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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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