Lesson 3 Flashcards

1
Q

What is muscle comprised of?

A

75% water

20% protein

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2
Q

Where is 50-75% of protein stored? What is that fact important when we are sick?

A

skeletal muscle

-amino acids in muscle become a big reserve for WBC production when sick

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3
Q

Describe skeletal muscle organization briefly.

A

myofilament (actin and myosin) -> sarcomere (contractile unit) -> myofibrils (sarcomeres in series) -> muscle fiber cells -> muscle fascicle -> whole muscle

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4
Q

What are costameres?

A
  • proteins that coordinately transduce contractile F from Z-line to basement membrane laterally, where it can then transmit F parallel to muscle cells’ long axis (become tensioned during contraction of sarcomere and transmit F to basement membrane)
  • 3 different cytoskeletal networks form costameres: integrin, spectrin, and dystroglycan
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5
Q

What happens in muscular dystrophy?

A

dystrophin impaired (another costamere) which destroys the muscle fibers

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6
Q

Where are intermediate filaments and what do mutations cause?

A
  • between myofibrils and form network around Z disks to keep sarcomeres in line
  • fragility with muscle contraction
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7
Q

Where does Titin run? What is PEVK’s role in Titin?

A
  • Titin runs from Z-line past myosin and has passive tension that can contribute to F production w/ sarcomere sliding/stretching
  • PEVK allows Titin to stretch b/c wound up and can unravel to provide passive tension to Titin
  • Titin helps guid/control sarcomere sliding
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8
Q

In the troponin-tropomyosin-actin complex, where is the tropomyosin and what does each troponin bind?

A

tropomyosin: “tail of myosin” spans 7 G-actin molecules
troponin:
T binds tropomyosin
I binds G-actin
C binds 4 calcium ions

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9
Q

Describe myosin structure and function.

A
  • thick filament with tail and globular head
  • globular head has 3 functions: 1) light chain responsible for speed of ATP hydrolysis on MHC 2) actin-binding 3) ATP-binding at ATP pocket; if pocket has no ATP, there is no binding to ATP
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10
Q

How does the myosin head play a role in Rigor Mortis?

A

ATP isn’t being hydrolyzed and is stuck in ATP pocket, so myosin bound to actin

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11
Q

What does the M line do? In which muscle fiber is it thickest?

A
  • stabilizes thick-filament lattice

- thicker in Type 1 (decreased F producing) > Type II fast twitch

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12
Q

Describe the overview of muscle contraction.

A

1) AP to motor neuron
2) AP propagates to pre-synapse, causing Calcium channels to open
3) Calcium flux causes vesicle emptying of ACh into synaptic drift
4) ACh diffuses to post-synapse and binds to ACh R’
5) Causes an increase in sodium/K permeability to depolarize muscle cell and create AP
6) AP travels in all directions through T-tubules, but diminishes as AP travels further into muscle cell (which is why Type II fibers are on the surface)
7) AP activates dihydropyridine R’ in T-tubule
8) DHP R’ physically connected to Ryanodine R’ in sarcoplasmic reticulum and causes SR to release calcium into cytosol
9) Calcium binds to C-subunit of troponin, which moves Tropomyosin away from F-actin binding site
10) myosin binds to actin, creating a cross bridge and muscle contraction follow in presence of ATP to ADP
11) APT then binds to myosin to release cross-bridge

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13
Q

Does the Type I or Type II fibers has higher threshold for stimulation.

A

Type I takes less depolarization as AP travels down T-tubule

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14
Q

How does chemo-mechanical coupling work in the SR? What is the Triad?

A
  • voltage-sensitive DHP receptors on the T-tubule are activated, which causes conformational change on Ryanodine R’ on the SR to release calcium
  • calcium binds to troponin and actin-myosin crossbridge forms (mechanical E)
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15
Q

How much does 1 myosin head produce in force?

A

4-6 pN w/ no gender difference

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16
Q

What is the difference between twitch and tetanic tension?

A

twitch: b/c decreased calcium
tetanic: b/c increased calcium

17
Q

Which myofibrils contract first?

A

superficial myofibrils (usually Type II a& b)

18
Q

If calcium stays out of SR, we will have contractures, so how do we get calcium back in to the SR after muscle contraction?

A

in myoplasm - calmodulin and parvalbumin help put Calcium back in to SR
in SR - calsequestrin

19
Q

What is the resting sarcomere length?

A

2.2 micrometers

20
Q

What is the winding filament hypothesis?

A

titin and PEVK help to rotate myosin around actin, which shortens sarcomere