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CHAPTER
Elaine N. Marieb
Katja Hoehn
Human
Anatomy
& Physiology
SEVENTH EDITION
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
9
PART B
Muscles and
Muscle Tissue
Depolarization

Initially, this is a local electrical event called end
plate potential

Later, it ignites an action potential that spreads in
all directions across the sarcolemma
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Action Potential: Electrical Conditions of a
Polarized Sarcolemma
 The outside
(extracellular) face is
positive, while the inside
face is negative

This difference in charge
is the resting membrane
potential
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.8a
Action Potential: Electrical Conditions of a
Polarized Sarcolemma

The predominant
extracellular ion is Na+

The predominant
intracellular ion is K+

The sarcolemma is
relatively impermeable
to both ions
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.8a
Action Potential: Depolarization and
Generation of the Action Potential

An axonal terminal of a
motor neuron releases
ACh and causes a patch
of the sarcolemma to
become permeable to
Na+ (sodium channels
open)
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.8b
Action Potential: Depolarization and
Generation of the Action Potential

Na+ enters the cell, and
the resting potential is
decreased
(depolarization occurs)

If the stimulus is strong
enough, an action
potential is initiated
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.8b
Action Potential: Propagation of the Action
Potential

Polarity reversal of the
initial patch of
sarcolemma changes the
permeability of the
adjacent patch

Voltage-regulated Na+
channels now open in
the adjacent patch
causing it to depolarize
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.8c
Action Potential: Propagation of the Action
Potential

Thus, the action
potential travels rapidly
along the sarcolemma

Once initiated, the action
potential is unstoppable,
and ultimately results in
the contraction of a
muscle
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.8c
Action Potential: Repolarization

Immediately after the
depolarization wave
passes, the sarcolemma
permeability changes

Na+ channels close and
K+ channels open

K+ diffuses from the
cell, restoring the
electrical polarity of the
sarcolemma
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.8d
Action Potential: Repolarization

Repolarization occurs
in the same direction as
depolarization, and
must occur before the
muscle can be
stimulated again
(refractory period)

The ionic concentration
of the resting state is
restored by the
Na+-K+ pump
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.8d
Excitation-Contraction Coupling


Once generated, the action potential:

Is propagated along the sarcolemma

Travels down the T tubules

Triggers Ca2+ release from terminal cisternae
Ca2+ binds to troponin and causes:

The blocking action of tropomyosin to cease

Actin active binding sites to be exposed
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Excitation-Contraction Coupling

Myosin cross bridges alternately attach and detach

Thin filaments move toward the center of the
sarcomere

Hydrolysis of ATP powers this cycling process

Ca2+ is removed into the SR, tropomyosin
blockage is restored, and the muscle fiber relaxes
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Action Potential Scan
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.9
Excitation-Contraction (EC) Coupling
1.
Action potential generated and
propagated along sarcomere to
T-tubules
2.
Action potential triggers Ca2+
release
3.
Ca++ bind to troponin;
blocking action of tropomyosin
released
4.
contraction via crossbridge
formation; ATP hyrdolysis
5.
Removal of Ca+2 by active
transport
6.
tropomyosin blockage restored;
contraction ends
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.10
Neurotransmitter released diffuses
across the synaptic cleft and attaches
to ACh receptors on the sarcolemma.
Axon terminal
Synaptic
cleft
Synaptic
vesicle
Sarcolemma
T tubule
1 Net entry of Na+ Initiates
ACh
ACh
an action potential which
is propagated along the
sarcolemma and down
the T tubules.
ACh
Ca2+
Ca2+
SR tubules (cut)
SR
Ca2+
Ca2+
2 Action potential in
T tubule activates
voltage-sensitive receptors,
which in turn trigger Ca2+
release from terminal
cisternae of SR
into cytosol.
ADP
Pi
6
Ca2+
Ca2+
Tropomyosin blockage restored,
blocking myosin binding sites on
actin; contraction ends and
muscle fiber relaxes.
Ca2+
Ca2+
3 Calcium ions bind to troponin;
Ca2+
troponin changes shape, removing
the blocking action of tropomyosin;
actin active sites exposed.
5 Removal of Ca2+ by active transport
into the SR after the action
potential ends.
Ca2+
4 Contraction; myosin heads alternately attach to
actin and detach, pulling the actin filaments toward
the center of the sarcomere; release of energy by
ATP hydrolysis powers the cycling process.
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.10
Axon terminal
Synaptic
cleft
Synaptic
vesicle
ACh
Neurotransmitter released diffuses
across the synaptic cleft and attaches
to ACh receptors on the sarcolemma.
ACh
ACh
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.10
Axon terminal
Neurotransmitter released diffuses
across the synaptic cleft and attaches
to ACh receptors on the sarcolemma.
Synaptic
cleft
Synaptic
vesicle
Sarcolemma
T tubule
1 Net entry of Na+ Initiates
ACh
ACh
ACh
an action potential which
is propagated along the
sarcolemma and down
the T tubules.
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.10
Neurotransmitter released diffuses
across the synaptic cleft and attaches
to ACh receptors on the sarcolemma.
Axon terminal
Synaptic
cleft
Synaptic
vesicle
Sarcolemma
T tubule
1 Net entry of Na+ Initiates
ACh
ACh
an action potential which
is propagated along the
sarcolemma and down
the T tubules.
ACh
Ca2+
Ca2+
SR tubules (cut)
SR
Ca2+
Ca2+
2 Action potential in
T tubule activates
voltage-sensitive receptors,
which in turn trigger Ca2+
release from terminal
cisternae of SR
into cytosol.
Ca2+
Ca2+
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Ca2+
Ca2+
Figure 9.10
Neurotransmitter released diffuses
across the synaptic cleft and attaches
to ACh receptors on the sarcolemma.
Axon terminal
Synaptic
cleft
Synaptic
vesicle
Sarcolemma
T tubule
1 Net entry of Na+ Initiates
ACh
ACh
an action potential which
is propagated along the
sarcolemma and down
the T tubules.
ACh
Ca2+
Ca2+
SR tubules (cut)
SR
Ca2+
Ca2+
2 Action potential in
T tubule activates
voltage-sensitive receptors,
which in turn trigger Ca2+
release from terminal
cisternae of SR
into cytosol.
Ca2+
Ca2+
Ca2+
Ca2+
3 Calcium ions bind to troponin;
Ca2+
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
troponin changes shape, removing
the blocking action of tropomyosin;
actin active sites exposed.
Figure 9.10
Neurotransmitter released diffuses
across the synaptic cleft and attaches
to ACh receptors on the sarcolemma.
Axon terminal
Synaptic
cleft
Synaptic
vesicle
Sarcolemma
T tubule
1 Net entry of Na+ Initiates
ACh
ACh
an action potential which
is propagated along the
sarcolemma and down
the T tubules.
ACh
Ca2+
Ca2+
SR tubules (cut)
SR
Ca2+
Ca2+
2 Action potential in
T tubule activates
voltage-sensitive receptors,
which in turn trigger Ca2+
release from terminal
cisternae of SR
into cytosol.
Ca2+
Ca2+
Ca2+
Ca2+
3 Calcium ions bind to troponin;
Ca2+
troponin changes shape, removing
the blocking action of tropomyosin;
actin active sites exposed.
4 Contraction; myosin heads alternately attach to
actin and detach, pulling the actin filaments toward
the center of the sarcomere; release of energy by
ATP hydrolysis powers the cycling process.
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.10
Neurotransmitter released diffuses
across the synaptic cleft and attaches
to ACh receptors on the sarcolemma.
Axon terminal
Synaptic
cleft
Synaptic
vesicle
Sarcolemma
T tubule
1 Net entry of Na+ Initiates
ACh
ACh
an action potential which
is propagated along the
sarcolemma and down
the T tubules.
ACh
Ca2+
Ca2+
SR tubules (cut)
SR
Ca2+
Ca2+
2 Action potential in
T tubule activates
voltage-sensitive receptors,
which in turn trigger Ca2+
release from terminal
cisternae of SR
into cytosol.
Ca2+
Ca2+
Ca2+
Ca2+
3 Calcium ions bind to troponin;
Ca2+
troponin changes shape, removing
the blocking action of tropomyosin;
actin active sites exposed.
5 Removal of Ca2+ by active transport
into the SR after the action
potential ends.
Ca2+
4 Contraction; myosin heads alternately attach to
actin and detach, pulling the actin filaments toward
the center of the sarcomere; release of energy by
ATP hydrolysis powers the cycling process.
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.10
Neurotransmitter released diffuses
across the synaptic cleft and attaches
to ACh receptors on the sarcolemma.
Axon terminal
Synaptic
cleft
Synaptic
vesicle
Sarcolemma
T tubule
1 Net entry of Na+ Initiates
ACh
ACh
an action potential which
is propagated along the
sarcolemma and down
the T tubules.
ACh
Ca2+
Ca2+
SR tubules (cut)
SR
Ca2+
Ca2+
2 Action potential in
T tubule activates
voltage-sensitive receptors,
which in turn trigger Ca2+
release from terminal
cisternae of SR
into cytosol.
ADP
Pi
6
Ca2+
Ca2+
Tropomyosin blockage restored,
blocking myosin binding sites on
actin; contraction ends and
muscle fiber relaxes.
Ca2+
Ca2+
3 Calcium ions bind to troponin;
Ca2+
troponin changes shape, removing
the blocking action of tropomyosin;
actin active sites exposed.
5 Removal of Ca2+ by active transport
into the SR after the action
potential ends.
Ca2+
4 Contraction; myosin heads alternately attach to
actin and detach, pulling the actin filaments toward
the center of the sarcomere; release of energy by
ATP hydrolysis powers the cycling process.
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.10
Role of Ionic Calcium (Ca2+) in the Contraction
Mechanism
 At low intracellular Ca2+
concentration:

Tropomyosin blocks
the binding sites on
actin

Myosin cross bridges
cannot attach to
binding sites on actin

The relaxed state of the
muscle is enforced
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.11a
Role of Ionic Calcium (Ca2+) in the Contraction
Mechanism

At higher intracellular
Ca2+ concentrations:

Additional calcium
binds to troponin
(inactive troponin
binds two Ca2+)

Calcium-activated
troponin binds an
additional two Ca2+ at
a separate regulatory
site
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.11b
Role of Ionic Calcium (Ca2+) in the Contraction
Mechanism
 Calcium-activated
troponin undergoes a
conformational change

This change moves
tropomyosin away from
actin’s binding sites
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.11c
Role of Ionic Calcium (Ca2+) in the Contraction
Mechanism

Myosin head can now
bind and cycle

This permits contraction
(sliding of the thin
filaments by the myosin
cross bridges) to begin
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.11d
Sequential Events of Contraction




Cross bridge formation – myosin cross bridge
attaches to actin filament
Working (power) stroke – myosin head pivots and
pulls actin filament toward M line
Cross bridge detachment – ATP attaches to myosin
head and the cross bridge detaches
“Cocking” of the myosin head – energy from
hydrolysis of ATP cocks the myosin head into the
high-energy state
PLAY
InterActive Physiology ®: Sliding Filament Theory, pages 3-29
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Myosin head
(high-energy
configuration)
ADP
Pi
1 Myosin head attaches to the actin
myofilament, forming a cross bridge.
Thin filament
ATP
hydrolysis
ADP
ADP
Thick filament
Pi
Pi
2 Inorganic phosphate (Pi) generated in the
previous contraction cycle is released, initiating
the power (working) stroke. The myosin head
pivots and bends as it pulls on the actin filament,
sliding it toward the M line. Then ADP is released.
4 As ATP is split into ADP and Pi, the myosin
head is energized (cocked into the high-energy
conformation).
ATP
ATP
Myosin head
(low-energy
configuration)
3 As new ATP attaches to the myosin head,
the link between myosin and actin weakens,
the cross
bridge detaches.
Copyright © 2006 Pearson Education, Inc., publishing as and
Benjamin
Cummings
Figure 9.12
Myosin head
(high-energy
configuration)
ADP
Pi
1 Myosin head attaches to the actin
myofilament, forming a cross bridge.
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.12
Myosin head
(high-energy
configuration)
ADP
Pi
1 Myosin head attaches to the actin
myofilament, forming a cross bridge.
ADP
Pi
2 Inorganic phosphate (Pi) generated in the
previous contraction cycle is released, initiating
the power (working) stroke. The myosin head
pivots and bends as it pulls on the actin filament,
sliding it toward the M line. Then ADP is released.
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.12
Myosin head
(high-energy
configuration)
ADP
Pi
1 Myosin head attaches to the actin
myofilament, forming a cross bridge.
ADP
Pi
2 Inorganic phosphate (Pi) generated in the
previous contraction cycle is released, initiating
the power (working) stroke. The myosin head
pivots and bends as it pulls on the actin filament,
sliding it toward the M line. Then ADP is released.
ATP
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.12
Myosin head
(high-energy
configuration)
ADP
Pi
1 Myosin head attaches to the actin
myofilament, forming a cross bridge.
ADP
Pi
2 Inorganic phosphate (Pi) generated in the
previous contraction cycle is released, initiating
the power (working) stroke. The myosin head
pivots and bends as it pulls on the actin filament,
sliding it toward the M line. Then ADP is released.
ATP
ATP
Myosin head
(low-energy
configuration)
3 As new ATP attaches to the myosin head,
the link between myosin and actin weakens,
the cross
bridge detaches.
Copyright © 2006 Pearson Education, Inc., publishing as and
Benjamin
Cummings
Figure 9.12
Myosin head
(high-energy
configuration)
ADP
Pi
1 Myosin head attaches to the actin
myofilament, forming a cross bridge.
Thin filament
ATP
hydrolysis
ADP
ADP
Thick filament
Pi
Pi
2 Inorganic phosphate (Pi) generated in the
previous contraction cycle is released, initiating
the power (working) stroke. The myosin head
pivots and bends as it pulls on the actin filament,
sliding it toward the M line. Then ADP is released.
4 As ATP is split into ADP and Pi, the myosin
head is energized (cocked into the high-energy
conformation).
ATP
ATP
Myosin head
(low-energy
configuration)
3 As new ATP attaches to the myosin head,
the link between myosin and actin weakens,
the cross
bridge detaches.
Copyright © 2006 Pearson Education, Inc., publishing as and
Benjamin
Cummings
Figure 9.12
Myosin head
(high-energy
configuration)
ADP
Pi
1 Myosin head attaches to the actin
myofilament, forming a cross bridge.
Thin filament
ATP
hydrolysis
ADP
ADP
Thick filament
Pi
Pi
2 Inorganic phosphate (Pi) generated in the
previous contraction cycle is released, initiating
the power (working) stroke. The myosin head
pivots and bends as it pulls on the actin filament,
sliding it toward the M line. Then ADP is released.
4 As ATP is split into ADP and Pi, the myosin
head is energized (cocked into the high-energy
conformation).
ATP
ATP
Myosin head
(low-energy
configuration)
3 As new ATP attaches to the myosin head,
the link between myosin and actin weakens,
the cross
bridge detaches.
Copyright © 2006 Pearson Education, Inc., publishing as and
Benjamin
Cummings
Figure 9.12
Contraction of Skeletal Muscle Fibers

Contraction – refers to the activation of myosin’s
cross bridges (force-generating sites)

Shortening occurs when the tension generated by
the cross bridge exceeds forces opposing
shortening

Contraction ends when cross bridges become
inactive, the tension generated declines, and
relaxation is induced
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Contraction of Skeletal Muscle (Organ Level)

Contraction of muscle fibers (cells) and muscles
(organs) is similar

The two types of muscle contractions are:


Isometric contraction – increasing muscle tension
(muscle does not shorten during contraction)
Isotonic contraction – decreasing muscle length
(muscle shortens during contraction)
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Motor Unit: The Nerve-Muscle Functional Unit

A motor unit is a motor neuron and all the muscle
fibers it supplies

The number of muscle fibers per motor unit can
vary from four to several hundred

Muscles that control fine movements (fingers,
eyes) have small motor units
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Motor Unit: The Nerve-Muscle Functional Unit
PLAY
InterActive Physiology ®:
Contraction of Motor Units, pages 3-9
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.13a
Motor Unit: The Nerve-Muscle Functional Unit

Large weight-bearing muscles (thighs, hips) have
large motor units

Muscle fibers from a motor unit are spread
throughout the muscle; therefore, contraction of a
single motor unit causes weak contraction of the
entire muscle
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Muscle Twitch

A muscle twitch is the response of a muscle to a
single, brief threshold stimulus

There are three phases to a muscle twitch

Latent period

Period of contraction

Period of relaxation
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Phases of a Muscle Twitch



Latent period – first few
msec after stimulus; EC
coupling taking place
Period of contraction –
cross bridges from;
muscle shortens
Period of relaxation –
Ca2+ reabsorbed; muscle
tension goes to zero
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.14a
Muscle Twitch Comparisons
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.14b
Graded Muscle Responses


Graded muscle responses are:

Variations in the degree of muscle contraction

Required for proper control of skeletal movement
Responses are graded by:

Changing the frequency of stimulation

Changing the strength of the stimulus
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Muscle Response to Varying Stimuli
 A single stimulus results in a single contractile
response – a muscle twitch

Frequently delivered stimuli (muscle does not have
time to completely relax) increases contractile
force – wave summation
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.15
Muscle Response to Varying Stimuli

More rapidly delivered stimuli result in
incomplete tetanus

If stimuli are given quickly enough, complete
tetanus results
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.15
Muscle Response: Stimulation Strength

Threshold stimulus – the stimulus strength at
which the first observable muscle contraction
occurs

Beyond threshold, muscle contracts more
vigorously as stimulus strength is increased

Force of contraction is precisely controlled by
multiple motor unit summation

This phenomenon, called recruitment, brings more
and more muscle fibers into play
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Stimulus Intensity and Muscle Tension
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.16
Size Principle
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.17
Treppe: The Staircase Effect


Staircase – increased contraction in response to
multiple stimuli of the same strength
Contractions increase because:

There is increasing availability of Ca2+ in the
sarcoplasm

Muscle enzyme systems become more efficient
because heat is increased as muscle contracts
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Treppe: The Staircase Effect
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Figure 9.18