Muscle Tissue Characteristics

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113 Terms

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excitability(responsiveness)

ability to receive and respond to stimuli and generation potential

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contractility

ability to shorten forcibly when stimulated

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extensibility

ability to stretch

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elasticity

ability to recoil to resting length

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Prefixes for muscle

myo, mys, and sarco

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muscle fibers

myocytes or muscle cells

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sarcoplasm

muscle cell cytoplasm

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Sarcoplasm contains

many glycogens storage as well as Myoglobin for O2 storage

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Sarcoplasmic reticulum (modified endoplasmic reticulum)

stores calcium ions

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Skeletal Muscle

attached to bones or (some fascial muscles) to skin

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Cell shape appearance of skeletal muscles

single very long cylindrical multinucleate cells with obvious striations

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Cardiac Muscle

Walls of the heart

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Cell shape and appearance of the cardiac muscle

Branching chains of cells, uni, or binucleate; striations

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Smooth Muscle

Unitary muscle in walls of hollow visceral organs (other than the heart); unit muscle in intrinsic eye muscles, airways, large arteries.

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Cell Shape appearance Smooth muscle

single fusiform uninucleate no striations

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Skeletal muscle tissue

is packaged into skeletal muscles organs that are attached to bones and skin

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Skeletal muscle fibers (muscles cells)

longest of all muscle and have striations (stripes)

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Skeletal muscles can also be called

voluntary muscle: can be consciously controlled

contract rapidly tired easily powerful

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Key words for skeletal muscle

skeletal, striated and voluntary

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Skeletal muscle is an organ made up of

different tissues

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Nerve

consciously controlled skeletal muscle has nerves supplying every fiber to control activity

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Cholinergic somatic

motoneuron axons form neuromuscular junctions

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<p>Tendons </p>

Tendons

attachments to bones

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contracting muscles fibers requires

huge amount of energy oxygen and nutrients

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Sarcoplasm

muscle cell cytoplasm contains many

glycosomes

myoglobin

mitochondria

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glycosomes

for glycogen storage as well as

myoglobin for O2

storage mitochondria produce ATP

also, nee waste produces to removed quickly

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Mitochondria produce

ATP

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Muscle (organ)

a muscle consists of hundreds of thousands of muscle cells plus connective tissue wrappings blood vessels and nerve fibers

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Muscle connective tissue wrappings

covered externally by the epimysium

<p>covered externally by the epimysium </p>
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<p>fascicle </p>

fascicle

is a discrete bundles of muscle cells segregated from the rest of the muscle by a connective tissue sheath

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<p>fascicle is surrounded by </p>

fascicle is surrounded by

perimysium

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muscle fiber

an elongated multinucleate cell it has a banded (striated) appearance

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Muscle fiber is surrounded by

endomysium

<p>endomysium </p>
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I bands are

light regions

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<p>A Bands are </p>

A Bands are

dark region

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Myofibrils are composed of

long myofilaments proteins responsible for the banding pattern including:

Actin

Myosin

Titin

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Actin

thin filaments anchored to Z disc with regularly protein Troponin and Tropomyosin

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Myosin

thick filaments

Extend length of A band

Connected at M line

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Titin

elastin and other proteins that hold them together

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<p>I Band </p>

I Band

thin filaments only in Actin

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<p>H Zone </p>

H Zone

thick filaments only myosin

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<p>M line </p>

M line

thick filaments linked by accessory proteins

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<p>outer edge of A band </p>

outer edge of A band

thick and thin filaments overlap

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Dystrophin

links thin filaments to proteins of sarcolemma nebulin, myomesin (M line), C proteins bind filaments or sarcomeres together. Maintain alignment of sarcomere

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<p>During a contraction </p>

During a contraction

A band stays the same width but the Z lines move closer together and the I band gets smaller

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<p>When the ends of a myofibril are to move </p>

When the ends of a myofibril are to move

the sarcomeres shorten simultaneously, and the ends of a myofibril are pulled toward its center

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In the relaxed state thin and think filaments

overlap only slightly at ends of A band

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sliding filament model of contraction states that during the contraction

thin filaments slide past thick filaments causing actin and myosin to overlap more

Neither thick nor thin filaments change length just overlap more

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When nervous system stimulates muscles fibers myosin heads are allowed

to bind to actin, forming cross bridges which causes sliding (contraction) process to begin

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Sarcomere

smallest contractile unit (functional unit) of muscle fiber

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Individual sarcomeres align

end to end along myofibril like boxcars of train

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Each sarcomere extends from

one Z disc to the next

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Striations

stripes formed from repeating series of dark and light bands along length of each myofibril

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A bands

dark regions

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H zone

lighter region in middle of dark A band

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M line

line protein (myomesin) that bisects H zone vertically

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I bands

lighter regions

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<p>Z disc (line) </p>

Z disc (line)

coined-shaped sheet of proteins on midline of light I band

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Actin myofilaments

are anchors to the Z disc

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Myofilaments orderly arrangement of

actin and myosin myofilaments within sarcomere

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Actin myofilaments

extend across I band and partway in A band

anchored to Z discs

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Myosin myofilaments

thick filaments

extend length of A band

connected at M line

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Thin Filament consists of

two strands of actin subunits twisted into a helix plus two types of regulatory proteins (troponin and tropomyosin)

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thick

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thin filaments composed of

protein actin

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actin

is polypeptide made up of kidney-shaped G actin (globular) subunits

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G actin

subunits bears active sites for myosin head attachment during contraction

G actin subunits link together to form long fibrous F actin (filamentous)

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Two F actins strands

twist together to form a thin filament

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Tropomyosin and troponin

regulatory proteins to actin

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Tropomyosin

covers active sites on G -actin

prevents actin-myosin interaction

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troponin

globular protein

binds tropomyosin, G-actin and Calcium (Ca+2)

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Sarcoplasmic reticulum (SR)

network of smooth endoplasmic reticulum tubules surrounding each myofibril

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SR functions in the

regulation of intracellular Ca+2 levels

stores and releases Ca+2

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<p>T tubes </p>

T tubes

tube formed by the protrusion of sarcolemma deep into interior. Increase muscle fibers surface area greatly. Allow the action potential to reach deep into interior of each muscle fiber.

Tubules penetrate cell’s interior at ach A-I band junction between terminal cisterns

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action potential generated by a

nerve stimulation along the sarcolemma and down the tubules

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<p>transmission of the  AP along the T tubules of the triads causes </p>

transmission of the AP along the T tubules of the triads causes

the voltage-sensitive tubule proteins to change shape. This shape change opens the Ca+2 release channels in the terminal cisterns of the sarcoplasmic reticulum (SR) allowing Ca+2 to flow into the cytosol

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A motor unit consists of

one motor neuron and all the muscle fibers it innervates

Branching axon terminals forms neuromuscular junctions one per muscle fiber

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<p>ALS (AKA Lou Gehrig’s disease) </p>

ALS (AKA Lou Gehrig’s disease)

a progressive neurodegenerative disease that affects nerve cells in the brain and spinal cord.

Healthy motor neurons stimulate muscles to contract

ALS kills motor neurons causing muscles to weaken

<p>a progressive neurodegenerative disease that affects nerve cells in the brain and spinal cord.</p><p>Healthy motor neurons stimulate muscles to contract </p><p>ALS kills motor neurons causing muscles to weaken </p>
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Neuromuscular junction or Synapse

between a neuron (motoneuron) and a skeletal muscle fiber at the level of the motor end plate.

Skeletal muscles are stimulated by somatic motor neurons

That are cholinergic (release Acetylcholine)

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<p>Action potential arrives at </p>

Action potential arrives at

axon terminal of motor neuron

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<p>Voltage-gated Ca+2 channels open in the </p>

Voltage-gated Ca+2 channels open in the

axon Ca+2 enters the axon terminal, moving down its electrochemical gradient

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<p>Ca+2 entry causes </p>

Ca+2 entry causes

ACh (a neurotransmitter) to be released by exocytosis in the synaptic cleft

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<p>ACh diffuses across the </p>

ACh diffuses across the

the synaptic cleft and binds to its receptors on the sarcolemma

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ACh binds opens ion channels in the receptors that allow

simultaneous passaged of Na+ into the muscle fiber and K+ out of the muscle fiber. More Na+ ions enter than K+ ions exit, which produces a local depolarization of post synaptic cell.

In the muscle fiber this depolarization is called end late potential

<p>simultaneous passaged of Na+ into the muscle fiber and K+ out of the muscle fiber.  More Na+ ions enter than K+ ions exit, which produces a local depolarization of post synaptic cell.</p><p>In the muscle fiber this depolarization is called end late potential </p>
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<p>ACh effects are terminated by it’s breakdown in the  </p>

ACh effects are terminated by it’s breakdown in the

synaptic cleft by acetylcholinesterase into choline (taken by the axon) and acetate that diffuses away from the junction

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Action potential is generated on the

muscle plasma membrane and reaches the T-tuble

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Excitation-Contraction Coupling

describes the rapid communication between electrical events occurring in the plasma membrane of skeletal muscle fibers and Ca+2 releases from the sarcoplasmic reticulum (SR) which leads to contraction

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<p>Action Potential propagates along the </p>

Action Potential propagates along the

sarcolemma and down the T tubules

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<p>transmission of the AP along the T-tubles of the triads causes the </p>

transmission of the AP along the T-tubles of the triads causes the

voltage-sensitive tuble proteins to change shape. This shape change opens the Ca+2 release channels in the terminal cisterns of the sarcoplasmic reticulum (SR) allowing Ca+2 to flow into the cytosol

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calcium binds to troponin and removes the blocking action of tropomyosin

when Ca binds troponin changes shape, exposing binding sites for myosin (active sites) on the thin filaments

4) contraction begins

<p>when Ca binds troponin changes shape, exposing binding sites for myosin (active sites) on the thin filaments </p><p>4) contraction begins </p>
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<p>Contraction begins:</p>

Contraction begins:

Myosin binding to actin forms cross bridges and contraction (cross bridge cycling) begins at this point E-C coupling is over

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EC-coupling Excitation-Contraction Coupling

describes the rapid communication between electrical events occurring in the plasma membrane of skeletal muscle fibers and Ca+2 release from the sarcoplasmic reticulum (SR), which leads to contraction

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<p>1) Cross Bridge formation</p>

1) Cross Bridge formation

energized myosin head attaches to an actin myofilament forming cross bridge

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<p>2) Power working stroke</p>

2) Power working stroke

ADP and P are released and the myosin head pivots and bends changing to its bent low-energy state. As a result it pulls the actin filament toward the M line.

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<p>3) Cross bridge detachment</p>

3) Cross bridge detachment

After ATP attaches to myosin the link between myosin and actin weakens and the myosin head detaches (cross bridge breaks)

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<p>4) Cocking of the myosin head </p>

4) Cocking of the myosin head

As ATP is hydrolyzed to ADP and P the myosin returns to its prestroke high energy or cocked position which is ready to bind again to actin.

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Rigor mortis

-34-4 hours after death, muscles begin to stiffen

-Peak rigidity occurs about 12 hours and postmortem

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Intracellular calcium levels increase because

ATP is no longer being synthesized, so Calcium cannot be pumped back into SR

results in cross bridge formation