section 4 muscle contraction
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Muscle Contraction
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Muscular SystemFunctions
Body movement
Maintenance of posture
Respiration Production of body heat
Communication
Constriction of organs and vessels Heart beat
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Properties of Muscle
Contractility
Ability of a muscle to shorten with force
Excitability
Capacity of muscle to respond to a stimulus Extensibility
Muscle can be stretched to its normal restinglength and beyond to a limited degree
Elasticity Ability of muscle to recoil to original resting
length after stretched
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Muscle Tissue Types
Skeletal Attached to bones
Nuclei multiple and peripherally located
Striated, Voluntary and involuntary (reflexes)
Smooth
Walls of hollow organs, blood vessels, eye, glands, skin Single nucleus centrally located
Not striated, involuntary, gap junctions in visceralsmooth
Cardiac Heart
Single nucleus centrally located
Striations, involuntary, intercalated disks
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Classification of the
MuscleAccording to the structure: Striated Muscle,
Smooth Muscle
According to the nerve innervation:Voluntary Muscle, Involuntary Muscle
According to the Function: Skeletal Muscle,Cardiac Contraction, Smooth Muscle
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Skeletal Muscle
Human body contains over 400 skeletal
muscles
40-50% of total body weightFunctions of skeletal muscle
Force production for locomotion and
breathingForce production for postural support
Heat production during cold stress
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I. Skeletal Muscle
A. Muscle fiber1. Sarcolemma
2. Sarcoplasm
3. Myofibrils contractile elements
a. Actin myofilament
F actin strands
tropomyosin
troponin (T, I, C)
b. Myosin myofilament
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4. Sarcomere
arrangement of myofibrils
a. Z disk attaches actin
b. I band actin myofilament
c. A band both actin and myosin
H zone only myosin
5. T Tubules
invagination of sarcolemma
6. Sarcoplasmic Reticulum
high conc. of calcium
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Fascicles: bundles, CT(connective tissue) covering on
each one
Muscle fibers: muscle cells
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Structure of skeletal musclefiber
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Structure of Skeletal Muscle:
Microstructure
Sarcolemma
Transverse (T) tubule
Longitudinal tubule (Sarcoplasmicreticulum, SR
Myofibrils (thin filament)
TroponinTropomyosin
Myosin (thick filament)
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Within the sarcoplasm
Transverse tubules
Sarcoplasmic reticulum -Storage sites for calcium
Terminal cisternae - Storage sites for calcium
Triad
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Microstructure of Skeletal
Muscle (myofibril)
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Sarcomeres Sarcomere : bundle of alternating thick and
thin filaments
Sarcomeres join end to end to form myofibrils
Thousands per fiber, depending on length of
muscle
Alternating thick and thin filaments create
appearance of striations
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Myosin head is hinged
Bends and straightens during contraction
Myosin
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Thin filaments (actin)Backbone: two strands of polymerized globular
actin fibrous actinEach actin has myosin binding site
Troponin
Binds Ca2+ ; regulates muscle contractionTropomyosin
Lies in groove of actin helix
Blocks myosin binding sites in absence of Ca2+
hi k fil i (h d d il)
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Thick filament: Myosin (head and tail)
Thin filament: Actin, Tropomyosin, Troponin
(calcium binding site)
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The Sliding Filament Model of Muscle Contraction
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Cross-Bridge Formation in
Muscle Contraction
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B. Signal transmission
1. Motor neuron
2. Presynaptic terminal
3. Endplate
region of skeletal fiber where synapse occurs
4. Nicotinic receptor
C. Muscle Contraction
1. Action Potential -> sarcolemma ->T tubules
2. T tubules -> Sarcoplasmic Retic
3. Voltage gated Ca++ channels open
4. Ca++ -> sarcoplasm
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I Signal Transmission Through
the Neuromuscular Junction
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Skeletal Muscle Innervation
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C 2+ i d f i fACh is released and
ACh binds to itsBinding of ACh opens
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40K+
Outsid
Inside
Na+
Na+
Na+Na+
Na+
Na+
Na+Na+ Na+
Na+
Na+
Na+
K+ K+
K+K+
K+K+
K+K+
K+
K+ K+
ACh
ACh
ACh
Ca2+ induces fusion of
vesicles with nerve
terminal membrane.
ACh is released and
diffuses across
synaptic cleft.
ACh
ACh binds to its
receptor on the
postsynaptic membrane
Binding of ACh opens
channel pore that is
permeable to Na+ and K+.
Na+
Na+
K+
Muscle membrane
Nerve
terminal Ca2+
Ca2+
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Uses of anti-ChE agents
Clinical applications (Neostigmine,Physostigmine
Insecticides (organophosphate )
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NMJ Diseases
Myasthenia GravisAutoimmunity to ACh receptor
Fewer functional ACh receptors
Low safety factor for NM transmissionLambert-Eaton syndromeAutoimmunity directed against Ca2
channelsReduced ACh release
Low safety factor for NM transmission
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Energy for Muscle Contraction
ATP is required for muscle contraction
Myosin ATPase breaks down ATP as fiber
contracts
Nerve Activation of Individual
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Nerve Activation of Individual
Muscle Cells (cont.)
Excitation/contraction coupling
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Action potential along T-tubule causes releaseof calcium from cisternae of TRIAD
Cross-bridge cycle
Excitation/contraction coupling
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1. Myosin heads form cross bridges
Myosin head is
tightly bound to
actin in rigor state
Nothing bound to
nucleotide binding
site
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3 ATP h d l i
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3. ATP hydrolysis
ATP is brokendown into:
ADP + Pi
(inorganic
phosphate)
Both ADP and Pi
remain bound to
myosin
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4 M i h d h
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4. Myosin head changes
conformation
Myosin headrotates andbinds to new
actinmolecule
Myosin is inhigh energyconfiguration
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Myosin cannot release actin until anew ATP molecule binds
Run out of ATP at death, cross-bridges never release
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Ca+2 binds to troponin during
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Ca binds to troponin during
contraction
Troponin-Ca+2 pulls tropomyosin,unblocking
myosin-bindingsites
Myosin-actin
cross-bridge cyclecan now occur
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The action potential triggersThe action potential triggers
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contractioncontractionHow does the AP trigger
contraction?This question has the
beginning (AP) and the end(contraction) but it misses lots
of things in the middle!
We should ask:how does the AP cause release of
Ca from the SR, so leading to anincrease in [Ca]i?
how does an increase in [Ca]i
cause contraction?
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Ca2+ Controls Contraction
Ca2+ Channels and Pumps Release of Ca2+ from the SR triggers
contraction
Reuptake of Ca2+ into SR relaxes muscle
So how is calcium released in responseto nerve impulses?
Answer has come from studies ofantagonist molecules that block Ca2+channel activity
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Dihydropyridine Receptor
In t-tubules of heart and skeletal muscle
Nifedipine and other DHP-like molecules bind
to the "DHP receptor" in t-tubules
In heart, DHP receptor is a voltage-gated Ca2+
channel
In skeletal muscle, DHP receptor is apparently
a voltage-sensing protein and probablyundergoes voltage-dependent conformational
changes
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Cardiac muscle
Cardiac muscle
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Cardiac muscleCardiac muscle
The AP:
moves down the t-tubule
voltage change detected by DHP
receptors (Ca channels) which
opens to allow small amount of(trigger) Ca into the fibre
Ca binds to ryanodine receptors
which open to release a large
amount of (activator) Ca(CACR)
Thus, calcium, not voltage,
appears to trigger Ca release in
Cardiac muscle!
out
in
voltage sensor
& Ca channel
(DHP receptor)
junctional foot
(ryanodine receptor)
sarcoplasmic
reticulum
sarcolemma
T-tubule
The Answers!
The Answers!
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The Answers!
Skeletal
The trigger for SR releaseappears to be voltage(Voltage Activated CalciumRelease- VACR)
The t-tubule membrane hasa voltage sensor (DHPreceptor)
The ryanodine receptor isthe SR Ca release channel
Ca2+ release is proportionalto membrane voltage
Cardiac
The trigger for SR releaseappears to be calcium
(Calcium Activated
Calcium Release - CACR)
The t-tubule membranehas a Ca2+ channel (DHP
receptor)
The ryanodine receptor is
the SR Ca release channel
The ryanodine receptor is
Ca-gated & Ca release is
proportional to Ca2+
entry
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Ca2+ release during Excitation-Contraction
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gcoupling
Ryanodyne R
Ca-release ch.
Action
potential onmotorendplatetravels
down Ttubules
Voltage -gated Ca2+ channels open, Ca2+ flows outSR into cytoplasm
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SR into cytoplasm
Ca2+ channels close when action potential ends.
Active transport pumps continually return Ca2+ to SR
Ca ATPase
(SERCA)
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Excitation-Contraction Coupling
Depolarization of motor end plate (excitation) iscoupled to muscular contraction
Nerve impulse travels along sarcolemma and down
T-tubules to cause a release of Ca2+
from SR Ca2+ binds to troponin and causes position change in
tropomyosin, exposing active sites on actin
Permits strong binding state between actin and
myosin and contraction occurs
ATP is hydrolyzed and energy goes to myosin head
which releases from actin
y: x -Coupling
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Coupling
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E. Phases of muscle movement
1. Lag Phase
AP in motor neuron to exposure of active sites
2. Contraction Phase
crossbridge -> power stroke
3. Relaxation Phase
calcium pumped into S. R.
4. Mechanical signal
measured as tension
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IV Factors that Affect the
Efficiency of Muscle Contraction
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T f C i I
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Types of Contractions I
Twitch: a brief mechanical contraction
of a single fiber produced by a single
action potential at low frequency
stimulation is known as single twitch.
Tetanus: It means a summation of
twitches that occurs at high frequencystimulation
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Effects of Repeated Stimulations
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p
Figure 10.15
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1/sec 5/sec 10/sec 50/sec
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Isotonic and Isometric Contractions
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Resistance and Speed of Contraction
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Muscle PowerMuscle Power
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Maximal power occurs where the product of
force (P) and velocity (V) is greatest(P=FV)
X Max Power=
4.5units
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