Human Physiology, 14th edition (2016)

(Tina Sui) #1
Muscle 373

The membrane of the sarcoplasmic reticulum also con-
tains a type of Ca^2 1 release channel that opens in response to
a rise in the Ca^2 1 concentration in the cytoplasm. These cal-
cium release channels are thus regulated by a Ca 2 1 -induced
Ca 2 1 release mechanism. This mechanism contributes signif-
icantly to excitation-contraction coupling in skeletal muscle,
and in cardiac muscle it is the mechanism most responsible
for excitation-contraction coupling (see fig. 12.34 , step 4).

Muscle Relaxation
As long as action potentials continue to be produced—which
is as long as neural stimulation of the muscle is maintained—
the calcium release channels in the sarcoplasmic reticulum will
remain open, Ca^2 1 will passively diffuse out of the sarcoplasmic
reticulum and the Ca^2 1 concentration of the sarcoplasm will
remain high. Thus, Ca^2 1 will remain attached to troponin and
the cross-bridge cycle will continue to maintain contraction.
To stop the cross-bridge cycle, the production of action
potentials must cease. The calcium release channels will
thereby close, so that Ca^2 1 can no longer passively diffuse
out of the terminal cisternae. Ca^2 1 in the cytoplasm must
then be moved against a concentration gradient back into the
lumen of the sarcoplasmic reticulum. The active transport
pumps for Ca^2 1 are in a family of sarcoplasmic/endoplasmic
reticulum  Ca  2 1 ATPase pumps (or SERCA pumps ) that
accumulate Ca^2 1 so that it is sequestered from the cytoplasm.
This will prevent Ca^2 1 from binding to troponin, so that tropo-
myosin can resume its position that blocks the myosin heads
from binding to actin. Because active transport pumps are
powered by the hydrolysis of ATP, ATP is required for muscle
relaxation as well as for muscle contraction (see fig. 12.34 ).

transverse tubules conduct action potentials, the voltage-gated
calcium channels undergo a conformational (shape) change.
There is a direct molecular coupling between these chan-
nels on the transverse tubules and the calcium release chan-
nels (ryanodine receptors) in the sarcoplasmic reticulum. The
conformational change in the voltage-gated channels in the
transverse tubules directly causes the calcium release chan-
nels in the sarcoplasmic reticulum to open. This releases Ca^2 1
into the cytoplasm, raising the cytoplasmic Ca^2 1 concentra-
tion and stimulating contraction ( fig. 12.16 ). The process by
which action potentials cause contraction is termed excitation-
contraction coupling ( fig. 12.17 ).
This excitation-contraction coupling mechanism in skel-
etal muscle has been described as an electromechanical release
mechanism, because the voltage-gated calcium channels and
the calcium release channels are physically (mechanically)
coupled. As a result, Ca^2 1 enters the cytoplasm from the sarco-
plasmic reticulum where it is stored. However, this electrome-
chanical release mechanism is not the full story of how action
potentials stimulate the contraction of skeletal muscles.


Figure 12.17 Summary of excitation-contraction
coupling. Electrical excitation of the muscle fiber—that is,
action potentials conducted along the sarcolemma and down
the transverse tubules—triggers the release of Ca^2 1 from the
sarcoplasmic reticulum. Because Ca^2 1 binding to troponin leads to
contraction, the Ca^2 1 can be said to couple excitation to contraction.


Sarcolemma Binds to nicotinic ACh receptors, opens ligand
(chemically)-gated channels

ACh released

Somatic motor neuron

Na+ diffuses in, producing depolarizing stimulus

Action potential produced

Transverse
tubules

Action potentials conducted along
transverse tubules

Action potentials open voltage-gated
Ca2+ channels

Sarcoplasmic
reticulum

Ca2+ release channels in SR open

Ca2+ diffuses out into sarcoplasm

Myofibrils Ca2+ binds to troponin, stimulating contraction

| CHECKPOINT

3a. With reference to the sliding filament theory, explain
how the lengths of the A, I, and H bands change
during contraction.
3b. Draw a sarcomere in a relaxed muscle and a
sarcomere in a contracted muscle and label the
bands in each. What is the significance of the
differences in your drawings?
4a. Describe a cycle of cross-bridge activity during
contraction and discuss the role of ATP in this cycle.
4b. Describe the molecular structure of myosin and
actin. How are tropomyosin and troponin positioned
in the thin filaments and how do they function in the
contraction cycle?
5a. Use a flowchart to show the sequence of events
from the time ACh is released from a nerve ending
to the time Ca^2 1 is released from the sarcoplasmic
reticulum.
5b. Explain the requirements for Ca^2 1 and ATP in muscle
contraction and relaxation.
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