So now that we've talked about the
noncontractile pacemaker cells of the heart,
let's take a look at the contractile muscle
fibers that make up the bulk of the heart
and are actually responsible for the pumping action itself.
These are going to be slightly different than
the skeletal muscle fibers and it's going to be
a slightly different type of contraction because
the cardiac muscle action potentials have a plateau.
So let's look a little more closely at the action potential
In the cardiac muscle fibers, depolarization
opens fast voltage-gated sodium channels
allowing for sodium to enter the cell.
Then by positive feedback, this influx of sodium
is going to cause a rise in the action potential
so that goes from -90 mV all the way up to +30 mV.
This is what's known as a rapid depolarization.
Next, depolarization by sodium is also
going to open the slow calcium channels.
At +30 mV, the sodium channels are gonna close but
the slow calcium channels are going to remain open
thus prolonging the depolarization.
This appears as a sort of plateau
or flattening out of the depolarization.
After about 200 milliseconds, these slow
calcium channels are now going to close themselves
and subsequently, the voltage-gated
potassium channels are going to open.
This causes a rapid efflux of potassium out of the cell, thus
repolarizing the cell to its resting membrane potential.
Calcium is pumped both back into the sarcoplasmic
reticulum and out of the cell into the extracellular space.
So how is this different from what
happens in our skeletal muscles?
Well first, the action potential in our skeletal
muscles only lasts about 1 to 2 milliseconds
while the action potential in our
cardiac muscle cells last 200 milliseconds.
Also, contraction in our skeletal muscle cells
is going to last about 15 to 100 milliseconds
whereas in a cardiac contraction,
it also lasts about 200 milliseconds.
so the action potential is about
as long as the contraction itself.
Because of this longer action potential and
contraction, we get a sustained contraction
that ensures an efficient ejection
of the blood from the ventricles.
Also, because of the longer refractory
period, we do not have the potential for tetanus
or tetanic contraction in our cardiac muscle cells.