Chapter 9
Muscles and Muscle Tissue
289
9
When intracellular calcium levels are low, the muscle cell is
relaxed, and tropomyosin molecules physically block the active
(myosin-binding) sites on actin. As Ca
2
1
levels rise, the ions
bind to regulatory sites on troponin. To activate its group of
seven actins, a troponin must bind two calcium ions, change
shape, and then roll tropomyosin into the groove of the actin
helix, away from the myosin-binding sites. In short, the tro-
pomyosin “blockade” is removed when sufficient calcium is
present. Once binding sites on actin are exposed, the events of
the cross bridge cycle occur in rapid succession, as depicted in
Focus on the Cross Bridge Cycle
(Figure 9.12)
on p. 292.
±e thin filaments continue to slide as long as the calcium
signal and adequate ATP are present. When nerve impulses
arrive rapidly, intracellular Ca
2
1
levels soar due to successive
“puffs” or rounds of Ca
2
1
released from the SR. In such cases,
the muscle cells do not completely relax between successive
stimuli and contraction is stronger and more sustained (within
limits) until nervous stimulation ceases.
As the Ca
2
1
pumps of the SR reclaim calcium ions from the
cytosol and troponin again changes shape, tropomyosin again
blocks actin’s myosin-binding sites. ±e contraction ends, and
the muscle fiber relaxes.
When the cycle is ready to start again, the myosin head is in
its upright high-energy configuration (see step
4
in Focus Fig-
ure 9.12), ready to take another “step” and attach to an actin site
farther along the thin filament. ±is “walking” of the myosin
heads along the adjacent thin filaments during muscle short-
ening is much like a centipede’s gait. ±e thin filaments can-
not slide backward as the cycle repeats again and again because
some myosin heads (“legs”) are always in contact with actin (the
“ground”). Contracting muscles routinely shorten by 30–35% of
their total resting length, so each myosin cross bridge attaches
and detaches many times during a single contraction. It is likely
that only half of the myosin heads of a thick filament are pulling
at the same instant. ±e others are randomly seeking their next
binding site.
fiber, restoring negatively charged conditions inside (also
see
Figure 9.10
).
During repolarization, a muscle fiber is said to be in a
refrac-
tory period
, because the cell cannot be stimulated again un-
til repolarization is complete. Note that repolarization restores
only the
electrical conditions
of the resting (polarized) state. ±e
ATP-dependent Na
1
-K
1
pump restores the
ionic conditions
of
the resting state, but hundreds of action potentials can occur
before ionic imbalances interfere with contractile activity.
Once initiated, the action potential is unstoppable. It ulti-
mately results in contraction of the muscle fiber. Although the
action potential itself lasts only a few milliseconds (ms), the
contraction phase of a muscle fiber may persist for 100 ms or
more and far outlasts the electrical event that triggers it.
Excitation-Contraction Coupling
Excitation-contraction (E-C) coupling
is the sequence of events
by which transmission of an action potential along the sarco-
lemma causes myofilaments to slide. ±e action potential is brief
and ends well before any signs of contraction are obvious.
As you will see, the electrical signal does not act directly on
the myofilaments. Instead, it causes the rise in intracellular lev-
els of calcium ions, which allows the filaments to slide.
Focus on Excitation-Contraction Coupling
(Figure 9.11)
on
pp. 290–291 illustrates the steps in this process. ±is Focus fea-
ture also reveals how the integral proteins of the T tubules and
terminal cisterns in the triads interact to provide the Ca
2
1
nec-
essary for contraction to occur. Make sure you understand this
material before continuing.
Summary: Channels Involved in Initiating Muscle
Contraction
So let’s summarize what has to happen to excite a muscle cell,
starting from the nerve ending. Essentially this process activates
four sets of ion channels:
1. ±e process begins when the nerve impulse reaches the
axon terminal and opens voltage-gated calcium channels
in the axonal membrane. Calcium entry triggers release of
ACh into the synaptic cle².
2. Released ACh binds to ACh receptors in the sarcolemma,
opening chemically gated Na
1
-K
1
channels. Greater in-
flux of Na
1
causes a local voltage change (the end plate
potential).
3. Local depolarization opens voltage-gated sodium chan-
nels in the neighboring region of the sarcolemma. ±is
allows more sodium to enter, which further depolarizes
the sarcolemma, generating and propagating an AP.
4. Transmission of the AP along the T tubules changes the
shape of voltage-sensitive proteins in the T tubules, which
in turn stimulate SR calcium release channels to release
Ca
2
1
into the cytosol.
Muscle Fiber Contraction: Cross Bridge Cycling
As we have noted, cross bridge formation (attachment of my-
osin heads to actin) requires Ca
2
1
. Let’s look more closely at
how calcium ions promote muscle cell contraction.
0
+30
–95
0
5
10
15
20
Time (ms)
Membrane potential (mV)
Na
+
channels
close, K
+
channels
open
K
+
channels
closed
Repolarization
due to K
+
exit
Na
+
channels
open
Depolarization
due to Na
+
entry
Figure 9.10
Action potential tracing indicates changes in Na
1
and K
1
ion channels.
(Text continues on p. 293.)
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