Muscle
291
restored to its original extremely low resting value by primary
active Ca
2+
-ATPase pumps and Na
+
/Ca
2+
countertransporters
in the sarcoplasmic reticulum and sarcolemma. The amount
of calcium returned to the extracellular fl uid and into the sar-
coplasmic reticulum exactly matches the amounts that entered
the cytosol during excitation. During a single twitch contrac-
tion of cardiac muscle in a person at rest, the amount of cal-
cium entering the cytosol is only suffi cient to expose about
30 percent of the cross-bridge attachment sites on the thin
fi lament. As Chapter 12 will describe, however, hormones and
neurotransmitters of the autonomic nervous system modulate
the amount of calcium released during excitation-contraction
coupling, enabling the strength of cardiac muscle contractions
to be varied. Cardiac muscle contractions are thus graded in a
manner similar to that of smooth muscle contractions.
The “L” in L-type calcium channels stands for “long-
lasting current,” and this property of cardiac calcium
channels underlies an important feature of this muscle
type—cardiac muscle cannot undergo tetanic contractions.
Unlike skeletal muscle, in which the membrane action
potential is extremely brief (1–2 ms) and force generation
lasts much longer (20–100 ms), in cardiac muscle the action
potential and twitch are both prolonged due to the long-
lasting calcium current (
Figure 9–41
). Because the plasma
membrane remains refractory to additional stimuli as long as
it is depolarized (review Figure 6–22), it isn’t possible to ini-
tiate multiple cardiac action potentials during the time frame
of a single twitch. This is critical for the heart’s function
as an oscillating pump, because it must alternate between
being relaxed and fi lling with blood, and contracting to eject
blood.
A fi nal question to consider is, “What initiates action
potentials in cardiac muscle?” Certain specialized cardiac
muscle cells exhibit pacemaker potentials that generate action
potentials spontaneously, similar to the mechanism for smooth
muscle described in Figure 9–36a. Because cardiac cells are
linked via gap junctions, when an action potential is initi-
ated by a pacemaker cell it propagates rapidly throughout the
entire heart. A single heartbeat corresponds to the initiation
and conduction of a single action potential. In addition to the
modulation of calcium release and the strength of contraction,
Chapter 12 will also discuss how hormones and autonomic
neurotransmitters modify the frequency of cardiac pacemaker
cell depolarization, and thus vary the heart rate.
Table 9–6
summarizes and compares the properties of
the different types of muscle.
“Excitation”
(depolarization of
plasma membrane)
Contraction
Cytosolic Ca
2+
concentration
Flow of Ca
2+
into cytosol
Flow of Ca
2+
into cytosol
steps
Multiple
Ca
2+
binds to Ca
2+
receptors
(ryanodine receptors)
on the external surface of the
sarcoplasmic reticulum
Opening of Ca
2+
channels intrinsic
to these receptors
Opening of plasma membrane
L-type Ca
2+
channels in T-tubules
Figure 9–40
Excitation-contraction coupling in cardiac muscle.
Figure 9–41
Timing of action potentials and twitch tension in skeletal and
cardiac muscles. Muscle tension not drawn to scale.
0
–90
Membrane potential (mV)
0
100
200
300
Time (ms)
Time (ms)
Refractory
period
Cardiac muscle
Muscle tension
Cardiac muscle cell action potential
0
100
200
300
Skeletal muscle
Skeletal muscle fiber action potential
0
–90
Membrane potential (mV)
Muscle tension
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