biol 223 muscles 1

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57 Terms

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muscle tissue

specialized for contraction

three types:

skeletal - attached to bone

  • striated, voluntary

cardiac - found in the heart

  • striated, involuntary

smooth - lines hollow organs

  • nonstriated, involuntary

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If binding Acetylcholine to a chemically gated sodium ion channel opens the channel

A. sodium ions will move into the cell causing a hyperpolarization

B. sodium ions will move out of the cell causing a hyperpolarization

C. sodium ions will move into the cell causing a depolarization

D. sodium ions will move out of the cell causing a depolarization

C. sodium ions will move into the cell causing a depolarization

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skeletal muscle functions

produce skeletal movement

maintain posture and body position (always contracting muscle to maintain posture)

support soft tissue

guard entrances and exits

maintain body temperature

nutrient reserves

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gross anatomy of skeletal muscle

attached to bone by tendon

  • origin - attached to bone that remains relatively stationary during movement

  • insertion - attached to the bone that moves

synergist muscles - muscles that work together for a common goal; ex. muscles working to create a fit

antagonistic muscles

  • flexors and extensors

exceptions: circular sphincter muscles

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endomysium

covers individual muscle fibers (1 fiber = 1 cell)

contains blood vessels and nerves

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perimysium

sheathes bundles of muscle fibers(muscle fascicles)

contains blood vessels and nerves

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epimysium

surrounds a muscle

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deep fascia

wrap groups of cooperating muscles together

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skeletal muscle cells (myo- & sarco-)

muscle cell = muscle fiber

multinucleate, very long cell

  • each muscle cell is as long as the muscle

  • like osteoclasts, multinucleate for transcription and translation

formed during embryogenesis by end-to-end fusion of uni-nucleate myoblasts

adult muscle repair is limited

  • new skeletal muscle cells come from stem cells called satellite cells

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structure of a skeletal muscle cell (muscle fiber)

contains large quantities of protein filaments = myofilaments (strands of certain proteins

  • actin and myosin

myofibrils

sarcoplasm

sarcolemma

sarcoplasmic reticulum

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actin

thin filaments

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myosin

thick filaments

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sarcoplasm

muscle cell cytoplasm

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sarcolemma

muscle cell membrane

excitable membrane

  • conducts action potentials

narrow tubes of sarcolemma extend into cell at right angles to cell surface

  • transverse tubules (t-tubules)

  • conduct action potential deep into cell

  • comes in close contact with sarcoplasmic reticulum

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sarcoplasmic reticulum

modified ER

similar to smooth ER

forms a tubular network around each myofibril

  • terminal cisternae form triads with t tubules

stores high concentration of Ca+2 ions needed for muscle contraction

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myofilaments

thick (myosin)

thin (actin)

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myofibril

bundles of myofilaments

  • anchored to inner surface of sarcolemma at either end of cell

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sarcomeres

repeating units of myofilaments in myofibrils

  • can actively shorten

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striated sarcomeres

differences in distribution of thick and thin myofilaments gives banded appearance

I bands

A bands

Z disk (line)

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I bands

LIght band

contains only thin filaments

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A bands

dArk band

contains thick filaments, and some overlap with thin filaments

H band contains only thick filaments

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Z disk (line)

border between sarcomeres

transition

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Muscles shorten during contraction because

A. the sarcoplamic reticulum pulls sarcomeres out of the myofilaments,

shortening them

B. the myosin and actin filaments can fold up like an accordion

C. the myosin and actin filaments are coiled like a spring and can recoil

after being stretched

D. the myosin and actin filaments slide between each other to shorten

each sarcomere

D. the myosin and actin filaments slide between each other to shorten

each sarcomere

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skeletal muscle (levels of functional organization in skeletal muscle fiber)

surrounded by: epimysium

contains: muscle fascicles

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muscle fascicle (levels of functional organization in skeletal muscle fiber)

surrounded by: perimysium

contains: muscle fibers

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muscle fiber (levels of functional organization in skeletal muscle fiber)

surrounded by: endomysium

contains: myofibrils

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myofibril (levels of functional organization in skeletal muscle fiber)

surrounded by: sarcoplasmic reticulum

consists of: sarcomeres (z line to z line)

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sarcomere (levels of functional organization in skeletal muscle fiber)

contains: thick and thin filaments

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sarcomere structure and function

myofibril in muscle cell consists of thousands of sarcomeres end to end

interactions between thin filaments and thick filaments are responsible for muscle contraction

thin filaments slide over thick filaments, shortening the sarcomere

shortening occurs in every sarcomere in the myofibril, thus shortens the myofibril

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sliding filament model of muscle contraction

thin actin filaments - attached to Z disk

as thin filaments move toward center of sarcomere

  • thin filaments slide ver thick filaments

  • Z lines are puller closer together

  • I bands and H band narrow

  • A band stays the same width

sarcomere is at maximum shortening when it is the width of the A band, no I band or H band are visible

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relaxed sarcomere

a relaxed sarcomere showing location of the A band, Z lines, and I band

<p>a relaxed sarcomere showing location of the A band, Z lines, and I band</p>
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contracted sarcomere

during a contraction, the A band stays the same width, but the Z lines move closer together and the I band gets smaller. when the ends of a myofibril are free to move, the sarcomeres shorten simultaneously and the ends of the myofibril are pulled toward its center

<p>during a contraction, the A band stays the same width, but the Z lines move closer together and the I band gets smaller. when the ends of a myofibril are free to move, the sarcomeres shorten simultaneously and the ends of the myofibril are pulled toward its center</p>
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what causes thin and thick myofilaments to slide across each other

myosin filaments have many short projections extending out from the filament

these projections can bind to sites on actin filaments, forming cross bridges

cross bridges, once formed, change shape pulling the actin past the myosin

cross bridges use energy of ATP to change shape and pull the actin - convert chemical energy to mechanical energy

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molecular anatomy of thick (myosin) myofilaments

composed of many (~100) identical myosin molecules bundled side by side, in staggered bipolar array

  • myosin molecules have elongate tail, globular head - golf club shape

  • arrayed with half facing each end, center is just tails

  • heads form cross bridges during contraction

  • interactions between myosin head and actin prevented by tropomyosin during rest

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molecular anatomy of thin (actin) myofilaments

composed of multiple actin molecules

  • twisted strand composed of two rows of individual globular actin molecules

  • each actin molecule in twisted strand has active site to which a myosin head can attach

  • strands of tropomyosin cover the actin active sites during rest

  • tropomyosin strands attached to actin by troponin

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sliding filament theory

explains the relationship between thick and thin filaments as contraction proceeds

cyclic process beginning with calcium release from SR

  • calcium binds to troponin

  • troponin moves, moving tropomyosin and exposing actin active site

  • myosin head forms cross bridge to actin, bends toward center of sarcomere, pulling the actin

    • ATP allows release of cross bridge

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role of ATP in molecular mechanism of contraction

ATP supplies the energy for the movement of the myosin head

  • converting chemical energy to mechanical energy of movement

myosin head in energized position binds to actin active site

  • releases ADP and P

  • pivots, pulling on actin and moving to un-energized state

ATP binds to un-energized myosin head

  • detaching myosin from action

  • ATP is split and head is energized

Active transport of ions

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role of calcium ions in molecular mechanism of contraction

concentration of Ca+2 around sarcomere controls sarcomere contraction

Ca+2 is low around sarcomere at rest

action potential in sarcolemma and t tubules results in contractions

  • causes voltage-gated Ca+2 channels of SR to open

  • releases Ca+2 into sarcoplasm around sarcomere

Ca+2 binds to troponin

  • causes troponin to change shape and pull tropomyosin off of actin active sites

myosin heads bind to available actin sites over and over until Ca+2 level falls

When Ca+2 level falls

  • tropomyosin covers actin active sites, ending contraction

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motor neuron

nerve cell that controls muscle contraction

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neuromuscular junction

synapse between motor neuron and muscle cell

where we have chemically gated ion channels

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control of skeletal muscle activity occurs at the neuromuscular junction

motor neuron

neuromuscular junction

action potential initiated in motor neuron in response to central nervous system commands

  • travels through motor neuron and arrives at synaptic neuron

AP in motor neuron causes the neurotransmitter Acetylcholine (ACh) to be released from motor neuron terminal

  • ACh diffuses across synaptic gap

  • ACh binds to receptors on chemically-gated sodium channels in muscle membrane

sodium ions flow into the muscle cell

  • depolarization the muscle cell membrane and starts an action potential in the muscle cell

chemically regulated gates stay open as long as ACh is present

Acetylcholine Esterase (AChE)

excitation of muscle cell

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acetylcholine esterase (ache) (Control of skeletal muscle activity occurs at the neuromuscular junction)

located in synaptic gap

rapidly breaks down acetylcholine

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excitation of muscle cell (Control of skeletal muscle activity occurs at the neuromuscular junction)

action potential is initiated which spreads across the entire muscle cell membrane including the t tubules

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activity at the neuromuscular junction 1

the cytoplasm of the axon terminal contains vesicles filled with molecules of acetylcholine, or ACh. acetylcholine is a neurotransmitter, a chemical released by a neuron to change the permeability or other properties of another cells’s plasma membrane. the synaptic cleft and the motor end plate contain molecules of the enzyme acetylcholinesterase (AChE), which breaks down ACh

the synaptic cleft is a narrow space that separates the axon terminal of the neuron from the opposing motor end plate

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activity at the neuromuscular junction 2

the stimulus for ACh release is the arrival of an electrical impulse, or action potential, at the axon terminal. an action potential is a sudden change in the membrane potential that travels along the length of the axon

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activity at the neuromuscular junction 3

when the action potential reaches the neuron’s axon terminal, permeability changes in its membrane trigger the exocytosis of ACh into the synaptic cleft. exocytosis occurs as vesicles fuse with the neuron’s plasma membrane

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activity at the neuromuscular junction 4

ACh molecules diffuse across the synaptic cleft and bind to ACh receptor membrane channels. ACh binding opens the membrane channel on the surface on the motor end plate. because the extracellular fluid contains a high concentration of sodium ions, and sodium ion concentration inside the cell is very low, sodium ions rush into the cytosol

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activity at the neuromuscular junction 5

the sudden inrush of sodium ions results in the generation of an action potential in the sarcolemma. ACh is removed from the synaptic cleft in two ways. ACh either diffuses away from the synapse, or it is broken down by AChE into acetic acid and choline. this removal closes the ACh receptor membrane channels. the muscle fiber pictured above indicates the propagation of the action potential along the sarcolemma

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excitation/contraction coupling

action potential along t tubule causes release of calcium from cisternae of SR

initiates contraction cycle

cycle repeats over and over until calcium ion concentration falls to resting level

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contraction cycle (excitation/contraction coupling)

Ca+2 binds to troponin, moving tropomyosin

attachment of myosin head to actin

pivot of myosin head pulls on actin

detachment of myosin head with binding of ATP

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Action potentials in the muscle cell membrane are conducted into the interior of the muscle via _ and cause Ca2+ ions to be released from the _

A. sarcoplasmic reticulum; myofibril

B. myofibril; mitochondria

C. myosin thick filaments; actin thin filaments

D. transverse tubules; sarcoplasmic reticulum

D. transverse tubules; sarcoplasmic reticulum

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how does calcium ion concentration return to resting level

AP depolarization ends, voltage-gated Ca+2 channels in SR close

  • calcium ion diffusion into sarcoplasm stops

Ca+2 is actively transported out of sarcoplasm

  • across sarcolemma to outside of cell

  • across sarcoplasmic reticulum membrane into SR

    • requires ATP for active transport protein to function

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duration of contraction depends on

  1. duration of stimulation at nerve-muscle synapse (neuromuscular junction)

  • multiple action potentials in motor neuron cause continued release of ACh and multiple AP in muscle fiber

  1. presence of calcium ions in sarcoplasm

  • contraction cycle continues until calcium ion concentration returns to resting level

  1. availability of ATP

  • if no ATP is available, contraction cycle stops even if action potential and calcium ions are present

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contraction ends and relaxation occurs when

action potentials stop in motor neuron

acetylcholinesterase breaks down ACh in the neuromuscular synaptic gap

ACh gated channels close

  • sodium ion influx stops

action potentials stop occurring in sarcolemma and t tubules

calcium ion levels in sarcoplasm return to resting levels

  • tropomyosin covers actin sites and no new myosin cross bridges can form

relaxation requires ATP

  • ATP needed to pump Ca+2 into the SR

  • ATP needed to disconnect myosin heads from actin

  • rigor mortis - lack of ATP after death

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steps that initiate a muscle contraction

  1. ACh released

    • ACh is released at the neuromuscular junction and binds to ACh receptors on the sarcolemma

  1. action potential reaches t tubule

    • an action potential is generated and spreads across the membrane surface of the muscle fiber and along the t tubules

  2. sarcoplasmic reticulum releases Ca+2

    • the sarcoplasmic reticulum releases stored calcium ions

  3. active sites exposed and cross-bridges form

    • calcium ions bind to troponin, exposing the active sites on the thin filaments. cross-bridges form when myosin heads bind to those active sites

    • contraction cycle begins as repeated cycles of cross-bridge binding, pivoting, and detachment occur—all powered by ATP

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steps that end a muscle contraction

  1. ACh is broken down

    • ACh is broken down by acetylcholinesterase (AChE), ending action potential generation

  2. sarcoplasmic reticulum reabsorbs Ca2+

    • as the calcium ions are reabsorbed, their concentration in the cytosol decreases

  3. active sites covered, and cross-bridge formation ends

    • without calcium ions, the tropomyosin returns to its normal position and the active sites are covered again

  4. contraction ends

    • without cross-bridge formation, contraction ends

  5. muscle relaxation occurs

    • the muscle returns passively to its resting length

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muscular system disorders

nervous system disorders that affect the coordination or control of muscle contraction

  • blockage of release of ACh (e.g. botulism)

  • interference with binding o ACh to receptors (e.g. myasthenia graves, autoimmune, can’t contract muscle)

  • interference with ACh esterase activity (blocks enzyme, continuous muscle contraction, spasm)

  • loss of motor neuron (e.g. polio)

  • loss of motor neuron axon - peripheral nerve damage

  • reduction of AP efficiency, damage to myelin (e.g. MS, autoimmune)

  • excessive stimulation of motor neuron (e.g. tetanus, excessive muscle contraction)