Cardiac muscle – Anatomy, Structure, Functions

Cardiac muscle (or myocardium) makes up the thick middle layer of the heart. It is one of three types of muscle in the body, along with skeletal and smooth muscle. The myocardium is surrounded by a thin outer layer called the epicardium (AKA visceral pericardium) and an inner endocardium. Coronary arteries supply to the cardiac muscle, and cardiac veins drain this blood. Cardiomyocytes are the individual cells that make up the cardiac muscle. The primary function of cardiomyocytes is to contract, which generates the pressure needed to pump blood through the circulatory system.

Cardiac muscle (also called heart muscle or myocardium) is one of three types of vertebrate muscle tissue, with the other two being skeletal muscle and smooth muscle. It is an involuntary, striated muscle that constitutes the main tissue of the wall of the heart. The cardiac muscle (myocardium) forms a thick middle layer between the outer layer of the heart wall (the pericardium) and the inner layer (the endocardium), with blood supplied via the coronary circulation. It is composed of individual cardiac muscle cells joined together by intercalated discs, and encased by collagen fibers and other substances that form the extracellular matrix.

The heart is a four-chambered organ responsible for pumping throughout the body. It receives deoxygenated blood from the body, sends it to the lung, receives oxygenated blood from the lungs, and then distributes the oxygenated blood throughout the body. At the histological level, the cellular features of the heart play a vital role in the normal function and adaptations of the heart.


The cardiac cells can only propagate action potentials because of an electrochemical potential gradient across cellular membranes. Ions, mainly sodium (Na+), potassium (K+), and calcium (Ca2+), are present in different concentrations inside the cells vs. their surrounding environments. Sodium and calcium concentrations are more extracellular, while potassium is present at a higher concentration inside the cell. Voltage-sensitive ion channels are available on cellular membranes to facilitate the movement of these ions. The tendency of ions to move down their chemical gradient and the tendency for charges to balance out across membranes contributes to a net electrochemical potential that varies with the status of ion channels. The term used for these variations in status is a phase. Cycles of these phases initiate when the cell membranes reach a threshold potential. This threshold potential is different for cardiomyocytes and pacemaker cells. Cells can reach threshold potential through stimulus by either adjacent cells, or, if they are pacemaker cells, possess automaticity.

The muscles of the heart, termed the myocardium, make up the middle and thickest layer of the heart wall. This layer lies between the single-cell endocardium layer, which lines the inner chambers, and the outer epicardium, which makes up part of the pericardium that surrounds and protects the heart. Histologically, heart muscles are composed of cells called cardiomyocytes that have unique structures and properties correlating to their contractile function. Cardiomyocytes are striated, uninucleated muscle cells found exclusively in the heart muscle. A unique cellular and physiological feature of cardiomyocytes are intercalated discs, which contain cell adhesions such as gap junctions, to facilitate cell-cell communication. These discs reduce internal resistance and allow action potentials to spread quickly throughout the entire heart muscle via the passage of charged ions. Thus, the heart muscle acts as a functional syncytium with rapid synchronized contractions that are responsible for pumping blood throughout the body. Functionally, the heart muscles rely on electrochemical gradients and the potentials to generate contractile force for each heartbeat.

Pacemaker Cells

Characteristically, a pacemaker action potential has only three phases, designated phases zero, three, and four.

  • Phase zero is the phase of depolarization. This phase starts when the membrane potential reaches -40 mV, the threshold potential for pacemaker cells. There is the opening of voltage-gated Ca2+ channels on reaching the threshold, causing the influx of Ca2+ ions. This influx of cation results in an upstroke in membrane potential from -40 mV to +10mV. Because calcium channels are slow channels (compared to sodium channels), the upstroke is not as steep as that of cardiomyocytes.
  • Phases one and two are not present in pacemaker cells. As a result, phase zero is followed by phase three.
  • Phase three is repolarization, involving the closing of Ca2+ channels, blocking the flow of Ca2+ ions. Voltage-gated K+ channels open, allowing for efflux of K+ ions. This efflux of cation contributes to a rapid decrease of membrane potential from +10 mV to -60mV.
  • Phase four, a phase of gradual depolarization, is unique to the pacemaker cells. This gradual depolarization mainly occurs via a depolarization current or pacemaker current (If). Pacemaker current occurs due to the slow influx of Na+ ions through the hyperpolarization-activated cyclic nucleotide-gated channel (HCN channel). This pacemaker current causes the membrane potential to change from -60mV to reach the threshold potential of -40mV. The slope of phase four determines heart rate and is different for pacemaker cells in different regions. SA node pacemaker cells depolarize at a rate of 60 to 100 per minute, while the AV node at 40 to 60 per minute. The pacemaker with the highest rate of depolarization takes over as the primary pacemaker. In healthy individuals, this is the SA node.


The myocardiocyte action potential is different from that of pacemaker cells and has five phases, zero through four. Phase 0 is the phase of depolarization; Phase 1 through 3 is the phase during which repolarization occurs; Phase 4 is the resting phase with no spontaneous depolarization.

  • During phase zero, the phase of rapid depolarization, voltage-gated Na+ channels open, resulting in a rapid influx of Na+ ions. Because of the influx of the cation, the membrane potential changes from -70mV to +50mV. The voltage-gated sodium channels are faster channels than calcium channels, and hence we get a steep upstroke of the action potential.
  • In phase one, there is inactivation of the previously opened voltage-gated Na+ channels along with the activation of transient outward potassium current (Ito). A slight drop in the membrane electrochemical potential results in the initiation of phase two.
  • During phase two or the Plateau phase, Ca2+ influx occurs through an opening of voltage-gated L-type Ca2+ channels. This calcium influx balances the K+ efflux, creating a plateau at around an electrochemical potential of +50mV. This plateau is a component of the Effective refractory period, during which the influx of Ca2+ also stimulates the calcium release from the sarcoplasmic reticulum, initiating muscle contraction. No initiation of new action potentials can occur during this period (Absolute Refractory Period)
  • Repolarization follows in phase three, involving K+ efflux through the opening of rapid delayed rectifier K+ channels and closing of the voltage-gated Ca2+ channels.

Dispersion of Repolarization

  • In the heart, the wave of depolarization current originates in the SA node under normal conditions and reaches the ventricular myocardium via the conduction system. Anatomically the ventricular depolarization travels from apex to base and from endocardium to epicardium. The wave of depolarization moves in the opposite direction from epicardium to endocardium. Thus the action potential duration is not the same across the thickness of the ventricular wall, with cardiomyocytes near the epicardium depolarizing last and repolarizing first. Time taken by M cells for repolarization is the longest, while that of endocardial cells is intermediate between epicardial and M cells. This difference is due to an intrinsic difference in the activity of the various ion channels between the three cell types. Hence there is a transmural dispersion in the process of repolarization. Thus dispersion of repolarization is defined as a difference in repolarization time (activation time plus action potential duration).
  • Transmural dispersion of repolarization is significant clinically because it can lead to arrhythmia by forming re-entry circuits. These re-entry circuits are an essential factor in maintaining Torsades de pointes.

Repolarization Reserve

Roden coined the concept of repolarization reserve to address the difficulty in predicting the development of Torsades de pointes with the use of drugs that prolongs repolarization in different individuals. Repolarization reserve means that under normal physiologic conditions, there is a significant reserve in outward repolarization current. Thus repolarization is not controlled by the action of a single ion channel, and there are considerable overlap and redundancy between the opening and closing of different ion channels. Thus a drug that blocks one channel, for example, IKs, will not cause the failure of depolarization or marked QT prolongation unless there is also a concurrent blocking of another channel; this shows that when one channel fails, other channels take over.

Some of the crucial currents that affect Repolarization reserve are:

  • Persistent inward sodium current (INa) – Normally, after phase 0, the current through the sodium channel decreases and does not contribute significantly to cardiac action potential duration. However, it does not entirely cease, and a small inward current exists during the plateau phase. There is an increase in this inward current in certain conditions like heart failure and Long QT syndrome Type 3 (LQTS 3). Because of this, more potassium should move outside the cell to balance this and cause repolarization, thus decreasing the outward repolarizing current reserve. INa is inherently more prominent in the M cells than the epicardial and endocardial cells
  • Rapid delayed rectifier outward potassium current (IKr) – This channel activates rapidly on depolarization, but its inactivation precedes depolarization mediated activation. Then around the end of phase 2, it opens rapidly when membrane potential becomes more negative and then inactivates slowly. This current is the primary repolarizing current, which contributes to phase 3 of the action potential. A drug that only blocks this channel, when given in higher concentration, can cause QT prolongation by itself (Class 3 anti-arrhythmic). It shows that this is the primary current responsible for maintaining the repolarization reserve. This channel’s activity is affected in many conditions, like in long QT syndrome type 2. Serum potassium levels also affect this current. When serum potassium levels decrease, more of these channels are internalized and hence decrease the strength of the current. Thus hypokalemia causes QT prolongation, while in hyperkalemia, QT interval becomes shortened. Also, due to the specific kinetics of this channel, when any cause prolongs the action potential duration, the activity of IKr decreases, thereby forming a positive loop and hence causing more QT prolongation
  • Slow delayed rectifier outward potassium current (IKs) – This channel activates slowly during phase 2 and deactivates rapidly. Under normal physiologic conditions, I do not significantly contribute to Phase 3 of repolarization. However, during conditions like increased sympathetic stimulation or blocked IKr, the current passing through this channel increases. Thus IKs provide a repolarization reserve or a physiologic check to prevent excess action potential duration lengthening and QT prolongation. This current is defective in Long QT syndrome type 1. This current is more active in the epicardial and endocardial cells and intrinsically weak in the M cells. Thus any physiologic or pathologic conditions that increase or decrease this current will affect the cells in these regions differently and increase the transmural dispersion of repolarization.
  • Inward rectifier potassium current (IK1) – This channel is open during diastole. Its primary function as repolarization reserve is to prevent spontaneous delayed after depolarization during Phase 4 of the action potential.

Other channels like Sodium Potassium ATPase, L-type Ca channel also affect the repolarization reserve. Thus, the degree of QT prolongation when we block a particular potassium channel by either cardiac or non-cardiac drug is dependent on which channel we are blocking and the functioning of the other channels that affect the repolarization reserve.

Microscopic Anatomy

Cardiac muscle appears striated due to the presence of sarcomeres, the highly organized basic functional unit of muscle tissue.

Key Points

Cardiac muscle, composed of the contractile cells of the heart, has a striated appearance due to alternating thick and thin filaments composed of myosin and actin.

Actin and myosin are contractile protein filaments, with actin making up thin filaments, and myosin contributing to thick filaments. Together, they are considered myofibrils.

Myosin and actin adenosine triphosphate ( ATP ) binding allows for muscle contraction. It is regulated by action potentials and calcium concentrations.

Adherens junctions, gap junctions, and desmosomes are intercalated discs that connect cardiac muscle cells. Gap junctions specifically allow for the transmission of action potentials within cells.

Key Terms

  • intercalated discs: Junctions that connect cardiomyocytes together, some of which transmit electrical impulses between cells.
  • sarcomere: The basic unit of contractile muscle which contains myosin and actin, the two proteins that slide past one another to cause a muscle contraction.

Cardiac muscle, like skeletal muscle, appears striated due to the organization of muscle tissue into sarcomeres. While similar to skeletal muscle, cardiac muscle is different in a few ways. Cardiac muscles are composed of tubular cardiomyocytes or cardiac muscle cells. The cardiomyocytes are composed of tubular myofibrils, which are repeating sections of sarcomeres. Intercalated disks transmit electrical action potentials between sarcomeres.


The cellular physiology for the heart is complicated and will be broken down into two sections: the action potential, which is unique in the heart to other action potentials in the body, and electrophysiology.

Action Potential

Please see the image following this article for visual representation

Cardiac Myocyte

The action potential (AP) in the heart is unique to other action potentials in the body. It has five distinct phases numbered 0-4. The resting potential or baseline of the AP is rough – 90 mV and is considered phase 4. For understanding, depolarization is considered the voltage change from the resting potential of – 90 mV toward a positive value. Repolarization will be represented by the return of the voltage of the cell from a positive value down to its resting potential of – 90 mV. The ultimate conclusion of a completed AP is a contraction of the cardiac myocyte.

There are multiple types of potassium channels involved in the cardiac myocyte AP. To begin, phase 4 is at resting potential and consists of the first set of potassium channels open, with positively-charged potassium flowing out of the cell and thus keeping the voltage low at approximately – 90 mV. This set of potassium channels is passively open and consistently outflows potassium during phase 4.

In the next phase, phase 0, sodium channels open at approximately – 70 mV. The initial depolarization from – 90 mV to – 70 mV is caused by positive sodium and calcium ions entering the cell through gap junctions from neighboring cells. These ions depolarize the voltage just enough to open these voltage-gated (VG) sodium channels which further depolarize the cell to approximately + 50 mV. These voltage-gated sodium channels close very quickly upon depolarizing the cell.

Upon reaching peak voltage, voltage-gated potassium channels open and move potassium out of the cell, decreasing voltage once again. This is known as phase 1.

In phase 2, the plateau phase, potassium channels are open out of the cell, and voltage-gated calcium channels begin to open into the cell. This creates a net balance of charge in the cell, creating a plateau.

With phase 3, the voltage-gated calcium channels close, leaving the outward-flowing potassium channels as the only open channels. This causes rapid repolarization, dropping the voltage of the cell to – 90 mV and closing the currently open potassium channel. At the resting potential, the cell has only the original potassium channel slowly leaking potassium out of the cell, and we are returned to phase 4 of the action potential.

In summary, the 5 phases of the cardiac myocyte are as follows:

  • Phase 4: Resting Potential at – 90 mV with minor depolarization from – 90 mV to – 70 mV; the passive outflow of potassium
  • Phase 0: Rapid depolarization from – 70 mV to + 50 mV; inward VG sodium channels
  • Phase 1: Minor repolarization; outward VG potassium channels
  • Phase 2: Plateau at + 50 mV; outward VG potassium channels and inward VG calcium channels
  • Phase 3: Repolarization from + 50 mV to – 90 mV; outward voltage-gated potassium channels

Cardiac Pacemaker Cell

The action potential for cardiac pacemaker cells (SA node, AV node, and Bundle of His/Purkinje Fibers) is unique to the AP of the general cardiac myocyte. These cells undergo automaticity and are responsible for the heart rate. Therefore, each AP corresponds to one beat of the heart and the inherent frequency of these cells is essential for maintaining proper rate control.

Additionally, the electrophysiology and anatomy of these pacemaker cells are discussed in a later section. We will use phases in line with the previous discussion of the cardiac myocyte; to explain, there are 3 basic phases of the pacemaker AP, but they are named phases 0, 3, and 4 correspondings with the phases of the myocyte action potential. The biggest difference to note in this AP is that calcium is the driving factor for rapid depolarization.

To begin, phase 4 involves sodium influx into the cell. This phase initiates at – 60 mV and the main ion influx is sodium. As the cell gains a positive charge due to the influx of positive ions, it reaches – 40 mV which is defined as the threshold for the pacemaker AP. As the voltage hits – 40 mV, voltage-gated calcium channels open into the cell to influx more positive ions. This influx of calcium ions denotes the beginning of phase 0, which is the action potential. The voltage continues to rise until it hits + 10 mV, which will shut off the voltage-gated calcium channels and open up voltage-gated potassium channels, which are efflux from the cell. The opening of the potassium channels begins phase 3 and the downslope of our voltage, and the voltage will drop back to the start of Phase 4 at – 60 mV where the potassium channels will close.

In summary, the 3 phases of the pacemaker action potential are as follows:

  • Phase 4: Minor depolarization from – 60 mV to – 40 mV; passive inflow of sodium
  • Phase 0: Rapid depolarization from – 40 mV to + 10 mV; inflow of VG calcium channels
  • Phase 3: Repolarization from + 10 mV to – 60 mV; outflow of VG potassium channels

Lastly, each pacemaker cell has a different inherent rate at which it can maintain the heart. The SA node is responsible for heart rate under normal conditions; this means that the inherent rate of the SA node is typically around 60 to 100 beats per minute (BPM). The AV node is the second pacemaker which takes over rate if the SA node begins to fail; the AV node keeps the rate at 40 to 60 BPM. There are other foci situated around the SA and AV nodes (e.g., atrial foci and ventricular foci) that can contribute to the rate. In pathology such as atrial fibrillation, these Foci can even create a disease state through rapid firing which increases heart rate, but this discussion is out of scope for this article.


The electrical circuit of the heart follows a distinct pathway from the right atrium down throughout the ventricles of the heart. The electrical circuit begins at the Sinoatrial node, or SA node, which is located in the right atrium. This node is a unique bundle of cells that undergoes automaticity; these cells have their inherent rate of depolarization that is independent of other cells in the heart. As the SA node depolarizes, an electrical signal is simultaneously transmitted across from the right atrium to the left atrium via a bundle of cells termed “Bachman’s Bundle.” Following the SA node conduction, the current travels down to the Atrioventricular node, or AV node. The AV node is located further inferior in the Right Atrium by the interatrial septum. An important distinction to make about the AV node is that it creates a small pause in the electrical circuit. This pause is important because it delays the ventricles from contracting, and thus establishes successive contraction of the ventricles following the atria. If this pause did not occur, the atria and ventricles would contract simultaneously, and blood would not flow appropriately through the heart. The current leaves the AV node down a bundle of cells named the “Bundle of His” located inferior to the AV node in the interventricular septum. The Bundle of His then transmits the conduction down two bundle branches that arc throughout the two ventricles; specifically, these are named the right and left bundle branches. The right and left bundle branches have many fascicles that divide off and supply much of the ventricles. The main continuation of the right and left bundle branch is the Purkinje Fiber system, which is a set of many small branches arcing throughout the remaining ventricular space and supplying it with the electrical output.

In summary, the order of flow through the electrical system is as follows:

  • SA node and Bachman’s Bundle
  • AV node
  • Bundle of His
  • Right and left bundle branches
  • Purkinje Fibers

Sarcomere Structure

A sarcomere is the basic unit of muscle tissue in both cardiac and skeletal muscle. Sarcomeres appear under the microscope as striations, with alternating dark and light bands. Sarcomeres are connected to a plasma membrane, called a sarcolemma, by T-tubules, which speed up the rate of depolarization within the sarcomere.

Individual sarcomeres are composed of long, fibrous proteins that slide past each other when the muscles contract and relax. The two most important proteins within sarcomeres are myosin, which forms a thick, flexible filament, and actin, which forms the thin, more rigid filament. Myosin has a long, fibrous tail and a globular head which binds to actin. The myosin head also binds to ATP, the source of energy for muscle movement. Actin molecules are bound to the Z-disc, which forms the borders of the sarcomere. Together, myosin and actin form myofibrils, the repeating molecular structure of sarcomeres.

Myofibril activity is required for muscle contraction on the molecular level. When ATP binds to myosin, it separates from the actin of the myofibril, which causes a contraction. Muscle contraction is a complex process regulated by calcium influx and the stimulus of electrical impulses.

This diagram illustrates the molecular mechanism of muscular contraction. With application of a stimulus, the myosin head binds to actin, resulting in ATP hydrolysis. The myosin head turns as P is released and is further distorted with the release of ATP. When ATP is present, it binds to myosin, which releases from the actin filament returning the myosin head to starting position. CA2 regulation either causes contractions to end or a new cycle to begin. When myosin heads remain bound to actin filaments, rigor mortis ensues.

Muscle Contraction and Actin-Myosin Interactions: Skeletal muscle contracts following activation by an action potential. The binding of Acetylcholine at the motor endplate leads to intracellular calcium release and interactions between myofibrils, eliciting contraction.


The Sarcomere: A single sarcomere unit with all functional areas labeled, including thick and thin filaments, Z lines, H zone, I bands, and A band.

Intercalated Discs

Intercalated discs are gap junctions that link cardiomyocytes so that electrical impulses (action potentials) can travel between cells. In a more general sense, an intercalated disk is any junction that links cells together between a gap in which no other cells exist, such as an extracellular matrix. In cardiac muscle tissue, they are also responsible for the transmission of action potentials and calcium during muscle contraction. In cardiac muscle, intercalated discs connecting cardiomyocytes to the syncytium, a multinucleated muscle cell, to support the rapid spread of action potentials and the synchronized contraction of the myocardium. Intercalated discs consist of three types of cell-cell junctions, most of which are found in other tissues besides cardiac muscle:

  • Adherens junctions, which anchor actin filaments to the cytoplasm of cardiomyocytes.
  • Desmosomes, which bind adhesion proteins to the cytoskeleton within cells, thus connecting the cells.
  • Gap junctions, which connect proteins to the cytoplasm of different cells and transmit action potentials between both cells, required for cellular depolarization. It is found primarily in nervous and muscular tissue.

Under light microscopy, intercalated discs appear as thin lines dividing adjacent cardiac muscle cells and running perpendicular to the direction of muscle fibers.

Mechanism and Contraction Events of Cardiac Muscle Fibers

Cardiac muscle fibers undergo coordinated contraction via calcium-induced calcium release conducted through the intercalated discs.

Key Points

Cardiac muscle fibers contract via excitation-contraction coupling, using a mechanism unique to a cardiac muscle called calcium-induced calcium release.

Excitation-contraction coupling describes the process of converting an electrical stimulus ( action potential ) into a mechanical response (muscle contraction).

Calcium-induced calcium release involves the conduction of calcium ions into the cardiomyocyte, triggering the further release of ions into the cytoplasm.

Calcium prolongs the duration of muscle cell depolarization before repolarization occurs. Contraction in cardiac muscle occurs due to the binding of the myosin head to adenosine triphosphate ( ATP ), which then pulls the actin filaments to the center of the sarcomere, the mechanical force of contraction.

Key Terms

  • excitation-contraction coupling (ECC): The physiological process of converting an electrical stimulus to a mechanical response.
  • calcium-induced calcium release (CICR): A process whereby calcium can trigger release of further calcium from the muscle sarcoplasmic reticulum.

Cardiomyocytes are capable of coordinated contraction, controlled through the gap junctions of intercalated discs. The gap junctions spread action potentials to support the synchronized contraction of the myocardium. In cardiac, skeletal, and some smooth muscle tissue, contraction occurs through a phenomenon known as excitation-contraction coupling (ECC). ECC describes the process of converting an electrical stimulus from the neurons into a mechanical response that facilitates muscle movement. Action potentials are the electrical stimulus that elicits the mechanical response in ECC.

Calcium-Induced Calcium Release

In cardiac muscle, ECC is dependent on a phenomenon called calcium-induced calcium release (CICR), which involves the influx of calcium ions into the cell, triggering the further release of ions into the cytoplasm. The mechanism for CIRC is receptors within the cardiomyocyte that bind to calcium ions when calcium ion channels open during depolarization, releasing more calcium ions into the cell.

Similarly to skeletal muscle, the influx of sodium ions causes an initial depolarization; however, in cardiac muscle, the influx of calcium ions sustains the depolarization so that it lasts longer. CICR creates a “plateau phase” in which the cell’s charge stays slightly positive (depolarized) briefly before it becomes more negative as it repolarizes due to potassium ion influx. Skeletal muscle, by contrast, repolarizes immediately.

Pathway of Cardiac Muscle Contraction

The actual mechanical contraction response in cardiac muscle occurs via the sliding filament model of contraction. In the sliding filament model, myosin filaments slide along actin filaments to shorten or lengthen the muscle fiber for contraction and relaxation. The pathway of contraction can be described in five steps:

  • An action potential, induced by the pacemaker cells in the sinoatrial (SA) and atrioventricular (AV) nodes, is conducted to contractile cardiomyocytes through gap junctions.
  • As the action potential travels between sarcomeres, it activates the calcium channels in the T-tubules, resulting in an influx of calcium ions into the cardiomyocyte.
  • Calcium in the cytoplasm then binds to cardiac troponin-C, which moves the troponin complex away from the actin-binding site. This removal of the troponin complex frees the actin to be bound by myosin and initiates contraction.
  • The myosin head binds to ATP and pulls the actin filaments toward the center of the sarcomere, contracting the muscle.
  • Intracellular calcium is then removed by the sarcoplasmic reticulum, dropping intracellular calcium concentration, returning the troponin complex to its inhibiting position on the active site of actin, and effectively ending contraction as the actin filaments return to their initial position, relaxing the muscle.

This diagram of the sliding filament model of contraction indicates the I-bands, H zone, cap Z, titin, Z disc, myosin head, myosin tail, actin filament, M line.

Sliding Filament Model of Contraction: Muscle fibers in relaxed (above) and contracted (below) positions


Animation of Myosin and Actin: This animation shows myosin filaments (red) sliding along the actin filaments (pink) to contract a muscle cell.

Energy Requirements

Cardiac cells contain numerous mitochondria, which enable continuous aerobic respiration and the production of adenosine triphosphate (ATP) for cardiac function.

Key Points

The myocardium requires significant energy to contract continually over the human lifetime.

These energy needs are met through mitochondria, myoglobins, and rich blood supply from the coronary arteries.

The mitochondria generate ATP for the contraction of cardiomyocytes.

Myoglobins are oxygen-storing and oxygen-transferring pigments in cardiomyocytes.

Aerobic metabolism occurs when oxygen is present, while anaerobic respiration occurs when tissue is deprived of oxygen. Aerobic metabolism accounts for nearly all of the metabolic functions in the heart, but anaerobic metabolism may contribute as well.

Glucose reservoirs and lactate recycling allow the heart to function even during malnutrition.

Key Terms

  • lactate: A molecule produced by anaerobic respiration that can be used to produce ATP without oxygen, albeit at lower levels.
  • myoglobin: A small globular protein containing a heme group that carries oxygen to muscles from the blood and stores reserve oxygen.

The heart muscle pumps continuously throughout life and is adapted to be highly resistant to fatigue. Cardiomyocytes contain large numbers of mitochondria, the powerhouse of the cell, enabling continuous aerobic respiration and ATP production required for mechanical muscle contraction. Cardiac muscle tissue has among the highest energy requirements in the human body (along with the brain) and has a high level of mitochondria and a constant, rich, blood supply to support its metabolic activity.

Aerobic Metabolism

Aerobic metabolism is a necessary component to support the metabolic function of the heart. Oxygen is necessary, and if even a small part of the heart is oxygen-deprived for too long, a myocardial infarction (heart attack) will occur. Coronary circulation branches from the aorta soon after it leaves the heart, and supplies the heart with the nutrients and oxygen needed to sustain aerobic metabolism. Cardiac muscle cells contain larger amounts of mitochondria than other cells in the body, enabling higher ATP production.

The heart derives energy from aerobic metabolism via many different types of nutrients. Sixty percent of the energy to power the heart is derived from fat (free fatty acids and triglycerides), 35% from carbohydrates, and 5% from amino acids and ketone bodies from proteins. These proportions vary widely with available dietary nutrients. Malnutrition will not result in the death of heart tissue in the way that oxygen deficiency will, because the body has glucose reserves that sustain the vital organs of the body and the ability to recycle and use lactate aerobically.


Myoglobin: The heme component of myoglobin, shown in orange, binds oxygen. Myoglobin provides a backup store of oxygen to muscle cells.

Heart muscle also contains large amounts of pigment called myoglobin. Myoglobin is similar to hemoglobin in that it contains a heme group (an oxygen-binding site). Myoglobin transfers oxygen from the blood to the muscle cell and stores reserve oxygen for aerobic metabolic function in the muscle cell.

Anaerobic Metabolism

While aerobic respiration supports normal heart activity, anaerobic respiration may provide additional energy during brief periods of oxygen deprivation. Lactate, created from lactic acid fermentation, accounts for the anaerobic component of cardiac metabolism. At normal metabolic rates, about 1% of energy is derived from lactate, and about 10% under moderately hypoxic (low oxygen) conditions. Under more severe hypoxic conditions, not enough energy can be liberated by lactate production to sustain ventricular contraction, and heart failure will occur.

Lactate can be recycled by the heart and provides additional support during nutrient deprivation. Recycling lactate is very energy-efficient in the nutrient-deprived myocardium since one NAD+ is reduced to NADH and H+ (equal to 2.5 or 3 ATP) when lactate is oxidized to pyruvate. The produced pyruvate can then be burned aerobically in the citric acid cycle (also known as the tricarboxylic acid cycle or Krebs cycle), liberating a significant amount of energy.

Blood Supply and Lymphatics

The process of contraction and relaxation requires a constant supply of oxygen and nutrients to meet the energy demands of cardiac muscle. Blood supply is delivered to the myocardium by coronary arteries, which are the first branches of the aortic root. Blood is drained away by the cardiac veins through the coronary sinus into the right atrium. There are left and right coronary arteries. The right coronary artery (RCA) arises from the right aortic sinus and supplies the right ventricle and the bundle of His. In 85% of the people (right dominance), it gives a branch known as the posterior descending artery (PDA), which supplies the AV node, posteromedial papillary muscle, and posterior portion of the interventricular septum and the ventricles. The left main coronary artery arises from the left aortic sinus. It branches off to give the left circumflex coronary artery (LCX) and the left anterior descending artery (LAD). The LCX supplies the lateral and posterior walls of the left ventricle, SA node, AV node, and anterolateral part of the papillary muscle. The LAD supplies the anterior part of the interventricular septum and the anterior surface of the left ventricle.

Lymph drains via a myocardial plexus located within the myocardium. Along with a subendocardial plexus with lymphatics from the ventricles, the myocardial plexus drains into a subepicardial plexus, which gives rise to a right and left coronary trunk. Lymph from the right side of the heart in the right coronary trunk travels to the brachiocephalic lymph nodes and then the thoracic duct. Lymph from the left side of the heart in the left coronary trunk travels to the inferior tracheobronchial lymph nodes and subsequently to the right lymphatic duct.


The autonomic nervous system (ANS) is a significant regulator of contractility, heart rate, stroke volume, and cardiac output. Parasympathetic innervation is provided from the right and left vagus nerves (CN X). Sympathetic innervation comes from fibers of the sympathetic trunk arising from the upper segments of the thoracic spinal cord. Afferent nerves also provide the central nervous system with feedback on blood pressure, blood chemistry, and to relay pain sensation from the heart.

Organ Systems Involved

Smooth muscle is present in all of the organ systems below:

  • Gastrointestinal tract
  • Cardiovascular – blood vessel and lymphatic vessels
  • Renal – urinary bladder
  • Genital – uterus, both male and female reproductive tracts
  • Respiratory tract
  • Integument – erector pili of the skin
  • Sensory – the ciliary muscle and iris of the eye


The primary function of smooth muscle is contraction. Smooth muscle consists of two types: single-unit and multi-unit. Single-unit smooth muscle consists of multiple cells connected through connexins that can become stimulated in a synchronous pattern from only one synaptic input. Connexins allow for cell-to-cell communication between groups of single-unit smooth muscle cells. This intercellular communication allows ions and molecules to diffuse between cells giving rise to calcium waves. This unique property of single-unit smooth muscle allows for synchronous contraction to occur. Multi-unit smooth muscle differs from single-unit in that each smooth-muscle cell receives its own synaptic input, allowing for the multi-unit smooth muscle to have much finer control.

The function of smooth muscle can expand on a much larger scale to the organ systems it helps regulate. The functions of smooth muscle in each organ system is an incredibly broad topic and beyond the overall scope of this article. For simplicity, the basic functions of smooth muscle in the organ systems appear listed below.

  • Gastrointestinal tract – propulsion of the food bolus
  • Cardiovascular – regulation of blood flow and pressure via vascular resistance
  • Renal – regulation of urine flow
  • Genital – contractions during pregnancy, propulsion of sperm
  • Respiratory tract – regulation of bronchiole diameter
  • Integument – raises hair with erector pili muscle
  • Sensory – dilation and constriction of the pupil as well as changing lens shape


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