1. Chapter 8 The Muscular System
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Copyright 2010 John Wiley & Sons, Inc. All rights reserved. Reproduction or translation of this work beyond that permitted in section 117 of the 1976 United States Copyright Act without express permission of the copyright owner is unlawful. Request for further information should be addressed to the Permission Department, John Wiley & Sons, Inc. The purchaser may make back-up copies for his/her own use only and not for distribution or resale. The Publishers assumes no responsibility for errors, omissions, or damages caused by the use of theses programs or from the use of the information herein.
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End of Chapter 8
Copyright 2010 John Wiley & Sons, Inc. All rights reserved. Reproduction or translation of this work beyond that permitted in section 117 of the 1976 United States Copyright Act without express permission of the copyright owner is unlawful. Request for further information should be addressed to the Permission Department, John Wiley & Sons, Inc. The purchaser may make back-up copies for his/her own use only and not for distribution or resale. The Publishers assumes no responsibility for errors, omissions, or damages caused by the use of theses programs or from the use of the information herein.
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4. Types of Muscle and Function
Skeletal - 40–50% of total body weight- voluntary
Mostly movement of bone & body parts
Stabilizing body positions
Cardiac - only in heart - involuntary
Heart only
Develops pressure for arterial blood flow
Smooth- grouped in walls of hollow organs
Sphincters regulate flow in tubes
Maintain diameter of tubes
Move material in GI tract and reproductive organs
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Muscle Functions
Produce body movements
Stabilize body positions
Store and move substances
Produce heat
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6. Skeletal Muscle Tissue
Muscle includes: muscle fibers, connective tissue, nerves & blood vessels
Wrapped in epimysium
Perimysium surrounds fiber bundles called fascicles
Endomysium surrounds each individual fiber
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7. Skeletal Muscle Tissue
Well-supplied with blood vessels and nerves
Terminal of a neuron on each muscle fiber
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8. Skeletal Muscle Tissue
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Muscle Histology
Elongated cylindrical cells = muscle fibers
Plasma membrane = sarcolemma
Transverse (T) tubules tunnel from surface to center of each fiber
Multiple nuclei lie near surface of cell
Cytoplasm = sarcoplasm
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Muscle Histology
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Muscle Histology
Throughout sarcoplasm is sarcoplasmic reticulum
Stores calcium ions
Sarcoplasm contains myoglobin
Red pigmented protein related to Hemoglobin that carries oxygen
Along entire length are myofibrils
Myofibrils made of protein filaments
Come in thick and thin filaments
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Sarcomere
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Sarcomere
Filaments overlap in repeating patterns
Unit structure is called sarcomere
Separated by Z discs
Darker area = A band associated with thick filaments
H zone has no thin filaments
I band has thin filaments no thick filaments
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Sarcomere
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Sarcomere
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Sarcomere
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Functional Structure
Thick filament (myosin) has moveable heads (like “heads” of golf clubs)
Thin filaments (actin) are anchored to Z discs
Contain myosin binding sites for myosin head
Also contain tropomyosin & troponin
Tropomyosin blocks myosin binding site when muscle is at rest
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18. Sliding Filament Mechanism
During contraction myosin heads bind actin sites
Myosins pull and slide actin molecules (and Z discs) toward H zone
I bands and H zones become more narrow
Sliding generates force and shortens sarcomeres and thus fibers.
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Axon terminal
Axon collateral of
somatic motor neuron
Sarcolemma
Myofibril
ACh is released
from synaptic vesicle
ACh binds to Ach
receptor
Junctional fold
Synaptic vesicle
containing
acetylcholine
(ACh)
Synaptic cleft
(space)
Motor
end
plate
(a) Neuromuscular junction
(b) Enlarged view of the
neuromuscular junction
(c) Binding of acetylcholine to ACh receptors in the motor end plate
Synaptic
end bulb
Neuromuscular
junction (NMJ)
Synaptic end bulb
Motor end plate
Nerve impulse
Muscle action
potential is produced
Na+ 2 3 1
Axon terminal
Axon collateral of
somatic motor neuron
Sarcolemma
Myofibril
ACh is released
from synaptic vesicle
ACh binds to Ach
receptor
Junctional fold
Synaptic vesicle
containing
acetylcholine
(ACh)
Synaptic cleft
(space)
Motor
end
plate
(a) Neuromuscular junction
(b) Enlarged view of the
neuromuscular junction
(c) Binding of acetylcholine to ACh receptors in the motor end plate
Synaptic
end bulb
Neuromuscular
junction (NMJ)
Synaptic end bulb
Motor end plate
Nerve impulse
Na+ 2 1
Axon terminal
Axon collateral of
somatic motor neuron
Sarcolemma
Myofibril
ACh is released
from synaptic vesicle
Junctional fold
Synaptic vesicle
containing
acetylcholine
(ACh)
Synaptic cleft
(space)
Motor
end
plate
(a) Neuromuscular junction
(b) Enlarged view of the
neuromuscular junction
(c) Binding of acetylcholine to ACh receptors in the motor end plate
Synaptic
end bulb
Neuromuscular
junction (NMJ)
Synaptic end bulb
Motor end plate
Nerve impulse
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20. Neuromuscular Interaction
Nerve signal triggers muscle action potential
Delivered by motor neuron
One neuron can trigger 1 or more fibers at the same time
Neuron plus triggered fibers = motor unit
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21. Neuromuscular Junction
Neuronal ending to muscle fiber = neuromuscular junction (NMJ)
Synaptic end bulbs (at neuron terminal)
Release neurotransmitter
Muscular area = Motor end plate
Between is synaptic cleft
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22. Neuromuscular Junction
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Action at NMJ
Release of acetylcholine (ACh)
Diffuses across cleft
Activation of ACh receptors
Generation of Muscle Action Potential
Repeats with each neuronal action potential
Breakdown of ACh
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Contraction Trigger
Muscle action potential → Ca2+ release from Sacroplasmic Reticulum (SR)
Ca2+ binds to troponin →
Moves tropomyosin off actin sites →
Myosin binds & starts cycle
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25. Neuromuscular Junctions Interactions Animations
You must be connected to the internet to run this animation.
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Contraction Cycle
Myosin binds to actin & releases phosphate group (forming crossbridges)
Crossbridge swivels releasing ADP and shortening sarcomere (power stroke)
ATP binds to Myosin → release of myosin from actin
ATP broken down to ADP & Pi → activates myosin head to bind and start again
Repeats as long as Ca2+ concentration is high
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Contraction Cycle
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Relaxation
Breakdown of ACh to stop muscle action potentials
Ca2+ ions transported back into SR lowering concentration →
This takes ATP
Tropomyosin covers actin binding sites
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Muscle Tone
Even at rest some motor neuron activity occurs = Muscle Tone
If nerves are cut fiber becomes flaccid (very limp)
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Metabolism
Rapid changes from very low ATP consumption to high levels of consumption
Creatine phosphate (high energy store)
Fast and good for ~ 15 sec
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ACh diffuses across
synaptic cleft, binds
to its receptors in the
motor end plate, and
triggers a muscle
action potential (AP).
Nerve impulse arrives at
axon terminal of motor
neuron and triggers release
of acetylcholine (ACh).
Synaptic vesicle
filled with ACh
ACh receptor
Acetylcholinesterase in
synaptic cleft destroys
ACh so another muscle
action potential does not
arise unless more ACh is
released from motor neuron.
Ca2+
Muscle action
potential
Nerve
impulse SR
Contraction: power strokes
use ATP; myosin heads bind
to actin, swivel, and release;
thin filaments are pulled toward
center of sarcomere.
Ca2+ binds to troponin on
the thin filament, exposing
the binding sites for myosin.
Muscle AP travelling along
transverse tubule opens Ca2+
release channels in the
sarcoplasmic reticulum (SR)
membrane, which allows
calcium ions to flood into the
sarcoplasm.
Elevated Ca2+ 1 2 3 4 5 6
Transverse tubule
ACh diffuses across
synaptic cleft, binds
to its receptors in the
motor end plate, and
triggers a muscle
action potential (AP).
Nerve impulse arrives at
axon terminal of motor
neuron and triggers release
of acetylcholine (ACh).
Synaptic vesicle
filled with ACh
ACh receptor
Acetylcholinesterase in
synaptic cleft destroys
ACh so another muscle
action potential does not
arise unless more ACh is
released from motor neuron.
Ca2+
Muscle action
potential
Nerve
impulse SR
Contraction: power strokes
use ATP; myosin heads bind
to actin, swivel, and release;
thin filaments are pulled toward
center of sarcomere.
Ca2+ active
transport pumps
Ca2+ release channels in
SR close and Ca2+ active
transport pumps use ATP
to restore low level of
Ca2+ in sarcoplasm.
Ca2+ binds to troponin on
the thin filament, exposing
the binding sites for myosin.
Muscle AP travelling along
transverse tubule opens Ca2+
release channels in the
sarcoplasmic reticulum (SR)
membrane, which allows
calcium ions to flood into the
sarcoplasm.
Elevated Ca2+ 1 2 3 4 5 6 7
Transverse tubule
ACh diffuses across
synaptic cleft, binds
to its receptors in the
motor end plate, and
triggers a muscle
action potential (AP).
Nerve impulse arrives at
axon terminal of motor
neuron and triggers release
of acetylcholine (ACh).
Synaptic vesicle
filled with ACh
ACh receptor
Acetylcholinesterase in
synaptic cleft destroys
ACh so another muscle
action potential does not
arise unless more ACh is
released from motor neuron.
Ca2+
Muscle action
potential
Nerve
impulse SR
Contraction: power strokes
use ATP; myosin heads bind
to actin, swivel, and release;
thin filaments are pulled toward
center of sarcomere.
Troponin–tropomyosin
complex slides back
into position where it
blocks the myosin
binding sites on actin.
Ca2+ active
transport pumps
Ca2+ release channels in
SR close and Ca2+ active
transport pumps use ATP
to restore low level of
Ca2+ in sarcoplasm.
Ca2+ binds to troponin on
the thin filament, exposing
the binding sites for myosin.
Muscle AP travelling along
transverse tubule opens Ca2+
release channels in the
sarcoplasmic reticulum (SR)
membrane, which allows
calcium ions to flood into the
sarcoplasm.
Elevated Ca2+ 1 2 3 4 5 6 7 8
Transverse tubule
ACh diffuses across
synaptic cleft, binds
to its receptors in the
motor end plate, and
triggers a muscle
action potential (AP).
Nerve impulse arrives at
axon terminal of motor
neuron and triggers release
of acetylcholine (ACh).
Synaptic vesicle
filled with ACh
ACh receptor
Acetylcholinesterase in
synaptic cleft destroys
ACh so another muscle
action potential does not
arise unless more ACh is
released from motor neuron.
Ca2+
Muscle action
potential
Nerve
impulse SR
Contraction: power strokes
use ATP; myosin heads bind
to actin, swivel, and release;
thin filaments are pulled toward
center of sarcomere.
Troponin–tropomyosin
complex slides back
into position where it
blocks the myosin
binding sites on actin.
Muscle relaxes.
Ca2+ active
transport pumps
Ca2+ release channels in
SR close and Ca2+ active
transport pumps use ATP
to restore low level of
Ca2+ in sarcoplasm.
Ca2+ binds to troponin on
the thin filament, exposing
the binding sites for myosin.
Muscle AP travelling along
transverse tubule opens Ca2+
release channels in the
sarcoplasmic reticulum (SR)
membrane, which allows
calcium ions to flood into the
sarcoplasm.
Elevated Ca2+ 1 2 3 4 9 5 6 7 8
Transverse tubule
ACh diffuses across
synaptic cleft, binds
to its receptors in the
motor end plate, and
triggers a muscle
action potential (AP).
Nerve impulse arrives at
axon terminal of motor
neuron and triggers release
of acetylcholine (ACh).
Synaptic vesicle
filled with ACh
ACh receptor
Acetylcholinesterase in
synaptic cleft destroys
ACh so another muscle
action potential does not
arise unless more ACh is
released from motor neuron.
Ca2+
Muscle action
potential
Nerve
impulse SR
Ca2+ binds to troponin on
the thin filament, exposing
the binding sites for myosin.
Muscle AP travelling along
transverse tubule opens Ca2+
release channels in the
sarcoplasmic reticulum (SR)
membrane, which allows
calcium ions to flood into the
sarcoplasm. 1 2 3 4 5
Transverse tubule
ACh diffuses across
synaptic cleft, binds
to its receptors in the
motor end plate, and
triggers a muscle
action potential (AP).
Nerve impulse arrives at
axon terminal of motor
neuron and triggers release
of acetylcholine (ACh).
Synaptic vesicle
filled with ACh
ACh receptor
Acetylcholinesterase in
synaptic cleft destroys
ACh so another muscle
action potential does not
arise unless more ACh is
released from motor neuron.
Ca2+
Muscle action
potential
Nerve
impulse SR
Muscle AP travelling along
transverse tubule opens Ca2+
release channels in the
sarcoplasmic reticulum (SR)
membrane, which allows
calcium ions to flood into the
sarcoplasm. 1 2 3 4
Transverse tubule
Nerve impulse arrives at
axon terminal of motor
neuron and triggers release
of acetylcholine (ACh).
Synaptic vesicle
filled with ACh
ACh receptor
Muscle action
potential
Nerve
impulse 1
ACh diffuses across
synaptic cleft, binds
to its receptors in the
motor end plate, and
triggers a muscle
action potential (AP).
Nerve impulse arrives at
axon terminal of motor
neuron and triggers release
of acetylcholine (ACh).
Synaptic vesicle
filled with ACh
ACh receptor
Muscle action
potential
Nerve
impulse 1 2
ACh diffuses across
synaptic cleft, binds
to its receptors in the
motor end plate, and
triggers a muscle
action potential (AP).
Nerve impulse arrives at
axon terminal of motor
neuron and triggers release
of acetylcholine (ACh).
Synaptic vesicle
filled with ACh
ACh receptor
Acetylcholinesterase in
synaptic cleft destroys
ACh so another muscle
action potential does not
arise unless more ACh is
released from motor neuron.
Muscle action
potential
Nerve
impulse 1 2 3
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32. Production of ATP for Muscle Contraction
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Glycolysis
Break down glucose to 2 pyruvates getting 2 ATPs
If insufficient mitochondria or oxygen, pyruvate → lactic acid
Get about 30–40 seconds more activity maximally
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34. Production of ATP for Muscle Contraction
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35. Aerobic Cellular Respiration
Production of ATP in mitochondria
Requires oxygen and carbon substrate
Produces CO2 and H2O and heat.
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Fatigue
Inability to contract forcefully after prolonged activity
Limiting factors can include:
Ca2+
Creatine Phosphate
Oxygen
Build up of acid
Neuronal failure
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37. Oxygen Use After Exercise
Convert lactic acid back to glucose in liver
Resynthesize creatine phosphate and ATP
Replace oxygen removed from myoglobin
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38. Control of Muscle Contraction
Single action potential(AP) → twitch
Smaller than maximum muscle force
Total tension of fiber depends on frequency of APs (number/second)
Require wave summation
Maximum = tetanus
Total tension of muscle depends on number of fibers contracting in unison
Increasing numbers = Motor unit recruitment
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Myogram
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Myogram
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Fiber Types
Slow oxidative (SO)- small diameter and red
Large amounts of myoglobin and mitochondria
ATP production primarily oxidative
Fatigue resistant
Fast oxidative- glycolytic (FOG)
Large diameter = many myofibrils
Many mitochondria and high glycolytic capacity
Fast glycolytic fibers (FG)
White, fast & powerful and fast fatiguing
For strong, short term use
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Recruitment
Muscle contractions only use the fibers required for the work
Recruited in order: SO → FOG → FG
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Effects of Exercise
SO/FG fiber ratio genetically determined
High FG → sprinters
High SO → marathoners
Endurance exercise gives FG → FOG
Increased diameter and numbers of mitochondria
Strength exercise increases size and strength of FG fibers
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Cardiac Muscle
Involuntary muscle found only in heart wall
Striated, branched short fibers with single, central nucleus in each fiber
Fibers connected by:
Intercalated discs (thickened cell membranes)
Gap junctions that allow spread of action potentials
ATP generated by abundant mitochondria and by lactic acid when cells lack oxygen
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Cardiac Muscle
Does not require nerve stimulation nerve
Has its own intrinsic pacemaker (and conduction system within cardiac muscle) that initiates cardiac contraction
Known as autorhythmicity
Ca2+released from S.R. and extracellular spaces
Intercalated discs with gap junctions transmit action potentials from ne muscle cell to the next
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Cardiac Muscle
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Smooth Muscle
Involuntary
Found in internal organs such as stomach, bladder, walls of arteries
Structure
Tapered cells each with single nucleus
Filaments not regular so tissue does not appear striated
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Smooth Muscle
Types
Visceral (single unit) type or
Form sheets and are autorhythmic
Contract as a unit
Multi-unit type
Each has own nerve and can contract independently
Graded contractions and slow responses
Often sustain long term tone
Often triggered by autonomic nerves
Modulated chemically, by nerves, by mechanical events (stretching)
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Smooth Muscle
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Aging
As with bone there is a slow progressive loss of skeletal muscle mass
Relative number of SO fibers tends to increase
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Movement
Muscles move one bone relative to another around one or more joint(s)
Origin → most stationary end
Location where the tendon attaches
Insertion → most mobile end
Location where tendon inserts
Action → the motion or function of the muscle
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52. Skeletal Muscle and Bones
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Movement
Generally arranged in opposing pairs
Flexors - extensors; abductors - adductors
The major actor: prime mover or agonist
Muscle with opposite effect: antagonist
Synergists - help prime mover
Fixators - stabilize origin of prime mover
Role of muscle varies with motion
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54. Basis of Muscle Names: Table 8.2
Direction of fibers relative to body axes
Examples: lateralis, medialis (medius), intermedius, rectus
Size of muscle
Examples: alba, brevis, longus, magnus, vastus
Shape of muscle
Examples: deltoid, orbicularis, serratus, trapezius
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55. Basis of Muscle Names: Table 8.2
Action of muscle
Examples: abductor, adductor, flexor, extensor
Number of tendons (heads) of origin
Examples: biceps, triceps, quadriceps
Location of muscle
Examples: abdominus, brachialis, cleido, oculo-, uro-,
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56. Superficial Skeletal Muscles
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57. Superficial Skeletal Muscles
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Muscles of the Head
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Muscles of the Eyeball
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Muscles of the Abdomen
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Muscles of the Abdomen
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Muscles of the Thorax
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Muscles of the Thorax
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64. Copyright 2010, John Wiley & Sons, Inc.
Muscles of the Thorax
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65. Copyright 2010, John Wiley & Sons, Inc.
Muscles of the Thorax
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66. Copyright 2010, John Wiley & Sons, Inc.
Muscles of the Thorax
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67. Copyright 2010, John Wiley & Sons, Inc.
Muscles of the Arm
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68. Copyright 2010, John Wiley & Sons, Inc.
Muscles of the Arm
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Muscles of the Forearm
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Muscles of the Forearm
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71. Muscles of the Neck and Back
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72. Muscles of the Gluteal Region
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73. Muscles of the Gluteal Region
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74. Muscles of the Leg: Foot and Toes
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75. Muscles of the Leg: Foot and Toes
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End of Chapter 8
Copyright 2010 John Wiley & Sons, Inc. All rights reserved. Reproduction or translation of this work beyond that permitted in section 117 of the 1976 United States Copyright Act without express permission of the copyright owner is unlawful. Request for further information should be addressed to the Permission Department, John Wiley & Sons, Inc. The purchaser may make back-up copies for his/her own use only and not for distribution or resale. The Publishers assumes no responsibility for errors, omissions, or damages caused by the use of theses programs or from the use of the information herein.
Copyright 2010, John Wiley & Sons, Inc.