Appendix A
9-7 d
Fast-oxidative-glycolytic fi
bers are an intermediate
type that are designed to contract rapidly but
to resist fatigue. They utilize both aerobic and
anaerobic energy systems, and thus they are red
fi bers with high myoglobin (which facilitates
production of ATP by oxidative phosphorylation),
but they also have a moderate ability to generate
ATP through glycolytic pathways. (Refer to
Table 9–3.)
9-8 c
In smooth muscle cells, dense bodies serve the
same functional role as Z lines do in striated muscle
cells—they serve as the anchoring point for the
fi laments.
9-9 b
When myosin light-chain kinase transfers a
phosphate group from ATP to the myosin light
chains of the cross-bridges, binding and cycling of
cross-bridges is activated.
9-10 d
Stretching a sheet of single-unit smooth muscle
cells opens mechanically gated ion channels, which
causes a depolarization that propagates through
gap junctions, followed by calcium entry and
contraction. This does not occur in multiunit
smooth muscle.
9-11 e
The amount of calcium released during a typical
resting heart beat exposes less than half of the thin
fi lament cross-bridge binding sites. Autonomic
neurotransmitters and hormones can increase or
decrease the amount of calcium released to the
cytosol during EC coupling.
Quantitative and Thought Questions
Under resting conditions, the myosin has already
bound and hydrolyzed a molecule of ATP, resulting
in an energized molecule of myosin (M · ADP · P
Because ATP is necessary to detach the myosin
cross-bridge from actin at the end of cross-bridge
movement, the absence of ATP will result in rigor
mortis, in which case the cross-bridges become
bound to actin but do not detach, leaving myosin
bound to actin (A · M).
No. The transverse tubules conduct the muscle action
potential from the plasma membrane into the interior
of the fi ber, where it can trigger the release of calcium
from the sarcoplasmic reticulum. If the transverse
tubules were not attached to the plasma membrane,
an action potential could not be conducted to the
sarcoplasmic reticulum, and there would be no
release of calcium to initiate contraction.
The length-tension relationship states that the
maximum tension developed by a muscle decreases at
lengths below L
. During normal shortening, as the
sarcomere length becomes shorter than the optimal
length, the maximum tension that can be generated
decreases. With a light load, the muscle will continue
to shorten until its maximal tension just equals the
load. No further shortening is possible because at
shorter sarcomere lengths the tension would be less
than the load. The heavier the load, the less the
distance shortened before reaching the isometric
Maximum tension is produced when the fi ber is
(1) stimulated by an action potential frequency that
is high enough to produce a maximal tetanic tension,
and (2) at its optimum length L
, where the thick
and thin fi laments have overlap suffi cient to provide
the greatest number of cross-bridges for tension
Moderate tension—for example, 50 percent of
maximal tension—is accomplished by recruiting
suffi cient numbers of motor units to produce this
degree of tension. If activity is maintained at this level
for prolonged periods, some of the active fi
bers will
begin to fatigue and their contribution to the total
tension will decrease. The same level of total tension
can be maintained, however, by recruiting new motor
units as some of the original ones fatigue. At this
point, for example, one might have 50 percent of
the fi bers active, 25 percent fatigued, and 25 percent
still unrecruited. Eventually, when all the fi bers have
fatigued and there are no additional motor units to
recruit, the whole muscle will fatigue.
The oxidative motor units, both fast and slow, will be
affected fi rst by a decrease in blood fl ow because they
depend on blood fl ow to provide both the fuel—
glucose and fatty acids—and the oxygen required
to metabolize the fuel. The fast-glycolytic motor
units will be affected more slowly because they rely
predominantly on internal stores of glycogen, which is
anaerobically metabolized by glycolysis.
Two factors lead to the recovery of muscle force.
(1) Some new fi bers can be formed by the fusion and
development of undifferentiated satellite cells. This
will replace some, but not all, of the fi bers that were
damaged. (2) Some of the restored force results from
hypertrophy of the surviving fi bers. Because of the
loss of fi bers in the accident, the remaining fi bers
must produce more force to move a given load. The
remaining fi bers undergo increased synthesis of actin
and myosin, resulting in increases in fi ber diameter
and thus their force of contraction.
In the absence of extracellular calcium ions, skeletal
muscle contracts normally in response to an action
potential generated in its plasma membrane because
the calcium required to trigger contraction comes
entirely from the sarcoplasmic reticulum within the
muscle fi bers. If the motor neuron to the muscle
is stimulated in a calcium-free medium, however,
the muscle will not contract because the infl
ux of
calcium from the extracellular fl uid into the motor
nerve terminal is necessary to trigger the release of
acetylcholine that in turn triggers an action potential
in the muscle.
In a calcium-free solution, smooth muscles would
not respond either to stimulation of the nerve or to
the plasma membrane. Stimulating the nerve would
have no effect because calcium entry into presynaptic
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