Download Ch 6 Contraction of a Single Muscle Fiber

Pages 187-191

Stimulus generated capabilities:
◦ Irritability (also called responsiveness)—ability to
receive and respond to a stimulus
◦ Contractility—ability to shorten when an
adequate stimulus is received

Movement capabilities:
◦ Extensibility—ability of muscle cells to be
stretched
◦ Elasticity—ability to recoil and resume resting
length after stretching
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
Skeletal muscles must be stimulated by a
motor neuron (nerve cell) to contract
Motor unit: consists of one motor neuron and
all the skeletal muscle cells stimulated by that
neuron
◦ (page 232 provides more elaboration about the
neurological make up of the motor unit)
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Figure 6.4a Motor units.
Axon terminals at
neuromuscular junctions
Spinal cord
Motor Motor
unit
unit
1
2
Nerve
Axon of
Motor neuron motor
cell bodies
neuron
Muscle
(a)
Muscle
fibers
Figure 6.4b Motor units.
Axon terminals at
neuromuscular junctions
Branching
axon to
motor unit (b)
Muscle
fibers

Neuromuscular junction
◦ Where the axon terminal (end) of the motor neuron
“meets up with” the sarcolemma (plasma
membrane) of a muscle
 These two components NEVER touch
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
Synaptic cleft
◦ Gap/space between axon terminal and muscle
◦ This gap is filled with interstitial (tissue) fluid

Neurotransmitter
◦ A chemical messenger released by the nerve when
the nerve impulse reaches the end of the axon
terminal
◦ Acetylcholine (ACh) is the neurotransmitter that
stimulates skeletal muscle
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Slide 2
Myelinated axon of motor neuron
Nerve impulse
Nucleus
1 Action potential reaches
axon terminal of motor neuron.
Axon terminal of
neuromuscular
junction
Sarcolemma of
the muscle fiber
Synaptic vesicle containing ACh
Axon terminal of motor neuron
Mitochondrion
Ca2+
ACh
receptor
Ca2+
Synaptic
cleft
ACh
Sarcolemma
Fusing synaptic
vesicle
Sarcoplasm
of muscle fiber
Folds of
sarcolemma
1.
Calcium channels open
◦ calcium ions enter the axon terminal
2.
The presence of Calcium causes the release
of acetylcholine (ACh) by way of vesicles
◦ ACh diffuses across the synaptic cleft (the gap) and
attaches to receptors on the sarcolemma
(membrane) of the muscle cell
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Slide 3
1 Action potential reaches
axon terminal of motor neuron.
Synaptic vesicle containing ACh
Axon terminal of motor neuron
Mitochondrion
2 Calcium (Ca2+) channels open, and
Ca2+ enters the axon terminal.
Ca2+
ACh
receptor
Ca2+
Synaptic
cleft
ACh
Sarcolemma
Fusing synaptic
vesicle
Sarcoplasm
of muscle fiber
Folds of
sarcolemma
Slide 4
1 Action potential reaches
axon terminal of motor neuron.
Synaptic vesicle containing ACh
Axon terminal of motor neuron
Mitochondrion
2 Calcium (Ca2+) channels open, and
Ca2+ enters the axon terminal.
3 Ca2+ entry causes some synaptic
vesicles to release their contents
(acetylcholine, a neurotransmitter)
by exocytosis.
Ca2+
ACh
receptor
Ca2+
Synaptic
cleft
ACh
Sarcolemma
Fusing synaptic
vesicle
Sarcoplasm
of muscle fiber
Folds of
sarcolemma
4.
If enough ACh is released, the sarcolemma
becomes temporarily more permeable to
sodium (Na) and potassium (K ) ions
◦ Sodium rushes into the cell
◦ Potassium leaves the cell
◦ This causes an imbalance of charge: the
sarcolemma becomes depolarized
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Slide 5
1 Action potential reaches
axon terminal of motor neuron.
Synaptic vesicle containing ACh
Axon terminal of motor neuron
Mitochondrion
2 Calcium (Ca2+) channels open, and
Ca2+ enters the axon terminal.
3 Ca2+ entry causes some synaptic
vesicles to release their contents
(acetylcholine, a neurotransmitter)
by exocytosis.
4 Acetylcholine diffuses across the
synaptic cleft and binds to
receptors in the sarcolemma.
Ca2+
ACh
receptor
Ca2+
Synaptic
cleft
ACh
Sarcolemma
Fusing synaptic
vesicle
Sarcoplasm
of muscle fiber
Folds of
sarcolemma
Slide 6
5 ACh binds and channels open that
allow simultaneous passage of Na+ into
the muscle fiber and K+ out of the
muscle fiber. More Na+ ions enter than
K+ ions leave, producing a local change
in the electrical conditions of the
membrane (depolarization). This
eventually leads to an action potential.
Na+ K+
Ion channel in
sarcolemma opens;
ions pass.
5.
Depolarization opens more sodium channels
that allow sodium ions to enter the cell
 Once started, the action potential cannot be stopped
 The action potential travels throughout the surface of
the sarcolemma via t-tubules of the sarcolemma,
causing the muscle to contract
6.
The enzyme Acetylcholinesterase (AChE)
breaks down acetylcholine into acetic acid
and choline to end muscle contraction
Slide 7
ACh
6 The enzyme acetylcholinesterase
breaks down ACh in the synaptic cleft,
ending the process.
Degraded ACh
Na+
AcetylcholineK+
sterase
Ion channel closed;
ions cannot pass.

Cell returns to its resting state when:
1. Potassium ions diffuse back out of the cell

Sodium-potassium pump moves sodium and

potassium ions back to their original positions
The muscle is ready to receive another stimulus
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
Calcium binds to regulatory proteins called
troponin and tropomyosin
◦ troponin stimulates tropomyosin to uncover the
actin binding sites
◦ This exposes myosin-binding sites
◦ myosin heads on the thick filaments attach
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
The attached heads pivot, sliding the thin
filaments toward the center of the sarcomere,
and contraction occurs (muscle shortens)
ATP provides the energy
◦ This continues as long as ionic calcium is present
Figure 6.7 Diagrammatic views of a sarcomere.
Myosin
Z
Actin
Z
H
A
I
I
(a) Relaxed sarcomere
Z
I
A
Z
I
(b) Fully contracted sarcomere
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