Cardiac muscle (heart muscle) is one of the three major types of
muscle, the others being skeletal and smooth muscle. It is an
involuntary, striated muscle that is found in the walls of the heart.
This muscle tissue is known as myocardium, and forms a thick middle
layer between the outer layer of the heart wall (the epicardium) and
the inner layer (the endocardium).
Myocardium is composed of
individual heart muscle cells (cardiomyocytes) joined together by
intercalated disks, encased by collagen fibres and other substances
forming the extracellular matrix.
Cardiac muscle contracts in a similar manner to skeletal muscle,
although with some important differences. An electrical stimulation in
the form of an action potential triggers the release of calcium from
the cell's internal calcium store, the sarcoplasmic reticulum. The
rise in calcium causes the cell's myofilaments to slide past each
other in a process called excitation contraction coupling.
Diseases of heart muscle are of major importance. These include
conditions caused by a restricted blood supply to the muscle including
angina pectoris and myocardial infarction, and other heart muscle
disease known as cardiomyopathies.
1.1 Gross anatomy
Cardiac muscle cells
220.127.116.11 Intercalated discs
1.2.3 Extracellular matrix
2.2 Differences between atria and ventricles
3 Clinical significance
4 See also
6 External links
Heart § Structure
3D rendering showing thick myocardium within heart wall.
Cardiac muscle tissue or myocardium forms the bulk of the heart. The
heart wall is a three layered structure with a thick layer of
myocardium sandwiched between the inner endocardium and the outer
epicardium (also known as the visceral pericardium). The inner
endocardium lines the cardiac chambers, covers the cardiac valves, and
joins with the endothelium that lines the blood vessels that connect
to the heart. On the outer aspect of the myocardium is the epicardium
which forms part of the pericardium, the sack that surrounds,
protects, and lubricates the heart. Within the myocardium there are
several sheets of cardiac muscle cells or cardiomyocytes. The sheets
of muscle that wrap around the left ventricle closest to the
endocardium are oriented perpendicularly to those closest to the
epicardium. When these sheets contract in a coordinated manner they
allow the ventricle to squeeze in several direction simultaneously –
longitudinally (becoming shorter from apex to base), radially
(becoming narrower from side to side), and with a twisting motion
(similar to wringing out a damp cloth) to squeeze out the maximum
amount of blood with each heartbeat.
When looked at microscopically, cardiac muscle can be likened to the
wall of a house. Most of the wall is taken up by bricks, which in
cardiac muscle are individual cardiac muscle cells or cardiomyocytes.
The mortar which surrounds the bricks is known as the extracellular
matrix, produced by supporting cells known as fibroblasts. In the same
way that the walls of a house contain electrical wires and plumbing,
cardiac muscle also contains specialised cells for conducting
electrical signals rapidly (the cardiac conduction system), and blood
vessels to bring nutrients to the muscle cells and take away waste
products (the coronary arteries, veins and capillary network).
Cardiac muscle cells
Cardiac muscle cells
Cardiac muscle cells
Cardiac muscle cells or cardiomyocytes are the contracting cells which
allow the heart to pump. Each cardiomyocyte needs to contract in
coordination with its neighbouring cells to efficiently pump blood
from the heart, and if this coordination breaks down then – despite
individual cells contracting – the heart may not pump at all, such
as may occur during abnormal heart rhythms such as ventricular
Viewed through a microscope, cardiac muscle cells are roughly
rectangular, measuring 100–150μm by 30–40μm. Individual
cardiac muscle cells are joined together at their ends by intercalated
disks to form long fibres. Each cell contains myofibrils, specialised
protein fibres that slide past each other. These are organised into
sarcomeres, the fundamental contractile units of muscle cells. The
regular organisation of myofibrils into sarcomeres gives cardiac
muscle cells a striped or striated appearance when looked at through a
microscope, similar to skeletal muscle. These striations are caused by
I bands composed mainly of a protein called actin, and darker
A bands composed mainly of myosin.
Cardiomyocytes contain T-tubules, pouches of membrane that run from
the surface to the cell's interior which help to which improve the
efficiency of contraction. The majority of these cells contain only
one nucleus (although they may have as many as four), unlike skeletal
muscle cells which typically contain many nuclei.
Cardiac muscle cells
contain many mitochondria which provide the energy needed for the cell
in the form of adenosine triphosphate (ATP), making them highly
resistant to fatigue.
Main article: T-tubules
T-tubules are microscopic tubes that run from the cell surface to deep
within the cell. They are continuous with the cell membrane, are
composed of the same phospholipid bilayer, and are open at the cell
surface to the extracellular fluid that surrounds the cell. T-tubules
in cardiac muscle are bigger and wider than those in skeletal muscle,
but fewer in number. In the centre of the cell they join together,
running into and along the cell as a transverse-axial network. Inside
the cell they lie close to the cell's internal calcium store, the
sarcoplasmic reticulum. Here, a single tubule pairs with part of the
sarcoplasmic reticulum called a terminal cisterna in a combination
known as a diad.
The functions of
T-tubules include rapidly transmitting electrical
impulses known as action potentials from the cell surface to the
cell's core, and helping to regulate the concentration of calcium
within the cell in a process known as excitation-contraction
Main article: Intercalated disc
Intercalated discs are part of the cardiac muscle sarcolemma and they
contain gap junctions and desmosomes.
The cardiac syncytium is a network of cardiomyocytes connected to each
other by intercalated discs that enable the rapid transmission of
electrical impulses through the network, enabling the syncytium to act
in a coordinated contraction of the myocardium. There is an atrial
syncytium and a ventricular syncytium that are connected by cardiac
connection fibres. Electrical resistance through intercalated discs
is very low, thus allowing free diffusion of ions. The ease of ion
movement along cardiac muscle fibers axes is such that action
potentials are able to travel from one cardiac muscle cell to the
next, facing only slight resistance. Each syncytium obeys the all or
Intercalated discs are complex adhering structures that connect the
single cardiomyocytes to an electrochemical syncytium (in contrast to
the skeletal muscle, which becomes a multicellular syncytium during
mammalian embryonic development). The discs are responsible mainly for
force transmission during muscle contraction. Intercalated discs
consist of three different types of cell-cell junctions: the actin
filament anchoring adherens junctions, the intermediate filament
anchoring desmosomes, and gap junctions. They allow action potentials
to spread between cardiac cells by permitting the passage of ions
between cells, producing depolarization of the heart muscle. However,
novel molecular biological and comprehensive studies unequivocally
showed that intercalated discs consist for the most part of mixed-type
adhering junctions named area composita (pl. areae compositae)
representing an amalgamation of typical desmosomal and fascia
adhaerens proteins (in contrast to various epithelia). The
authors discuss the high importance of these findings for the
understanding of inherited cardiomyopathies (such as arrhythmogenic
right ventricular cardiomyopathy).
Under light microscopy, intercalated discs appear as thin, typically
dark-staining lines dividing adjacent cardiac muscle cells. The
intercalated discs run perpendicular to the direction of muscle
fibers. Under electron microscopy, an intercalated disc's path appears
more complex. At low magnification, this may appear as a convoluted
electron dense structure overlying the location of the obscured
Z-line. At high magnification, the intercalated disc's path appears
even more convoluted, with both longitudinal and transverse areas
appearing in longitudinal section.
Main article: Fibroblasts
Cardiac fibroblasts are vital supporting cells within cardiac muscle.
They are unable to provide forceful contractions like cardiomyocytes,
but instead are largely responsible for creating and maintaining the
extracellular matrix which forms the mortar in which cardiomyocyte
bricks are embedded.
Fibroblasts play a crucial role in responding
to injury, such as a myocardial infarction. Following injury,
fibroblasts can become activated and turn into myofibroblasts –
cells which exhibit behaviour somewhere between a fibroblast
(generating extracellular matrix) and a smooth muscle cell (ability to
contract). In this capacity, fibroblasts can repair an injury by
creating collagen while gently contracting to pull the edges of the
injured area together.
Fibroblasts are smaller but more numerous than cardiomyocytes, and
several fibroblasts can be attached to a cardiomyocyte at once. When
attached to a cardiomyocyte they can influence the electrical currents
passing across the muscle cell's surface membrane, and in the context
are referred to as being electrically coupled. Other potential
roles for fibroblasts include electrical insulation of the cardiac
conduction system, and the ability to transform into other cell types
including cardiomyocytes and adipocytes.
Main article: Extracellular matrix
Continuing the analogy of heart muscle as being like a wall, the
extracellular matrix is the mortar which surrounds the cardiomyocyte
and fibroblasts bricks. The matrix is composed of proteins such as
collagen and elastin along with polysaccharides(sugar chains) known as
glycosaminoglycans. Together, these substances give support and
strength to the muscle cells, create elasticity in cardiac muscle, and
keep the muscle cells hydrated by binding water molecules.
The matrix in immediate contact with the muscle cells is referred to
as the basement membrane, mainly composed of type IV collagen and
laminin. Cardiomyocytes are linked to the basement membrane via
specialised glycoproteins called integrins.
An isolated cardiac muscle cell, beating
Main article: Excitation-contraction coupling
The physiology of cardiac muscle shares many similarities with that of
skeletal muscle. The primary function of both muscle types is to
contract, and in both cases a contraction begins with a characteristic
flow of ions across the cell membrane known as an action potential.
The action potential subsequently triggers muscle contraction by
increasing the concentration of calcium within the cytosol.
However, the mechanism by which calcium concentrations within the
cytosol rise differ between skeletal and cardiac muscle. In cardiac
muscle, the action potential comprises an inward flow of both sodium
and calcium ions. The flow of sodium ions is rapid but very
short-lived, while the flow of calcium is sustained and gives the
plateau phase characteristic of cardiac muscle action potentials. The
comparatively small flow of calcium through the L-type calcium
channels triggers a much larger release of calcium from the
sarcoplasmic reticulum in a phenomenon known as calcium-induced
calcium release. In contrast, in skeletal muscle, minimal calcium
flows into the cell during action potential and instead the
sarcoplasmic reticulum in these cells is directly coupled to the
surface membrane. This difference can be illustrated by the
observation that cardiac muscle fibres require calcium to be present
in the solution surrounding the cell in order to contract, while
skeletal muscle fibres will contract without extracellular calcium.
During contraction of a cardiac muscle cell, the long protein
myofilaments oriented along the length of the slide over each other in
what is known as the sliding filament hypothesis. There are two kinds
of myofilaments, thick filaments composed of the protein myosin, and
thin filaments composed of the proteins actin, troponin and
tropomyosin. As the thick and thin filaments slide past each other the
cell becomes shorter and fatter. In a mechanism known as crossbridge
cycling, calcium ions bind to the protein troponin, which along with
tropomyosin then uncover key binding sites on actin. Myosin, in the
thick filament, can then bind to actin, pulling the thick filaments
along the thin filaments. When the concentration of calcium within the
cell falls, troponin and tropomyosin once again cover the binding
sites on actin, causing the cell to relax.
Dog cardiac muscle (400X)
Until recently, it was commonly believed that cardiac muscle cells
could not be regenerated. However, a study reported in the April 3,
2009 issue of Science contradicts that belief. Olaf Bergmann and
his colleagues at the
Karolinska Institute in
Stockholm tested samples
of heart muscle from people born before 1955 who had very little
cardiac muscle around their heart, many showing with disabilities from
this abnormality. By using DNA samples from many hearts, the
researchers estimated that a 4-year-old renews about 20% of heart
muscle cells per year, and about 69 percent of the heart muscle cells
of a 50-year-old were generated after he or she was born.
One way that cardiomyocyte regeneration occurs is through the division
of pre-existing cardiomyocytes during the normal aging process.
The division process of pre-existing cardiomyocytes has also been
shown to increase in areas adjacent to sites of myocardial injury. In
addition, certain growth factors promote the self-renewal of
endogenous cardiomyocytes and cardiac stem cells. For example,
insulin-like growth factor 1, hepatocyte growth factor, and
high-mobility group protein B1 increase cardiac stem cell migration to
the affected area, as well as the proliferation and survival of these
cells. Some members of the fibroblast growth factor family also
induce cell-cycle re-entry of small cardiomyocytes. Vascular
endothelial growth factor also plays an important role in the
recruitment of native cardiac cells to an infarct site in addition to
its angiogenic effect.
Based on the natural role of stem cells in cardiomyocyte regeneration,
researchers and clinicians are increasingly interested in using these
cells to induce regeneration of damaged tissue. Various stem cell
lineages have been shown to be able to differentiate into
cardiomyocytes, including bone marrow stem cells. For example, in one
study, researchers transplanted bone marrow cells, which included a
population of stem cells, adjacent to an infarct site in a mouse
model. Nine days after surgery, the researchers found a new band of
regenerating myocardium. However, this regeneration was not
observed when the injected population of cells was devoid of stem
cells, which strongly suggests that it was the stem cell population
that contributed to the myocardium regeneration. Other clinical trials
have shown that autologous bone marrow cell transplants delivered via
the infarct-related artery decreases the infarct area compared to
patients not given the cell therapy.
Differences between atria and ventricles
Cardiac muscle forms both the atria and the ventricles of the heart.
Although this muscle tissue is very similar between cardiac chambers,
some differences exist. The myocardium found in the ventricles is
thick to allow forceful contractions, while the myocardium in the
atria is much thinner. The individual myocytes that make up the
myocardium also differ between cardiac chambers. Ventricular
cardiomyocytes are longer and wider, with a denser
Although the fundamental mechanisms of calcium handling are similar
between ventricular and atrial cardiomyocytes, the calcium transient
is smaller and decays more rapidly in atrial myocytes, with a
corresponding increase in calcium buffering capacity. The
complement of ion channels differs between chambers, leading to longer
action potential durations and effective refractory periods in the
ventricles. Certain ion currents such as IK(UR) are highly specific to
atrial cardiomyocytes, making them a potential target for treatments
for atrial fibrillation.
Diseases affecting cardiac muscle are of immense clinical
significance, and are the leading cause of death in developed
nations. The most common condition affecting cardiac muscle is
ischaemic heart disease, in which the blood supply to the heart is
reduced. In ischaemic heart disease, the coronary arteries become
narrowed by atherosclerosis. If these narrowings gradually become
severe enough to partially restrict blood flow, the syndrome of angina
pectoris may occur. This typically causes chest pain during
exertion that is relieved by rest. If a coronary artery suddenly
becomes very narrowed or completed blocked, interrupting or severely
reducing blood flow through the vessel, a myocardial infarction or
heart attack occurs. If the blockage is not relieved promptly by
medication, percutaneous coronary intervention, or surgery, then a
region of heart muscle may become permanently scarred and damaged.
Heart muscle can also become damaged despite a normal blood supply.
The heart muscle may become inflamed in a condition called
myocarditis, most commonly caused by a viral infection but
sometimes caused by the body's own immune system.
Heart muscle can
also be damaged by drugs such as alcohol, long standing high blood
pressure or hypertension, or persistent abnormal heart racing.
Specific diseases of heart muscle called cardiomyopathies can cause
heart muscle to become abnormally thick (hypertrophic
cardiomyopathy), abnormally large (dilated cardiomyopathy), or
abnormally stiff (restrictive cardiomyopathy). Some of these
conditions are caused by genetic mutations and can be inherited.
Many of these conditions, if severe enough, can damage the heart so
much that the pumping function of the heart is reduced. If the heart
is no longer able to pump enough blood to meet the body's needs, this
is described as heart failure.
Wikimedia Commons has media related to Cardiac muscle.
This article uses anatomical terminology; for an overview, see
Frank–Starling law of the heart
Regional function of the heart
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Cardiac muscle histology
Anatomical terms of muscle
List of muscles of the human body
Vascular smooth muscle
Laminin, alpha 2
(a, i, and h bands;
z and m lines)
Connective tissue in skeletal muscle
Sliding filament mechanism
Anatomy of the heart
(venae cavae, coronary sinus) → right atrium (atrial appendage,
fossa ovalis, limbus of fossa ovalis, crista terminalis, valve of
inferior vena cava, valve of coronary sinus) → tricuspid valve →
right ventricle (infundibulum, moderator band/septomarginal trabecula)
→ pulmonary valve → (pulmonary artery and pulmonary circulation)
(pulmonary veins) → left atrium (atrial appendage) → mitral valve
→ left ventricle → aortic valve (aortic sinus) → (aorta and
bundle of His
fold of left vena cava