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Anatomy Lecture BIOL 223 > Exam 2: Structure of Skeletal Muscle cells > Flashcards

Exam 2: Structure of Skeletal Muscle cells Flashcards

1
Q

Muscle Tissue

Musscle Tissue

A

Specialized for contraction

Three Types:
* Skeletal Muscle - Striated, volumtary
* Cardiac Muscle - Found in the heart, striated involuntary
* Smooth - lines hollow organs, nonstriated involuntary

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2
Q

Functions

Skeletal Muscle Functions

A
  • Produce skeletal movement
  • Maintain posture and bodt positions
  • Support soft tissues
  • Guard entrances and exits\
  • Maintain body temp (cellular resp at a high rate ATP and Heat is produced)
  • Nutrient Reserves (Glycogen and protein)
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3
Q

Gross Anatomy of Skeletal Muscles

Gross Anatomy of Skeletal Muscles

A

Attached to bone by tendon
* Origin - attached to bone that remains relativley stationary during movement
* Insertion - attached to the bone that moves
* Synergistic Muscles - muscles that work together
* Antagonistic Muscles - muscles that appose ech other (flexors and extensors)
* Exceptions (Circular sphincter muscles)

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4
Q

Orginization of connective tissue in skeletal muscles

Orginization of connective tissue in skeletal muscles

A
  • Endomysium - covers individual muscle fibers (cells)
  • Perimysium - sheaths bundles of muscle fibers (muscle Fasicles)
  • Epimysium - Surrounds a muscle
  • Endomysium and Perimysium contain blood vessels and nerves
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5
Q

Skeletal Muscle Cells

Skeletal Muscle Cells (Myo and Sacro) = muscles

A
  • Muscle cell = muscle fiber
  • Multinucleate , very long cell (each muscle cell is as long as the muscle)
  • Formed during embryogenesis by end-to-end fusion of uni-necleate myoblasts (fusion of stem cells)
  • Adult muscle repair is limited - new skeletal muscle cells come from stem cells called satellite cells
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6
Q

Structure of Skeletal Muscle cell

Structure of Skeletal Muscle Cell (Muscle Fiber)

A

Contains large quantities of protein filaments = myofilaments
* Actin - thin myofilament
* Myosin - thick myofilament

Myofibrils = bundles of myofilaments
Sarcoplasm = (muscle cell cytoplasm)
Sarcolemma (cell membrane) - sarcoplasmic reticulum (moddified ER)

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7
Q

Sarcolemma

Sarcolemma (muscle cell membrane)

A

Excitable membrane
* Conduct action potentials
Narrow Tubes of sarcolemma extended into cell at right angles to cell surface
* Transverse tubules (t-tubules)
* Conduct action potentials deep into cell
* Come in close contact with sarcoplasmic reticulunm

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8
Q

Sarcoplasmic Reticulum (SR)

Sarcoplasmic Reticulum (SR)

A
  • Simmilar to smooth ER
  • Forms a tubular network around each myofibril
  • Terminal cisternae form triads with T Tubules
  • Stores high concentrations of Ca2+ ions needed for muscle contrations
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8
Q

Sarcoplasmic Reticulum (SR)

Sarcoplasmic Reticulum (SR)

A
  • Simmilar to smooth ER
  • Forms a tubular network around each myofibril
  • Terminal cisternae form triads with T Tubules
  • Stores high concentrations of Ca2+ ions needed for muscle contrations
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9
Q

Arrangement of Myofilaments in a muscle fiber (muscle cell)

Arrangement of Myofilaments in a muscle fiber (muscle cell)

A

Myofilaments
* Thick (myosin)
* Thin (actin)

Myofibril - bundels of myofilaments
* anchored to inner surface of sarcolemma at either end of cell

Sarcomeres - repeting unints of myofiliments in myofibril
* Can activly shorten
* Myofibrils create sarcomers

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10
Q

Arrangement of Myofilaments in a muscle fiber (muscle cell)

Arrangement of Myofilaments in a muscle fiber (muscle cell)

A

Myofilaments
* Thick (myosin)
* Thin (actin)

Myofibril - bundels of myofilaments
* anchored to inner surface of sarcolemma at either end of cell

Sarcomeres - repeting unints of myofiliments in myofibril
* Can activly shorten
* Myofibrils create sarcomers

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11
Q

Striated Sarcomeres

Striated Sarcomeres

A

Differences in distrobution of thick anf thin myofilaments gives banded apperance
* I bands - LIght band - contains only thin filaments
* A bands - dArk band - contain thick filaments, and some overlap with thin filaments
* H band - only thick filaments
* Z disk (line) - border between sarcomeres

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12
Q

Sarcomere Structure and Function

Sarcomere Structure and Function

A
  • Myofibril in muscle cell consists of thousands of sarcomeres end to end
  • Interactions between thin filaments and thick filaments are responsible for muscle contration
  • Thin filaments slide over thic filaments, shortening the sarcomere
  • Shorterning occurs in every sarcomere in the myofibril, thus shortens the myofibril
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13
Q

Sliding Filament Model of Muscle Contraction

Sliding Filament Model of Muscle Contraction

A
  • Thin actin filaments - attached to z disk
  • As thin filaments move toward ceneter of sarcomere:
  • Thin Filaments slide over thick filaments
  • Z lines are pulled closer together
  • I band and H band narrow
  • A band stays the same
  • 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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14
Q

What causes thin and thick myofilaments to slide across eachother?

What causes thin and thick myofilaments to slide across eachother?

A
  • Myosin filaments have many short projections extending out of the filament
  • These projections can bind to site an 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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15
Q

Molecular Anatomy of thick (myosin) myofilaments

Molecular Anatomy of thick (myosin) myofilaments

A

Composed of many (-100) identical myosin molecules bundeld side by side, in stagerd bipolar arrays
* Myosin molecules have elongate tails, globular head - golf club shape
* Arrayed with half facing each end, center is just tails
* Heads form cross bridges during contraction
* Intersections between myosin head and actin provented by tropomyosin during rest

16
Q

Molecular Anatomy of thin (actin) myofilaments

Molecular Anatomy of thin (actin) myofilaments

A

Composed of multiple actin molecule
* Twisted strand composed of two rows of individual globular actin molecules
* Each actin molecule in twisted strand has active to which a myosin head can bind
* Strands of Tropomyosin cover the actin active site during rest
* Tropomyosin strands attached to actin by Troponin

17
Q

Silding Filament Theory

Silding Filament Theory

A

Explains the relationship between thick and thin filaments

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 towards center of sarcomere, pulling the actin
* ATP allows release of cross bridge

18
Q

Role of ATP in moleculare mechanism of Contraction

Role of ATP in moleculare mechanism of Contraction

A

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 mysoin from actin
* ATP is split and head is energized

19
Q

Role of Calcium Ions

Role of Calcium Ions

A

Concentration of CA2+ around sarcomere controls sarcomere contraction
* ca2+ is low around sarcomere at rest
* Action potential in sarcolema and T tubules results in contraction
* Causes coltage gateded Ca2+ chanels of SR to open
* Releaeses Ca2+ into sarcoplasm around sarcomere
* Ca2+ binds to troponin - causes troponin to change shape and pull tropomyosin off actin active sites
* Myosin heads bind to avaliable actin sites over and over until Ca2+ level falls
* When Ca2+ levels fall - tropomyosin covers actin active site, ending contraction

20
Q

Control of skeletal muscle activity occurs at the neuromuscular Junction

Control of skeletal muscle activity occurs at the neuromuscular Junction

A
  • Motor Neuron - nerve cell that controls muscle contraction
  • Neuromusclar Junction - synapse between motor neuron and muscle cell
  • Action potential initiated in motor neuron in response to central nervous system commands
  • Travels theough motor neuron and arraives at synaptic terminal
21
Q

Control of skeletal muscle activity occurs at the neuromuscular Junction

Control of skeletal muscle activity occurs at the neuromuscular Junction

A
  • AP in motor neuron causes the neurotransmiter Acetylcholine (ACH) to be released from motor neuron terminal
  • ACh diffuses across synaptic gap
  • ACh binds to receptors on chemicaly-gated sodium chanelsin muscle membrane
  • Sodium flows into muscle cell
  • Depolarizes the muscle cell membrane and starts an action potential in the muscle cell
22
Q

Control of skeletal muscle activity occurs at the neuromuscular Junction

Control of skeletal muscle activity occurs at the neuromuscular Junction

A

chemically regulated gates stay open as long as ACh is present
* Acetylcholine Esterase (AChE) - enzymne
* Located in the synpatic gap
* Rapidly Breaks down acetylcholine

Excitation of Muscle cell
* Action potential is initiated which spreads across the entire muscle cell membrane including the T tubuels

23
Q

Excitation/Contraction coupling

Excitation/Contraction coupling

A

Action potentials along T-tubule causes release of calcium from cisternae of SR
Initiates Contraction cycle
* Ca2+ binds to troponin, moving tropomysoin
* Attachment of myosin head to actin
* Pivot of mysoin head pulls on actin
* Detachment of myosin head with binding of ATP

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

24
Q

How does calcium ion concentrtion return to resting level?

How does calcium ion concentrtion return to resting level?

A

AP depolirization ends, voltage gated Ca2+ channels in SR close
* Calcium ion diffusion into sarcoplasm stops

Ca2+ is activly transported out of sarcoplasm
* Across sarcolemma to outside of cell (some)
* Across sarcoplasmic reticulum membrane into SR (Most)
* Requires ATP for active transport protein to function

25
Q

Duration of Contraction Depends on:

Duration of Contraction Depends on:

A
  1. Duration of stimulation at nerve-muscle synapse (nueromusclar junction)
    * Multiple action potentials in motor neuron cause continued release of ACh and multiple AP in muscle fiber
  2. Presence of calcium ions in sarcoplasm
    * Contraction cycle continues until calcium concentration returns to resting level
  3. Availability of ATP
    * If no ATP is avalible, contraction cycle stops even if action potential and calcium ions are present
    * Needed to power myosin head
26
Q

Duration of Contraction Depends on:

Duration of Contraction Depends on:

A
  1. Duration of stimulation at nerve-muscle synapse (nueromusclar junction)
    * Multiple action potentials in motor neuron cause continued release of ACh and multiple AP in muscle fiber
  2. Presence of calcium ions in sarcoplasm
    * Contraction cycle continues until calcium concentration returns to resting level
  3. Availability of ATP
    * If no ATP is avalible, contraction cycle stops even if action potential and calcium ions are present
    * Needed to power myosin head
27
Q

Contraction ends and relaxation occurs when:

Contraction ends and relaxation occurs when:

A
  • Action potential stops in motor neuron
  • Acettylcholine esterase breaks down the ACh in the neuromuscular synaptic gap
  • ACh gated chanels close (sodium ion influx stops)
  • Action potentials stop occuring in sarcolemma and T-tubules
28
Q

Contraction ends and relaxation occurs when:

Contraction ends and relaxation occurs when:

A

calcium ion levels in sarcoplasm return to resting levels
* Tropomyosin covers actin sites and now no new myosin cross bridges can form

Relaxation requires ATP
* ATP needed to pump Ca2+ into the SR, pump Na+/K+
* ATP needed to disconnect myosin heads from actin
* Rigot morits - lack of ATP after death

29
Q

Muscular System Disorders

Muscular System Disorders

A

Nevrous system disorders that affecr the coordination or control of muscle contraction
* Blockage of release of ACH (EX. Botulism)
* Interference with binding of ACh to receptors (EX. Myasthenia Gravis)
* Interference with ACh esterase activity (uncontrolled muscle contraction)
* Loss of motor Neuron (EX. polio)
* Loss of motor neuron axon (Peripheral nerve damage)
* Reduction of AP effecinecy (damage to myelin (MS))
* Excessive stimulation of motor neuron (EX. Tetanus)

Anatomy Lecture BIOL 223 (10 decks)

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