heart rate set by AV node (40 to 50 bpm)

pacemaker physiology

• SA node doesn’t have stable resting membrane potential

  • starts at -60 mV and drifts upward due to slow Na+ inflow (gradual depolarization is called pacemaker potential)

• when it reaches threshold of -40 mV, voltage-gated fast Ca2+ and Na+ channels open

  • faster depolarization occurs peaking at 0 mV

  • Ca2+ moves slowly; long AP allows to contract as one unit

• K+ channels then open and K+ leaves the cell causing repolarization

  • once K+ channels close, pacemaker potential starts over

• When SA node fires, it sets off heartbeat

  • typically fires every 0.8 seconds, setting resting rate at 75 bpm

impulse conduction to myocardium

• signal from SA node stimulates 2 atria to contract almost simultaneously

• signal slows down through AV node (thin cardiomyocytes with fewer gap junctions)

• signals travel very quickly though AV bundle and subendothelial conducting network

  • entire ventricular myocardium depolarizes and contracts in near unison

• ventricular systole progresses up from the apex of the heart

  • spiral arrangement of myocardium twists ventricles slightly

3 phases of cardiomyocyte AP

• cardiomyocytes have a stable resting potential of -90 mV, and then depolarize only when stimulated

• phases: depolarization, plateau, repolarization

depolarization phase of cardiomyocyte AP

• stimulus opens voltage-regulated Na+ gates (Na+ rushes in), membrane depolarizes rapidly

• AP peaks at +30 mV

• Na+ gates close quickly

plateau phase of cardiomyocyte AP

• lasts 200 to 250 ms, sustains contraction for expulsion of blood from heart

• voltage-gated slow Ca2+ channels open admitting Ca2+ which triggers opening of Ca2+ channels on sarcoplasmic reticulum (SR)

• Ca2+ (mostly from SR) binds to troponin triggering contraction

repolarization phase of cardiomyocyte AP

• Ca2+ channels close, K+ channels open, rapid diffusion of K+ out of the cell returns it to resting potential

• has a long absolute refractory period of 250 ms

  • prevents wave summation and tetanus which would stop the pumping action of the heart

electrocardiogram (EKG OR ECG)

• Composite of all APs of nodal and myocardial cells detected, amplified and recorded by electrodes on arms, legs, and chest

• tells atrial/electrical depolarization (p-wave) not heart contraction

normal EKG figure

• p-wave: SA node fires, atrial depolarizes and contract; atrial systole begins 100ms after SA signal

• t-wave: ventricular repolarization and relax

• QRS complex: ventricular depolarization

• PR interval: signal conduction through AV node, before activating ventricles

• QT interval: during ventricular depolarization

• ST segment: ventricular systole; corresponds to plateu in myocardial AP

deviations from ECG/EKG from normal may indicate

• myocardial infarction (MI)

• abnormalities in conduction pathways

• heart enlargement (hypertension, energy drinks)

• electrolyte and hormone imbalance

sinus rhythm and EKGs

• normal EKG

• P, T, QRS complex present

ventricular fibrillation

• serious arrhythmia (irregular heartbeat) caused by electrical signals travelling randomly (heart can’t pump blood; no coronary perfusion)

• hallmark of heart attack (MI)

• kills quickly if stopped

  • defibrillation: strong electrical shock with intent to depolarize entire myocardium and reset hear to sinus rhythm

  • not cure for artery disease

atrial fibrillation

chaotic depolarizations that do no stimulate ventricles; common in elderly and alcoholics

heart block

failure of any part of cardiac conduction system to conduct signals, usually result of disease or degeneration of conduction system

premature ventricular contraction

ventricular ectopic focus with extra beat; may result from stress, lack of sleep, or stimulants

cardiac cycle

one complete contraction and relaxation of all 4 chambers of the heart

2 main variables govern fluid movement

• pressure causes flow and resistance opposes it

• fluid only flow if there is a pressure gradient

  • fluid flows from high-pressure to low

  • pressure measured in mm Hg with manometer (sphygmomanometer for BP)

events occurring on left side of heart

• when ventricle relaxes and expands, internal pressure fails

• if mitral valve is open, blood flows into left ventricle

• when ventricle contracts, internal pressure rises

• AV valve close, aortic valve is pushed open and blood flows into aorta from left ventricle

• opening and closing of valves governed by pressure changes

  • AV valves limp when ventricles relaxed

  • semilunar valves under pressure from blood in vessels when ventricles relaxed

Valvular insufficiency (incompetence)

any failure of a valve to prevent reflux (regurgitation), backward flow of blood; valve that leaks

valvular stenosis

• cusps are stiffened and opening is constricted by scar tissue

• result in rheumatic fever, autoimmune attack on mitral and aortic valves

• heart overworks and may become enlarged

• heart murmur: abnormal heart sound produced by regurgitation of blood through incompetent valves; valve leaks

Mitral valve prolapse

• insufficiency in which one or both mitral valve cusps bulge into atria during ventricular contraction

• Hereditary in 1 out of 40 people

• May cause chest pain and shortness of breath

heart sounds

• auscultation - listening to sounds made by body

• S₁: 1st heart sound, louder and longer “lubb”, occurs with closure of AV valves, turbulence in the bloodstream, movement of heart wall

• S₂: 2nd heart sound, softer and sharper “dupp”, occurs with closure of semilunar valves, turbulence in bloodstream, movement of heart wall

• S₃: rarely heard in people over 30

phases of the cardiac cycle

• Ventricular filling (during diastole) 1

• Isovolumetric contraction (during systole) 2

• Ventricular ejection (during systole) 3

• Isovolumetric relaxation (during diastole) 4

• The entire cardiac cycle (all four of these phases) is completed in less than 1 second

Ventricular filling (1) - cardiac cycle

• ventricles expand and their pressure drops below that of atria

• AV valves open and blood flows into ventricles

• filling occurs in 3 phases:

  • rapid ventricular filling: first 1/3

  • diastasis: second 1/3; slower filling

    • P wave occurs at the end of diastiasis

  • atrial systole: final 1/3; atria contract

    • end-diastolic volume (EDV) achieved in each ventricle (~130 mL blood)

Isovolumetric contraction (2) - cardiac cycle

• atria repolarize, relax and remain in diastole for rest of cardiac cycle

• ventricles depolarize causing QRS complex, and begin to contract

• AV valves close as ventricular blood surges back against the cusps

• heart sound S₁ occurs at beginning of phase

• “isovolumetric” because ventricles contract but they don’t eject blood

  • pressures in aorta and pulmonary trunck are still greater than in ventricles

• cardiomyocytes exert force, but with all 4 valves closed, blood can’t go anywhere

ventricular ejection (3) - cardiac cycle

• begins when ventricular pressure exceeds arterial pressure and semilunar valves open

• pressure peaks in left ventricle at about 120 mm Hg and 25 mm Hg in the right

• 1st: rapid ejection; blood spurts out of ventricles quickly

• then: reduced ejection; slower flow with lower pressure

• ejection lasts about 200 to 250 ms; corresponds to plateau phase of cardiac AP

• T wave of EKG occurs late in phase

• stroke volume (SV) about 70 mL

  • ejection fraction is about 54% EDV (130mL)

  • 60mL remaining blood is end-systolic volume (ESV)

isovolumetric relaxation (4) - cardiac cycle

• T wave ends and ventricles begin to expand

• blood from aorta and pulmonary trunk briefly flows backward filling cusps and closing semilunar valves

  • creates pressure rebound that appears as dicrotic notch in graph of artery pressure

  • heart sound S₂ occurs

• “isovolumetric” because semilunar valves are closed, and AV valves have not yet opened; ventricles taking no blood

• AV valves open, ventricular filling begins again

stroke volume and cardiac output

• SV = EDV - ESV

• CO = HR * SV

in a resting person (cardiac cycle)

• atrial systole lasts about 0.1 second

• ventricular systole lasts about 0.3 second

• quiescent period, when all 4 chambers are in diastole, lasts about 0.4 second

• total duration of cardiac cycle is 0.8 second in heart beating 75 bpm

overview of volume changes in heart

• ESV 60 mL

• passively added to ventricle during atrial diastole +30mL

• added by atrial systole +40mL

• total: EDV 130 mL

• SV ejected by ventricular systole -70mL

• leaves: ESV 60mL

• both ventricles must eject same amount of blood

congestive heart failure (CHF)

• results from failure of either ventricle to eject blood effectively

• usually due to heart weakened by myocardial infarction, chronic hypertension (HTN), valvular insufficiency or congenital defects in heart structure

• normally, right and left sides eject same volume of blood

left vs right ventricular failure

• blood backs up into lungs causing pulmonary edema

  • shortness of breath or sense of suffication

• blood backs up into vena cava causing systemic or generalized edema

  • enlargement of liver, ascites (pooling of fluid in abdominal cavity), distension of jugular veins, etc.

  • eventually lead to total heart failure

autonomic innervation of the heart

• heart rhythm and contraction are controlled by cardiac centers in medulla oblongata

• cardioacceleratory center sends sympathetic innervation via cardiac nerves

• cardioinhibitory center sends parasympathetic innervation via vagus nerve

autonomic innervation - sympathetic nerves

• increase heart rate and contraction

• pathway to heart originates in the lower cervical to upper thoracic segments of the spinal cord

• continues to adjacent sympathetic chain ganglia and some ascend to cervical ganglia

• postganglionic fibers pass through cardiac plexus in mediastinum and continue as cardiac nerves to heart

• fibers terminate in SA and AV nodes, in atrial and ventricular myocardium (also aorta, pulmonary truck, coronary arteries)

• alpha receptors = smooth muscle relax

• beta receptors = smooth muscle contract

autonomic innervation - parasympathetic nerves

• slows heart rate

• pathways begins with nuclei of vagus nerves in medulla oblongata

• extend to cardiac plexus and continue to heart by way of cardiac nerves

• fibers of right vagus nerve lead to SA node

• fibers of left vagus nerve lead to AV node

• little or no vagal stimulation of myocardium

cardiac output

• amount ejected by each ventricle in 1 minute

• CO = HR * SV

• about 4 to 6 L/min at rest

• RBC leaving left ventricle will arrive back at the left ventricle in about 1 min

• vigorous exercise increases CO to 21 L/min for a fit person and up to more >40 L/min for world class athlete

• cardiac reserve: difference between a person’s max and resting CO

  • increases with fitness, decrease with disease

pulse

• surge of pressure produced by heart beat that can be felt by palpatating a superficial artery

• infants have HR of 120 bpm or more

• young adult females 72 to 80 bpm

• young adult mails 64 to 72 bpm

• heart rate rises again in elderly

tachycardia

• resting adult heart rate above 100 bpm

• stress, anxiety, drugs, heart disease, or fever

• loss of blood or damage to myocardium

bradycardia

• resting adult heart rate of less than 60 bpm

• in sleep, low body temp, endurance-trained athletes

positive vs negative chronotropic agents

• factors that raise the heart rate

• factors that lower the heart rate

• iontropic

chronotropic effects of autonomic nervous system

• autonomic nervous system doesn’t initiate heartbeat, it modulates rhythm and force

• cardiac centers in reticular formation of medulla oblongata initiate autonomic output to the heart

• cardiostimulatory effect: some neurons of cardiac center transmit signals to heart by sympathetic pathways

• cardioinhibitory effect: others transmit parasympathetic signals by vagus nerve

chronotropic effects - sympathetic system part 1

• postganglionic fibers are adrenergic

• release norepinephrine

• bind to beta-adrenergic fibers in the heart

• active cAMP 2nd messenger system in cardiomyocytes in nodal cells

• lead to opening of Ca2+ channels in plasma membrane

chronotropic effects - sympathetic system part 2

• increased Ca2+ inflow accelerates depolarization of SA node

• cAMP accelerates Ca2+ uptake by sarcoplasmic reticulum allowing cardiomyocytes to relax more quickly

• by accelerating both contraction and relaxation, norepinephrine (through cAMP) increases heart rate as high as 230 bmp

• excessively high heart rates (>180bpm), diastole becomes too brief for adequate filling (both SV and CO reduced)

chronotropic effects - parasympathetic system

• parasympathetic vagus nerves have cholinergic, inhibitory effects on SA and AV nodes

• acetylcholine (ACh) binds to muscarinic receptors

• opens K+ gates in nodal cells

• as K+ leaves cells, they become hyperpolarized and fire less frequently

• heart slows down

• K+ leaving cell = repolatization

without influences from ___, heart has an intrinsic firing rate of 100 bpm

• cardiac centers

• vagal tone: holds down the heart rate to 70 to 80 bpm at rest

• steady background firing rate of vagus nerves

inputs to cardiac centers in medulla

• are diverse

• sources include higher brain centers such as cerebral cortex, limbic system, hypothalamus

• medulla also receive input from muscles, joints, arteries, and brainstem

• proprioceptors in muscles and joints inform cardiac centers about changes in activity, so HR increases before metabolic demands on muscle arise

baroreceptors signal cardiac center

• pressure sensors in aorta and internal carotid arteries

• BP decreases, signal rate drops, cardiac center increases HR

• if BP increases, signal rate rises, cardiac center decreases HR

• responses to fluctuation in BP and chemistry; negative feedback loop

• brain knows O2 demands (roreceptors)

chemoreceptors

• in aortic arch, carotid arteries, medulla oblongata

• sensitive to blood pH, CO2, O2 levels

• more important in respiratory control than cardiac control but will trigger increase in HR when high CO2 levels (hypercapnia) lead to acidosis

• also respond to hypoxemia (O deficiency in blood) usually by slowing down heart

• responses to fluctuation of BP and chemistry; negative feedback loops

several chemicals affect HR

• autonomic neurotransmitters (NE, ACh)

• blood-borne adrenal catecholamines (NE and epinephrine) are potent cardiac stimulants

• nicotine stimulates catecholamine secretion

• thyroid hormone increases # of adrenergic receptors on heart so it’s more responsive to adrenergic stimulation

• caffine inhibits cAMP breakdown, prolonging adrenergic effect

electrolytes and chronotropic effects

• K+ greatest chronotropic effect

• hyperkalemia - excess K+ diffuses into cardiomyocytes

  • myocardium less excitable, HR slows and becomes irregular

• hypokalemia - deficiency in K+

  • cells hyperpolarized, require increased stimulation

• hypercalcemia - excess of Ca2+; decreases HR and contraction strength

• hypocalcemia - deficiency of Ca2+; increases HR and contraction strength

stroke volume

• other factor in CO besides HR

• 3 variables that govern it: preload, contractility, afterload

• increased preload or contractility increases SV

• increased afterload decreases SV

preload - SV

• amount of tension in ventricular myocardium immediately before it begins contract

• increased preload cause increased force of contraction

• exercise increases venous return and stretches myocardium

• cardiomyocytes generate more tension during contraction

• increased CO matches increased venous return

frank-starling law of heart

• SV directly proportional EDV

• ventricles eject almost as much blood as they receive

• more stretched, harder it is to contract

• relates to length-tension relationship of striated muscle

contractility - SV

• refers to how hard the myocardium contracts for a given preload

• positive inotropic agents increase it

  • hypercalcemia can cause strong, prolonged contractions and cardiac arrest in systole

  • catecholamines increase Ca levels

  • glucagon stimulates cAMP production

  • digitalis raises intracellular Ca levels and contraction strength

negative inotropic agents ___ contractility

• reduce

• hypocalcemia can cause weak, irregular heartbeat and cardiac arrest in diastole

• \hyperkalemia reduces strength of myocardial APs and release Ca2+ into sarcoplasm

• vagus nerves have effect on atria but too few nerves to ventricles for significant effect

afterload - SV

• sum of all forces (pressure) opposing ejection of blood from ventricle (to open valves)

• largest part of afterload is blood pressure in aorta and pulmonary trunk

  • opposes opening of semilunar valves

  • limits SV

• HTN increases afterload and opposes ventricular ejection

anything that impedes arterial circulation can also ____ afterload

• increase

• lung diseases that restrict pulmonary circulation

• Cor pulmonale: right ventricular failure due to obstructed pulmonary circulation

exercise and CO

• exercise makes the heart work harder and increases CO

• proprioceptors signal cardiac center

  • at beginning of exercise, signals from joints and muscles reach cardiac center of brain

  • sympathetic output from cardiac center increases cardiac output

• increased muscular activity increases venous return

  • increased preload and ultimately CO

increases in HR and SV cause an ___ in CO

• increase

• exercise produces very little ventricular hypertrophy

  • increased SV allows heart to beat more slowly at rest

  • athletes with increased cardiac reserve can tolerate more exertion than sedentary person