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Physiology > B1W3: Skeletal Muscle > Flashcards

B1W3: Skeletal Muscle Flashcards

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?

A

AcH

Ca2+

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
Q

Triad

A

T tubule

SR–terminal cisternae

26
Q

Excitation-Contraction Coupling

A

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
Q

Maliganant hyperthermia

A

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
Q

Isometric

A

Same length, contraction without shortening of muscle

i.e. lifting bar

29
Q

Isotonic

A

Same force, muscle contraction with shortening of muscle

Lifting dumbell over and over again

30
Q

Quantal summation

A

As more motor units are recruited, the strength of the muscle contraction increases

31
Q

Temporal summation

A

Stimulating contractions at a higher frequency, causing increased strength

32
Q

Treppe

A

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
Q

Tetanization

A

Contrations so frequent muscle cannot relax bc Ca2+ not pumped into SR fast enough

34
Q

Twitch contractions

A

Summate to one steady contraction

35
Q

Passive tension

A

Tension developed by stretching muscle to diff. lengths

36
Q

Active tension

A

Total tension-passive tension

=degree overap between filaments capable of generating cross bridges

37
Q

What happens to muscle as length increases above normal?

A

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
Q

Resting length and filaments

A

Optimal overlap thin and thick filaments

39
Q

Force-Velocity relationships

A

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
Q

When is active force maximum?

A

Normal length, resting length, or optimal length (all the same)

41
Q

Fast fibers (white)

A

Larger fibers

Fast twitch myosin isoform

Less extensive blood supply

No myoglobin; abundant glycolytic enzymes, fewer mitochondria

42
Q

Slow fibers (red)

A

smaller fibers

slow twitch myosin isoform

more mitochondria, contain myoglobin

extensive blood supply

adapted for slow, continuous activity

Physiology (9 decks)

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