B1W3: Skeletal Muscle Flashcards

(42 cards)

1
Q

Organization of Muscles

A
  1. Whole muscle
  2. Muscle fiber (muscle cell)
  3. Myofibrils (within cell, sarcomeres)
  4. Contractile filaments/proteins/structural proteins
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2
Q

Titin

A

Attaches to Z line and keeps thick filaments in line during contraction

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3
Q

CapZ

A

attaches actin filaments to Z line

prevents actin depolarization

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4
Q

Nebulin

A

On thin filament

Maintains constant length of each filament

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5
Q

Z line

A

Boundary of sarcomere

Where thin filaments attch

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6
Q

I band

A

Thin filaments (and z disks)

“I is a thin letter”

Disappears during contraction

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7
Q

A band

A

length of thick filaments

Thhin and thick filaments may overlap here

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8
Q

H zone

A

Thick filaments only

“H is a thick letter”

disappears during contraction

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9
Q

M line

A

Center of the thick filament

Structural protein

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10
Q

Label

A
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11
Q

Myosin components

A

Thick filaments

Two heavy chains for the tail, 4 light chains that form two globular heads

–actin binding site

–ATPase activity

Two of the light chains necessary, other two regulatory for smooth muscle

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12
Q

Thin filaments

A

Two F-actin strands and two strands tropomyosin

Actin contains myosin binding sites

Troponin: 3 subunits, one binds Ca2+ and the other two bind tropomyosin and actin

Tropomyosin: regulatory protein that binds to actin and troponin (blocks active myosin binding sites)

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13
Q

Hinges of myosin

A

One allows head to reach up and grab onto the myosin filament, another is at the myosin head and grabs onto actin

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14
Q

Muscle Contraction Steps

A
  1. Mysoin head is attached to actin in rigor state
  2. ATP binds to myosin and myosin head releases actin
  3. Myosin hydrolyzes ATP to “cock” myosin head
  4. Myosin binds actin to form new cross bridge
  5. Phosphate is released and myosin head has power stroke
  6. ADP released
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15
Q

How would no ATP impact skeletal muscle contraction?

A
  1. Myosin head would not release actin
  2. Ca2+ not pumped out of cell via (Ca/H+) pump
  3. Ca2+ not pumped into SR
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16
Q

How are skeletal muscles activated? How many nerve action potentials are needed for a muscle action potential?

A

Motor nerve impulses

Every nerve action potential will cause a muscle action potential

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17
Q

What is the neurotransmitter released and ion that helps release it at neuromuscular junction?

18
Q

What kind of receptors does AcH in muscle cells bind to?

A

Ach binds to nicotinic receptor, increasing Na+ and K+ conductance

Depolarization because Na+ conductance has greater effect

19
Q

How does curare block muscle contraction?

A

Blocks Ach binding to nicotinic receptor completely

20
Q

Are you supposed to see end plate potentials?

A

NO! Every EPP=AP

if you see one, the neuromuscular transmission is fucked up (maybe Curare?)

21
Q

How does botulinum toxin block muscle contraction?

A

Cleaves V and T Snares on vesicles of presynaptic neuron

AcH is not released, muscle will not contract

22
Q

How would giving a patient with myasthenia gravis neostigmine (Acetylcholine esterase inhibitor) help treat their condition?

A

Neostigmine inhibits acetylcholinesterase

By blocking that enzyme, AcH builds up and not deraded, increases likelihood of muscle contraction

23
Q

T Tubules

A

Network of muscle cell membrane that carries depolarizations from action potentials

Contains DHP receptors that attach to ryanodine receptors on SR

24
Q

Sarcoplasmic reticulum

A

Stores calcium, releases it and re-uptakes it

Ryanodine receptors are opened by voltage-gated DHP receptors, cause release of Ca2+ into cell

Calsequestrin binds to calcium in SR to maintain low free conc.

SERCA helps pump Ca2+ in

25
Triad
T tubule SR--terminal cisternae
26
Excitation-Contraction Coupling
Action potential due to Na+ current leads to Ca2+ release into the cell from the sarcoplasmic reticulum AP causes depolarization of DHP receptor, which releah opens ryanodine channel and Ca2+ into cell from SR When done, SERCA pumps Ca back into cell
27
Maliganant hyperthermia
SR Ca2+ channels genetically altered, and this appears under anesthesia SR Ca2+ channels do not close properly, Ca2+ leaks into cytoplasm causing sustained contractions, generating heat (NOT GOOD!)
28
Isometric
Same length, contraction without shortening of muscle i.e. lifting bar
29
Isotonic
Same force, muscle contraction with shortening of muscle Lifting dumbell over and over again
30
Quantal summation
As more motor units are recruited, the strength of the muscle contraction increases
31
Temporal summation
Stimulating contractions at a higher frequency, causing increased strength
32
Treppe
after a long period of rest, initial muscle contraction may not be as strong as later stimuli of same strength (i.e. why warm up before working out)
33
Tetanization
Contrations so frequent muscle cannot relax bc Ca2+ not pumped into SR fast enough
34
Twitch contractions
Summate to one steady contraction
35
Passive tension
Tension developed by stretching muscle to diff. lengths
36
Active tension
Total tension-passive tension =degree overap between filaments capable of generating cross bridges
37
What happens to muscle as length increases above normal?
Tension before contraction increases and contractile force decreases at longer lengths At a long enough length, tension before contraction=total force, no contractile force generated
38
Resting length and filaments
Optimal overlap thin and thick filaments
39
Force-Velocity relationships
Velocity decreases as load increases Vmax constant for specific given skeletal muscle Load is so much, V=o at isometric contraction V=max when load is 0
40
When is active force maximum?
Normal length, resting length, or optimal length (all the same)
41
Fast fibers (white)
Larger fibers Fast twitch myosin isoform Less extensive blood supply No myoglobin; abundant glycolytic enzymes, fewer mitochondria
42
Slow fibers (red)
smaller fibers slow twitch myosin isoform more mitochondria, contain myoglobin extensive blood supply adapted for slow, continuous activity