Transcript Human Anatomy & Physiology I

Chapter 8
The Muscular System
Copyright 2010, John Wiley & Sons, Inc.
Types of Muscle and Function
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Skeletal - 40–50% of total body weight- voluntary
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Cardiac - only in heart - involuntary
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Mostly movement of bone & body parts
Stabilizing body positions
Heart only
Develops pressure for arterial blood flow
Smooth- grouped in walls of hollow organs
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Sphincters regulate flow in tubes
Maintain diameter of tubes
Move material in GI tract and reproductive organs
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Muscle Functions
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Produce body movements
Stabilize body positions
Store and move substances
Produce heat
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Skeletal Muscle Tissue
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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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Skeletal Muscle Tissue
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Well-supplied with blood vessels and nerves
Terminal of a neuron on each muscle fiber
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Skeletal
Muscle
Tissue
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Muscle Histology
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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
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Throughout sarcoplasm is sarcoplasmic
reticulum
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Sarcoplasm contains myoglobin
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Stores calcium ions
Red pigmented protein related to Hemoglobin that
carries oxygen
Along entire length are myofibrils
Myofibrils made of protein filaments
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Come in thick and thin filaments
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Sarcomere
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Sarcomere
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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
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Thick filament (myosin) has moveable
heads (like “heads” of golf clubs)
Thin filaments (actin) are anchored to Z
discs
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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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Sliding Filament Mechanism
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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 collateral of
somatic motor neuron
Axon terminal
Nerve impulse
Synaptic vesicle
containing
acetylcholine
(ACh)
Synaptic
end bulb
Sarcolemma
Axon terminal
Synaptic
end bulb
Motor
end
plate
Neuromuscular
junction (NMJ)
Synaptic cleft
(space)
Sarcolemma
Myofibril
(b) Enlarged view of the
neuromuscular junction
(a) Neuromuscular junction
1 1ACh is released
from synaptic vesicle
Synaptic end bulb
Synaptic cleft
(space)
2
2 ACh binds to Ach
receptor
Motor end plate
Na+
Junctional fold
3 Muscle action
potential is produced
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(c) Binding of acetylcholine to ACh receptors in the motor end plate
Neuromuscular Interaction
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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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Neuromuscular Junction
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Neuronal ending to muscle fiber =
neuromuscular junction (NMJ)
Synaptic end bulbs (at neuron terminal)
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Release neurotransmitter
Muscular area = Motor end plate
Between is synaptic cleft
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Neuromuscular
Junction
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Action at NMJ
1. Release of acetylcholine (ACh)
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Diffuses across cleft
2. Binding & Activation of ACh receptors
3. Opening of Na+ channels & Na+ influx
4. Generation of Muscle Action Potential
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5.
Repeats with each neuronal action potential
Breakdown of ACh
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Contraction Trigger
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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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Neuromuscular Junctions
Interactions Animations
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Neuromuscular Junctions
You must be connected to the internet to run this animation.
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Contraction Cycle
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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
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Breakdown of ACh to stop muscle action
potentials
Ca2+ ions transported back into SR lowering
concentration →
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This takes ATP
Tropomyosin covers actin binding sites
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NMJ Poisons & Toxins - I
1. Botulinum toxin
- dangerous bacterial toxin; blocks presynaptic ACh
release at the NMJ
- leads to flaccid paralysis
- active component of the very popular"Botox" therapy
2. Tetanus toxin
- bacterial toxin; blocks neurotransmitter release
from inhibitory neurons;
- leads to spastic paralysis and a serious, often fatal,
clinical symptom called "Tetanus"
NMJ Poisons & Toxins - II
3. Curare
- plant-derived toxin; “blow gun poison” used for hunting
by native SA Indians
- prevents binding of Ach to its receptor
4. Organophosphates, Carbamates
- synthetic chemicals commonly used in agriculture,
homes and offices for pest control in US and other parts
of the world; also part of biological warfare chemicals
("nerve gas");
- inhibit the NMJ enzyme acetylcholinesterase;
- recently scientists showed causal connection of
carbamate and organophosphates exposure to the
"Gulf War veteran illness";
Muscle Tone
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Even at rest some motor neuron activity
occurs = Muscle Tone
If nerves are cut fiber becomes flaccid (very
limp)
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Metabolism
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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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Nerve
impulse
1 Nerve impulse arrives at
axon terminal of motor
neuron and triggers release
of acetylcholine (ACh).
2 ACh diffuses across
synaptic cleft, binds
to its receptors in the
motor end plate, and
triggers a muscle
action potential (AP).
ACh receptor
3 Acetylcholinesterase in
Synaptic vesicle
synaptic cleft destroys
filled with ACh
ACh so another muscle
action potential does not
arise unless more ACh is
released from motor neuron.
Muscle action
potential
Transverse tubule
4 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.
SR
Ca2+
9 Muscle relaxes.
8 Troponin–tropomyosin
complex slides back
into position where it
blocks the myosin
binding sites on actin.
5 Ca2+ binds to troponin on
the thin filament, exposing
the binding sites for myosin.
Elevated Ca2+
Ca2+ active
transport pumps
7 Ca2+ release channels in
SR close and Ca2+ active
transport pumps use ATP
to restore low level of
Ca2+ in sarcoplasm.
6 Contraction: power strokes
use ATP; myosin heads bind
to actin, swivel, and release;
thin filaments are pulled toward
center of sarcomere.
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Production of ATP for Muscle
Contraction
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Glycolysis
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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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Production of ATP for Muscle
Contraction
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Aerobic Cellular Respiration
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Production of ATP in mitochondria
Requires oxygen and carbon substrate
Produces CO2 and H2O and heat.
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Fatigue
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Inability to contract forcefully after prolonged
activity
Limiting factors can include:
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Ca2+
Creatine Phosphate
Oxygen
Build up of acid
Neuronal failure
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Oxygen Use After Exercise
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Convert lactic acid back to glucose in liver
Resynthesize creatine phosphate and ATP
Replace oxygen removed from myoglobin
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Control of Muscle Contraction
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Single action potential(AP) → twitch
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Total tension of fiber depends on
frequency of APs (number/second)
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Smaller than maximum muscle force
Require wave summation
Maximum = tetanus
Total tension of muscle depends on
number of fibers contracting in unison
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Increasing numbers = Motor unit recruitment
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Myogram
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Myogram
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Fiber Types
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Slow oxidative (SO)- small diameter and red
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Fast oxidative- glycolytic (FOG)
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Large amounts of myoglobin and mitochondria
ATP production primarily oxidative
Fatigue resistant
Large diameter = many myofibrils
Many mitochondria and high glycolytic capacity
Fast glycolytic fibers (FG)
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White, fast & powerful and fast fatiguing
For strong, short term use
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Recruitment
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Muscle contractions only use the fibers
required for the work
Recruited in order: SO → FOG → FG
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Effects of Exercise
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SO/FG fiber ratio genetically determined
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Endurance exercise gives FG → FOG
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High FG → sprinters
High SO → marathoners
Increased diameter and numbers of
mitochondria
Strength exercise increases size and
strength of FG fibers
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Cardiac Muscle
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Involuntary muscle found only in heart wall
Striated, branched short fibers with single,
central nucleus in each fiber
Fibers connected by:
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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
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Does not require nerve stimulation nerve
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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
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Involuntary
Found in internal organs such as stomach,
bladder, walls of arteries
Structure
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Tapered cells each with single nucleus
Filaments not regular so tissue does not appear
striated
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Smooth Muscle
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Types
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Visceral (single unit) type or
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Multi-unit type
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Form sheets and are autorhythmic
Contract as a unit
Each has own nerve and can contract independently
Graded contractions and slow responses
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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
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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
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Muscles move one bone relative to another
around one or more joint(s)
Origin → most stationary end
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Insertion → most mobile end
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Location where the tendon attaches
Location where tendon inserts
Action → the motion or function of the
muscle
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Skeletal
Muscle and
Bones
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Movement
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Generally arranged in opposing pairs
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Flexors - extensors; abductors - adductors
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The major actor: prime mover or agonist
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Muscle with opposite effect: antagonist
Synergists - help prime mover
Fixators - stabilize origin of prime mover
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Role of muscle varies with motion
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Basis of Muscle Names: Table 8.2
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Direction of fibers relative to body axes
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Size of muscle
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Examples: lateralis, medialis (medius),
intermedius, rectus
Examples: alba, brevis, longus, magnus, vastus
Shape of muscle
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Examples: deltoid, orbicularis, serratus,
trapezius
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Basis of Muscle Names: Table 8.2
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Action of muscle
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Number of tendons (heads) of origin
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Examples: abductor, adductor, flexor, extensor
Examples: biceps, triceps, quadriceps
Location of muscle
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Examples: abdominus, brachialis, cleido,
oculo-, uro-,
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Superficial
Skeletal
Muscles
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Superficial
Skeletal Muscles
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Muscles of the Head
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Muscles of the Head
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Muscles of the Eyeball
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Muscles of the Abdomen
 flexes
 compresses
 Flexes
 compresses
 compresses
 flexes
 compresses
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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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Muscles that move pectoral girdle
 elev./rot.
 elev. med./rot.
 depress./
lat. fwd
 “boxer
muscle”
Not shown:
- Rhomboid major (post.)
 have scapula as insertion
(Trapezius  also clavicle)
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Muscles that move pectoral girdle
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Muscles of the Thorax
 have humerus as insertion
 abduct
 abduct
 rot.med.
 adduct
 flex
 extends
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Muscles of the Thorax
Rhomboid major
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Muscles that move forearm
 extensor
 flexor
 flexor
Not shown:
- Brachioradialis (ant.)
- Supinator, Pronator
 have radius or ulna as insertion
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Muscles of the Arm
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Muscles that move wrist, hand & fingers
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Muscles of the Forearm
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Muscles of
the Neck and
Back
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Muscles which move femur (thigh)
Flexor
Extensor
Rotator
Adductor
Abductor
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Muscles which move femur
Flexor
Extensor
Rotator
Adductor
Abductor
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Muscles which move lower leg
Flexor
Extensor
Rotator
Adductor
Abductor
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Muscles that move the foot & toes
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Muscles that move the foot & toes
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Muscles that move foot & toes
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Muscular Pathology – Disease
& disorders affecting muscles
1. Achondroplasia
Autosomal dominant inherited or
acquired (80% of all cases) genetic
disorder which is responsible for
most common form of dwarfism in
humans.
Characterized by the appearance of
short stature with disproportionately
short arms, short legs, a large head
with pronounced forehead due to
impaired cartilage formation.
Connection to mutations in the gene
coding for the receptor (FGFR) of
the growth hormone
fibroblast growth factor (FGF).
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2. Myasthenia gravis (MG)
Fatal autoimmune disease characterized by chronic, progressive
damage of the neuromuscular junction (NMJ).
Caused by auto-antibodies that bind to and block some ACh
receptors at the motor endplates of muscles.
75% of patients with MG have hyperplasia or tumor of the
thymus (--> over-reactive immune system?).
Common clinical symptoms:
- Muscles of MG patients become increasingly weaker and
fatigue more easily;
- Trouble with eye and eyelid movement,
- Problems with facial expressions and swallowing
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3. Muscular Dystrophy
Group of inherited fatal muscle-destroying
disorder characterized by progressive
degeneration of skeletal muscle fibers.
Most common form is X chromosome-linked
Duchenne muscular dystrophy (DMD)
which almost exclusively affects males at
an early age.
By age of 12 most boys with DMD are
unable to walk and respiratory or cardiac
failure usually causes death between the
ages of 20 and 30.
Caused by mutation of a gene which
codes for the protein dystrophin
- plays an important role in the
structural reinforcement of
the skeletal muscle sarcolemma
Copyright 2010, John Wiley & Sons, Inc.