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POWERPOINT® LECTURE SLIDE PRESENTATION
by LYNN CIALDELLA, MA, MBA, The University of Texas at Austin
Additional Material by J. Padilla exclusively for Physiology 31 at ECC
UNIT 2
12
PART A
Muscles
HUMAN PHYSIOLOGY
AN INTEGRATED APPROACH
DEE UNGLAUB SILVERTHORN
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FOURTH EDITION
The Three Types of Muscle
Cylindrical shaped,
multinuclei, straited,
voluntary, fibers of
different speeds
Branched, uni/binuclei, involuntary,
striated, rhythmic
contractions
Spindled shaped, one
nucleus, involuntary,
non-straited, internal
organs
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Figure 12-1a
Muscles: Summary
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Skeletal Muscle
 Usually attached to bones by tendons- sometimes
attached directly to bone (pectoralis major)
 Origin: closest to the trunk- usually does not move a
joint when contracts.
 Insertion: more distal- moves joint when contracts
 Flexor: brings bones together- decreases angle at
joint
 Extensor: bones move away- increases angle at joint
 Antagonistic muscle groups: flexor-extensor pairsantagonistic muscles are usually in opposite sides.
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Anatomy Summary: Skeletal Muscle
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Figure 12-3a (1 of 2)
Anatomy Review: Muscle Fiber Structure
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Ultrastructure of Muscle
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Figure 12-3b
Anatomy Summary: Skeletal Muscle
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Figure 12-3a (2 of 2)
Ultrastructure of Muscle
Myosin are motor proteins. 250 myosins join to form the thick
filaments. The thin filament is made up of a string of actin with
tropomyosin and tropnin attached. Titin and nebulin anchor and
stabilize.
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Figure 12-3e
Ultrastructure of Muscle
Actin and myosin form crossbridges
Sarcomere
A band
(c)
Z disk
Z disk
Myofibril
M line
I band
H zone
(d)
Titin
Z disk
M line
Z disk
M line
Thin filaments
Thick filaments
(f)
(e)
Myosin tail
Myosin
heads
Hinge
region
Tropomyosin
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Myosin molecule
Titin
Troponin Nebulin
G-actin molecule
Actin chain
Figure 12-3c–f
Summary of Muscle Contraction
Muscle tension:
force created by
muscle
Load: weight that
opposes
contraction
Contraction:
creation of
tension in muscle
Relaxation:
release of tension
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Figure 12-7
Neuromuscular Junction: Overview
 Terminal boutons- insulate the site of the
neuromuscular juction and secrete supportive growth
factors
 Synaptic cleft- space between the axon terminal and
the sarcolemma
 Acetylcholine- neurotransmitter released involves
calcium and binds to nicotinic receptors
 Motor end plate- folds on the sarcolemma of the
muscle
 On muscle cell surface
 Nicotinic receptors
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Anatomy of the Neuromuscular Junction
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Figure 11-12 (1 of 3)
Anatomy of the Neuromuscular Junction
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Figure 11-12 (2 of 3)
Anatomy of the Neuromuscular Junction
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Figure 11-12 (3 of 3)
Mechanism of Signal Conduction
 Axon terminal (of presynaptic cell)
 Action potential signals acetylcholine release
 Motor end plate – series of folds in the plasma
membrane of the postsynaptic cell
 Two acetylcholine bind
 Opens cation channel
 Na+ influx – K+ efflux
 Membrane depolarized
 Stimulates fiber contraction as a result in increased
intracellular calcium concentration
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Events at the Neuromuscular Junction
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Figure 11-13a
T-tubules and the Sarcoplasmic Reticulum
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Figure 12-4
Excitation-Contraction Coupling
1
Somatic motor neuron
releases ACh at neuromuscular junction.
(a)
1
Axon terminal of
somatic motor neuron
ACh
Muscle fiber
Motor end plate
Sarcoplasmic reticulum
T-tubule
Ca2+
DHP
receptor
Tropomyosin
Z disk
Troponin
Actin
M line
Myosin
head
Myosin thick filament
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Figure 12-11a, step 1
Excitation-Contraction Coupling
1
Somatic motor neuron
releases ACh at neuromuscular junction.
2
(a)
Net entry of Na+ through ACh
receptor-channel initiates
a muscle action potential.
1
Axon terminal of
somatic motor neuron
ACh
Muscle fiber
potential
K+
2
Action potential
Na+
Motor end plate
Sarcoplasmic reticulum
T-tubule
Ca2+
DHP
receptor
Tropomyosin
Z disk
Troponin
Actin
M line
Myosin
head
Myosin thick filament
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Figure 12-11a, steps 1–2
Excitation-Contraction Coupling
3
Action potential in
t-tubule alters
conformation of
DHP receptor.
4
DHP receptor opens Ca2+
release channels in
sarcoplasmic reticulum
and Ca2+ enters cytoplasm.
5
Ca2+ binds to troponin,
allowing strong actinmyosin binding.
(b)
4
3
Ca2+
Ca2+
released
5
7
6
Myosin thick filament
M line
6
Myosin heads execute
power stroke.
Distance actin moves
7
Actin filament slides
toward center of
sarcomere.
PLAY Animation: Muscular System: The Neuromuscular Junction
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Figure 12-11b
Changes in Sarcomere Length
during Contraction
PLAY Animation: Muscular System: Sliding Filament Theory
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Figure 12-8
Regulatory Role of Tropomyosin and Troponin
In the
relaxed state
the myosin
head is at
90o but it is
unbound to
actin
because the
binding sites
on actin are
blocked.
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Figure 12-10a
Regulatory Role of Tropomyosin and
Troponin**
(b) Initiation of contraction
1
Ca2+ levels increase
in cytosol.
2
Ca2+ binds to
troponin.
3
Troponin-Ca2+
complex pulls
tropomyosin
away from G-actin
binding site.
4 Power stroke
3
Tropomyosin shifts,
exposing binding
site on G-actin
Pi
ADP
TN
4
Myosin binds
to actin and
completes power
stroke.
5
2
5
Actin filament
moves.
G-actin moves
1
Cytosolic Ca2+
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Figure 12-10b
The Molecular Basis of Contraction
Tight binding in the rigor
1 state. The crossbridge is
at a 45° angle relative to
the filaments.
2
45 °
ATP
binding
site
Myosin
binding
sites
1
2
3
ATP binds to its binding site
on the myosin. Myosin then
dissociates from actin.
Myosin
filament
4
ATP
1
2
3
4
G-actin molecule
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Figure 12-9, steps 1–2
The Molecular Basis of Contraction
The ATPase activity of myosin
3 hydrolyzes the ATP. ADP and
Pi remain bound to myosin.
The myosin head swings over
4 and binds weakly to a new
actin molecule. The crossbridge is now at 90º relative to
the filaments.
ADP
90°
Pi
Pi
1
2
3
4
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1
2
3
4
Figure 12-9, steps 3–4
The Molecular Basis of Contraction
Release of Pi initiates the power
5 stroke. The myosin head rotates
on its hinge, pushing the actin
filament past it.
At the end of the power stroke,
6 the myosin head releases ADP
and resumes the tightly bound
rigor state.
ADP
Pi
1
2
3
4
5
1
2
3
4
5
Actin filament
moves toward M line.
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Figure 12-9, steps 5–6
The Molecular Basis of Contraction
Myosin filament
1
Tight binding in the rigor
state. The crossbridge is
at a 45° angle relative to
the filaments.
Myosin
binding
sites
1
45°
ATP
binding
site
2 3 4
2
ATP binds to its binding site
on the myosin. Myosin then
dissociates from actin.
G-actin molecule
ADP
2
1
6
3
4
ATP
1
5
At the end of the power stroke,
the myosin head releases ADP
and resumes the tightly bound
rigor state.
3
2
3
4
Actin filament
moves toward M line.
Release of Pi initiates the power
5
stroke. The myosin head rotates
on its hinge, pushing the actin
filament past it.
90°
1
4
ADP
Pi
Sliding
filament
5
3
The ATPase activity of myosin
hydrolyzes the ATP. ADP and
Pi remain bound to myosin.
Contractionrelaxation
Pi
1
2
1
2
3
4
Pi
2
3
4
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4
The myosin head swings over and
binds weakly to a new actin molecule.
The crossbridge is now at 90º relative
to the filaments.
Figure 12-9
Muscle Fatigue: Multiple Causes
 Extended submaximal
exercise
 Depletion of glycogen
stores
 Short-duration maximal
exertion
 Increased levels of
inorganic phosphate
 May slow Pi release from
myosin
 Decrease calcium release
 Potassium is another factor
in fatigue
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Length-Tension Relationships
in Contracting Muscle
The strength of the contraction is related to the length before the
muscle contracts. Very short fibers do not produce much tension
because there is a lot of overlap not allowing for much sliding
and not many new crossbridges. At optimum lenght there is an
optimum number of cross-bridges to there is optimum tension.
At a longer length there is less overlap and less ability to
produce optimal force
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Figure 12-16
Electrical and Mechanical Events
in Muscle Contraction
A twitch is a single contraction-relaxation cycle
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Figure 12-12
Summation of Contractions
Stimuli is too far
apart and allows the
muscle to relax and
lose tension
If action potentials
come in at a closer
time they recruit
more fibers and the
additive effect
results in increased
muscle tension
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Figure 12-17a
Summation of Contractions
The more
stimulus the
more fibers
recruited until
there is a
maximum
tension but is
there is alot of
time between the
stimulus the
muscle relaxes
resulting in an
unfused tetanus
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Figure 12-17c
Summation of Contractions
Complete
tetanus results
when action
potentials arrive
close enough to
not allow the
muscle to relax.
Maximum
tension can only
be sustained for
a limited time
because fatigue
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Figure 12-17d
Motor Units: Fine motor movements have
more innervations
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Mechanics of Body Movement
 Isotonic contractions create force and move loadcreates force and moves a load.
 Concentric action is a shortening action- contraction
that flexes the joint while working against a load
 Eccentric action is a lengthening action- contraction
that extends the joint while resisting a load
 Isometric contractions create force without moving
a load- the muscle produces tension and contracts but
does not move the joint.
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Isotonic and Isometric Contractions
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Figure 12-19
Muscle Contraction
Duration of muscle contraction of the three types
of muscle- in smooth muscle contraction and
relaxation happen slower and can be sustained for a
longer time.
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Figure 12-24
Smooth Muscle: Properties
 Uses less energy- can maintain maximum tension
while using only a small percentage of the total
maximum cross bridge
 Maintain force for long periods- allows organs to
be tonically contracted and maintain tension for a
long time (sphincter muscles)
 Low oxygen consumption- allows for to maintain
tension for a long time without fatiguing (bladder).
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Smooth Muscle
 Smooth muscle is not studied as much as skeletal muscle because
 It has more variety- impossible to come up with a single
muscle function model- special types for vascular,
gastrointestinal, urinary, respiratory, reproductive, and ocular
 Anatomy makes functional studies difficult- fibers within
cells and muscle layers within organs run indifferent directions.
 It is controlled by hormones, paracrines, and
neurotransmitters
 It has variable electrical properties- contraction is not
triggered only action potential
 Multiple pathways influence contraction and relaxation- acts
as an integrating center to interpret mutiple excitatory and
inhibitory signals that may arrive at the same time
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Smooth Muscle Locations
 IV. Smooth Muscle- A
tissue formed by
uninucleated spindle
shaped cells found in six
areas of the body: blood
vessel walls, respiratory
tract, digestive tubes,
urinary organs,
reproductive organs, and
the eye.
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Smooth Muscle layer orientations
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Cellular details of smooth muscle
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Muscle Disorders
 Muscle cramp: sustained painful contraction –
hyperexcitability of the motor unit, countered with stretching
 Overuse – excessive use that causes tearing in the muscle
structures (fibers, sheaths, tendon connection)
 Disuse- loss of muscle activity causes muscle atrophy because
of loss of blood flow, can recover is disuse is less than a year
 Acquired disorders – infectious diseases and toxin poisoning
that lead to muscle weakness or paralysis
 Inherited disorders  Duchenne’s muscular dystrophy – muscle degenrates from
pelvis up, happens most often in women, people live to be 2030, die of respiratory failure
 Dystrophin –links actin to proteins in cell membrane
 McArdle’s disease – limited exercise tolerance
 Glycogen to glucose-6-phosphate – enzyme missing thus
muscles
do not
have asthe
energy
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Pearson Education,
Inc., publishing
Benjamin
Cummingssource available.