Cardiac muscle.

Cardiac
muscle (heart muscle) is
an involuntary,
striated muscle that is
found in the walls and
histological foundation of
the heart, specifically the
myocardium. Cardiac
muscle is one of three
major types of muscle, the
others being skeletal and
smoothmuscle. rdiac
muscle Your heart beats about
once a second for the whole of
your life, and of course has no
opportunity to rest. Its output
must adjust rapidly to meet the
needs of the body, and can
increase from about 5 litres of
blood/min at rest to more than
25 litres/min in heavy exercise.
The special requirements of the
heart call for a special type of
muscle, cardiac muscle, which
is not found anywhere else in
the body. Cardiac muscle is in
some ways similar
to skeletal and smooth muscle.
For example, all three contract
when a rise in calcium inside
the muscle cell allows
interaction
between actin and myosin fila
ments. However, cardiac
muscle has a unique structure,
and differs in the way that
contraction is initiated and
regulated.
Structure
Under the microscope, cardiac
muscle is seen to consist of
interlacing bundles of cardiac
myocytes (muscle cells). Like
skeletal muscle it is striated
with narrow dark and light
bands, due to the parallel
arrangement of actin and
myosin filaments that extend
from end to end of each
myocyte. However, cardiac
myocytes are narrower and
much shorter than skeletal
muscle cells, being about 0.02
mm wide and 0.1 mm long,
and are more rectangular than
smooth muscle cells, which are
normally spindle-shaped. They
are often branched, and contain
one nucleus but
many mitochondria, which
provide the energy required for
contraction. A prominent and
unique feature of cardiac
muscle is the presence of
irregularly-spaced dark bands
between myocytes. These are
known as intercalated discs,
and are due to areas where the
membranes of adjacent
myocytes come very close
together. The intercalated discs
have two important functions:
one is to ‘glue’ the myocytes
together so that they do not
pull apart when the heart
contracts; the other is to allow
an electrical connection
between the cells, which, as we
will see, is vital to the function
of the heart as a whole. The
electrical connection is made
via special junctions (gap
junctions) between adjoining
myocytes, containing pores
through which small ions and
therefore electrical current can
pass. As the myocytes are
electrically connected, cardiac
muscle is often referred to as
a functional
syncytium (continuous cellular
material).
diac myocytes contract when
the voltage across the
membrane, the resting
membrane potential, is reduced
sufficiently to initiate an action
potential. In most parts of the
heart this is caused by an
action potential in an adjacent
myocyte being transmitted
through the gap junctions. The
action potential starts with a
very rapid reduction in voltage
toward zero, which is due to
sodium ions entering the
myocyte. This phase of the
action potential is also seen in
skeletal muscle and nerves. In
cardiac muscle, however, the
membrane potential then
remains close to zero for about
0.3 sec — the plateau phase,
which is largely due to entry of
calcium ions. It is this entry of
calcium that leads to
contraction. At the end of the
plateau phase the membrane
potential returns to resting
levels. The plateau means that
cardiac muscle action
potentials last much longer
than those in skeletal muscle or
nerves, where calcium does not
enter the cell and there is
therefore no plateau phase.
When an action potential is
initiated in one myocyte, it
causes an electrical current to
pass through gap junctions in
the intercalated discs to its
neighbours. This current
initiates action potentials in
these cells, which in turn
stimulate their neighbours. As
a result, a wave of activation,
and therefore contraction,
passes through the heart. This
process allows synchronization
of contraction throughout the
heart, and is vital for proper
function. When it is disrupted,
as in some types of heart
disease, the myocytes may lose
synchronization. In severe
cases, such as ventricular
fibrillation, the heart cannot
pump at all, and is said to look
like a ‘bag of (writhing)
worms’.

The amount of calcium

entering the myocyte during an
action potential is not enough
to cause contraction. However,
its entry causes more calcium
to be released from stores in
the sarcoplasmic reticulum, a
membranous structure within
the myocyte. This is known
as calcium-induced calcium
release. The amount of
calcium released depends on
the amount that enters during
the action potential, so that
contractile force can therefore
be regulated by controlling
calcium entry. This is
increased by adrenaline and
the autonomic nervous system.
At the end of the beat, calcium
is rapidly taken back into the
sarcoplasmic reticulum,
causing relaxation. Excess
calcium — the amount that
entered during the action
potential — is expelled from
the myocyte during the interval
between beats by pumps in the
membrane. If the heart rate
increases there is less time to
remove this calcium. As a
result there is more calcium in
the myocyte for the next beat,
and so the force developed
increases. This staircase
effect allows the heart to expel
blood more rapidly when the
heart rate is increased. Drugs
that inhibit removal of calcium
from the myocyte can similarly
increase cardiac muscle force.
An example is digitalis, which
was originally derived from the
foxglove and has been used for
treating heart disease for
centuries. Some areas of the
heart contain myocytes that
have specialized functions.
One is the sino-atrial
node or pacemaker region in
the right atrium, where
modified myocytes generate
action potentials automatically,
and are responsible for
initiating the heartbeat.
Although nervous activity is
not required for the heart to
beat, the autonomic nervous
system can modulate the
activity of the pacemaker, and
hence heart rate. The atria and
ventricles are separated by a
non-conducting band except at
the atrio-ventricular node.
This node consists of small
myocytes that do conduct, but
delay the impulse from the
pacemaker, thus allowing the
atria to contract before the
ventricles. From here the
impulse is distributed rapidly
around the ventricles via
bundles of specialized large
myocytes called Purkinje
fibres. Defects in any part of
this conduction system can
lead to a disordered heartbeat.