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ZOOL 461 > Muscles > Flashcards

Muscles Flashcards

1
Q

What are the 2 categories of muscle?

A

Smooth and striated

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2
Q

2 types of striated muscle

A

Skeletal (voluntary) and cardiac

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3
Q

2 types of smooth muscle cell

A

Single or multi-unit
- has to do with how connected the cells are

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4
Q

Muscle cell is also known as what other two things?

A

Muscle fiber and myocyte

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5
Q

Skeletal muscles are (uninucleated/multinucleated)
- explain why

A

Multinucleate (fusion of precursor cells)
- Important because there’s a lot of metabolism which requires a lot of DNA

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6
Q

Muscle cells contain strands of…

A

Proteins called myofibrils

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7
Q

Sarcomere

A

Subunit of myofibril

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8
Q

I band

A

Distance between end of one thick filament and end of adjacent thick filament in another sarcomere

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9
Q

A band

A

Distance of thick filament

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10
Q

Z line/disc

A

Backbone of sarcomere
- Holds up the thin filaments

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11
Q

H zone

A

Distance between thin filaments

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12
Q

M line

A

Line that goes down the middle of the sarcomere (vertically)

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13
Q

Titin

A

Large elastic protein that is made of titanium, and anchors the thick filaments to the thin filaments

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14
Q

__ region is only thin filaments, while __ region is only thick filaments

A

I (band), H (zone)

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15
Q

Draw two sarcomeres adjacently and label the I band, A band, Z lines, M line, H zone and titin

A
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16
Q

In vertebrates, there’s _ thin to _ thick filament

A

2 thin to 1 thick filament

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17
Q

Myosin heavy chain is composed of what 3 components?

A

Head, neck and tail

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18
Q

The head on the myosin heavy chain contains what two things?

A

ATPase and an actin binding site

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19
Q

The neck of the myosin heavy chain is…

A

Just the part where it bends

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20
Q

Where is the essential myosin light chain located?

A

Just below the myosin head

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21
Q

Where is the regulatory myosin light chain located?

A

At the neck of the myosin heavy chain

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22
Q

True or false: myosin heavy chains are isolated

A

False; myosin heavy chains usually come in pairs

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23
Q

Describe the thick filament structure in general

A

Tails form “body” of filament and heads stick out
- Tails pointing toward the middle of the thick filament with head pairs sticking out

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24
Q

Where is the “bare zone” in the thick filament?

A

The area where there are no myosin heads in the center of the thick filament

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25
Q

Actin monomers
- What do they contain?

A

g-actin, each contain a binding site for attachment with myosin cross bridge

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26
Q

Actin polymer

A

f-actin

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27
Q

Where is troponin located?

A

Scattered along the length of the thin filament

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28
Q

Where is tropomyosin located (and its general structure)?

A

Long strand-like protein
- sits on top of myosin binding sites by wrapping around actin filament

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29
Q

In f-actin alone, myosin binding site (is always/is not) available

A

Is always available

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30
Q

Thin filament is composed of which 3 things? What does this result in?

A

f-actin, tropomyosin and troponin
Results in regulated binding

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31
Q

Whole muscles are made of ______ which are packed with _____,which are packed with ______

A

Whole muscles are made of fascicles which are packed with muscle fibers, which are packed with myofibrils

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32
Q

What surround the fascicles and whole muscle? What is its composition?

A

Connective tissue sheaths around fascicles and whole muscle - stretchy (elastic)

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33
Q

How is muscle contraction defined?

A

When the cross-bridge cycle is occurring

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34
Q

Describe the cross-bridge cycle (6 steps)

A
  1. ATP bound to myosin head, which bends neck
  2. ATPase hydrolyzes ATP -> releases energy, which pulls back on myosin head (straightens neck) -> charges “spring” in myosin
  3. Actin + myosin get closer and associate in a weak bond (reversible)
  4. Pi leaves myosin -> releases energy from “spring” -> head snaps into bent conformation -> pulls on actin as it bends -> usually moves thin filament, results in muscle force aka power stroke. Strong bond between actin and myosin in this step (irreversible)
  5. ADP leaves myosin
  6. New ATP binds to myosin head -> binding of new ATP is what releases the strong bond
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35
Q

What happens to muscles if there’s Ca2+ present but no ATP?

A

Muscles seize up because ATP can’t release the strong bond
- happens in rigor mortis, muscles seize up until protein decomposition occurs

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36
Q

TN-I function

A

Troponin I, acts as an anchor (attach troponin to g-actin)

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37
Q

TN-C function

A

Binds to Ca2+

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38
Q

TN-T function

A

Binds to tropomyosin

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39
Q

What happens to TN-I, TN-C, TN-T and TM “complex” upon Ca2+ binding to TN-C?

A

The chain straightens out, so TM does not bind to myosin binding site

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40
Q

During contraction, what happens to the Z lines?

A

The move toward each other

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41
Q

In a muscle fiber, contraction occurs in…

A

All sarcomeres simultanenously

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42
Q

During contraction, ____ and ____ both shorten

A

Sarcomeres and muscle fiber
- so cell is physically getting shorter

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43
Q

True or false: contraction and shortening are the same thing

A

False
- they are related, but they are not the same thing

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44
Q

Assuming there is no ATP and no Ca2+ present, would you expect binding to occur in a mixture of pure g-actin (no troponin or tropomyosin) and myosin?

A

Yes, you would get a weak bond but no strong bonding as there is no ATP to be hydrolyzes for this strong bond to eventually occur in cross-bridge cycling

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45
Q

Assuming there is no ATP and no Ca2+ present, would you expect binding to occur in a mixture of thin filaments and myosin?

A

No
- myosin binding site on actin would be blocked by tropomyosin

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46
Q

During shortening, the A band (increases/decreases/stays the same length)

A

Stays the same length

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47
Q

During shortening, the I band (increases/decreases/stays the same length)

A

Decreases

48
Q

During shortening, the H zone (increases/decreases/stays the same length)

A

Decreases

49
Q

What are the 3 parts of a length-tension curve?

A
  1. Ascending limb
  2. Plateau
  3. Descending limb
50
Q

What causes the decrease in force (tension) at higher sarcomere lengths?

A

Decreased/no overlap between thin and thick filaments

51
Q

Peak muscle force (tension) at the end of the plateau phase happens when?

A

Happens when all of the myosin heads overlap with the thin filaments

52
Q

In the ascending limb of the length-tension curve, what causes the lower tension at smaller sarcomere lengths? What happens to the H zone in this scenario?

A

Thin filaments from opposite sides start to overlap with each other. This decreases the force because the thin filaments are getting in each others way, and the thick filaments on one side can’t bind to the thin filaments on the opposite side.
- There is no longer an H zone because there’s no gap between our thin filaments

53
Q

What happens to the sarcomere band prior to the drop in tension at smaller sarcomere lengths?

A

A band compression -> A band is no longer a straight line in the sarcomere, which drastically decreases force (thin filaments getting distorted)

54
Q

When thin filaments overlap, what happens to Ca2+ availability in the cytoplasm and the affinity of TN-C for Ca2+?

A

-less Ca2+ available in the cytoplasm
- TN-C will have lower affinity for Ca2+

55
Q

What are the two types of synapses?

A

Electrical and chemical

56
Q

Describe the contact between cells in electrical synapses

A

Direct contact between excitable cells

57
Q

What links electrical synapses?

A

Channels called connexons
- permit many different ions to move through

58
Q

Connexons are (unidirectional/bidirectional)

A

Bidirectional

59
Q

Electrical synapses are (faster/slower) than chemical synapses

A

Faster (near synchronous signals)

60
Q

Electrical synapses (sometimes/always) transmits signal

A

Always

61
Q

What are two downsides of electrical synapses

A

Not selective about what ions are passed (i.e. toxins can also be passed), and no fine-tuning signals (because they’re so fast)

62
Q

What connects chemical synapses?

A

Chemical intermediates that cross the space (cleft) between cells

63
Q

True or false: all chemical synapses are uniform

A

False
- Chemical synapses vary in type based on neurotransmitters and receptors

64
Q

Chemical synapses are (unidirectional/bidirectional)

A

Unidirectional

65
Q

True or false: chemical synapses can modulate signals and responses

A

True

66
Q

What is a downside of chemical synapses?

A

There’s more places for things to go wrong (because there’s more parts to a chemical synapse)

67
Q

Cells that surround axon terminal and provide support

A

Schwann cells (not the myelin Schwann cells, these Schwann cells just provide support)

68
Q

Region of axon terminal where vesicles are

A

Active zone

69
Q

Membrane of skeletal fiber in a neuromuscular junction is called…

A

Sarcolemma

70
Q

Sarcolemma contains ______ folds, with what type of channels within these folds?

A

Junctional folds, containing ligand-gated ion channels specific to Ach (that lets Na+ into sarcolemma) and voltage-gated Na+ channels

71
Q

Where are junctional folds located in the sarcolemma relative to the axon terminal in a neuromuscular junction?

A

Junctional folds located at each active zone

72
Q

What channels are found on the axon terminal at the NMJ?

A

Voltage-gated Ca2+ channels

73
Q

Where are SNAREs found in the NMJ? (2)

A
  1. Found on vesicle
  2. Found on axon terminal membrane in active zone
74
Q

6 steps for stimulating a muscle at the neuromuscular junction

A
  1. Action potential opens voltage-gated Ca2+ channel
  2. SNAREs link up between vesicle and membrane
  3. Exocytosis
  4. Diffusion across synaptic cleft
  5. Ach binds to AchRs (ligand-gated Na+ channels), causes Na+ channels to open, Na+ enters fiber. This causes a slight depolarization at the membrane where Ach binds, causing an excitatory post-synaptic potential (EPSP), which is like a little “flicker” of depolarization -> rise from Na+; fall as channels randomly close.
  6. EPSP opens voltage-gated Na+ channels causing a depolarization of the post-synaptic cell, resulting in an action potential.
75
Q

3 ways to classify chemical synapses

A
  1. Fast vs. slow
  2. Strong vs. weak
  3. Excitatory vs. inhibitory
76
Q

Receptor for fast chemical synapse

A

Ligand-gated ion channels

77
Q

Receptor for slow chemical synapse

A

G-protein coupled receptors

78
Q

Strong chemical synapse

A

1 EPSP is strong enough to reach threshold and trigger an action potential

79
Q

Weak chemical synapse

A

Need multiple EPSPs to reach threshold and trigger an action potential

80
Q

Excitatory vs inhibitory chemical synapses

A

Excitatory: depolarizes the cell
Inhibitory: hyperpolarizes the cell

81
Q

Neuromuscular junction is a (fast/slow) chemical synapse

A

Fast

82
Q

Neuromuscular junction is a (strong/weak) chemical synapse

A

Strong

83
Q

Neuromuscular junction is a (excitatory/inhibitory) chemical synapse

A

Excitatory

84
Q

How could signal transmission be disrupted on the presynaptic side of the NMJ? (4)

A

Disrupting SNAREs, disrupting voltage-gated Ca2+ channels, problem with neurotransmitter formation/packaging into vesicles, not enough vesicle formation

85
Q

After an action potential is produced at the NMJ in the sarcolemma, how does the action potential get carried deep into the cell?

A

Travels down T-tubules

86
Q

T-tubules contain…

A

A DHPR (type of receptor), which is voltage-sensitive

87
Q

Sarcoplasmic reticulum contains…

A

A RyR (type of receptor), which is a Ca2+ channel

88
Q

DHPR and RyR are…

A

Physically linked

89
Q

Describe what happens after the action potential travels down the T-tubule (4 steps)

A
  1. DHPR changes shape
  2. Physical link makes RyR change shape too
  3. Ca2+ “spills out” of sarcoplasmic reticulum
  4. Ca2+ causes muscle contraction
90
Q

What would happen if you stimulate a muscle fiber repeatedly?

A

Continuously triggering opening of Ca2+ channels -> leads to continual contraction

91
Q

Myasthenia gravis is an autoimmune disease where antibodies block or destroy AChRs. How would this disease impact muscular function?

A

Signal from NMJ no longer received -> muscle is paralyzed

92
Q

What are two ways that the signal is stopped at the neuromuscular junction to end contraction?

A
  1. Enzyme breaks ACh down
  2. A little ACh diffuses out (but most ACh is degraded by acetylcholinesterases)
93
Q

True or false: acetylcholinesterase is always running

A

True. It is always running but the enzyme gets overwhelmed by so much ACh that it can’t keep up

94
Q

How is Ca2+ removed from the cytoplasm after muscle contraction?

A

ATP-dependent pump constantly moves Ca2+ back into sarcoplasmic reticulum

95
Q

What is latency?

A

The delay between muscle excitation and subsequent events
- Key idea: stuff takes time!
- Excitation, then Ca2+ release, then force, then shortening

96
Q

Contraction vs. shortening

A

Contraction: Cross-bridge cycles are occurring
Shortening: The actual physical change in size of the sarcomere

97
Q

Concentric contraction and example

A

Generating force and length is getting shorter
ex: shoulder muscle as you raise your arm to the side

98
Q

Eccentric contraction and example

A

Generating force and length is getting longer
- cross-bridge cycle is occurring, but muscle is getting longer; the cross-bridges allow for control of muscle lengthening
ex: Triceps during descending phase of overhead extension

99
Q

Isometric contraction and example

A

Generating force and no length change
ex: Quad muscle during a wall sit

100
Q

Isometric vs. isotonic contraction

A

Isometric: constant length of muscle
Isotonic contraction: Constant force in muscle (can only occur in lab setting because force is typically a vector)

101
Q

Draw the length-tension graph for sarcomeres, the elasticity of a muscle and the whole muscle

A

(the sarcomere curve is smoothed out because we’re looking at the whole muscle now (lots of sarcomeres) and the sarcomeres aren’t all in sync)

102
Q

What are the 4 sources of elasticity in a muscle?

A
  1. Myosin neck (small contribution)
  2. Sarcolemma - cell membrane itself has a little stretchiness (also a small contribution)
  3. Connective tissue sheaths
  4. Tendon -> works like a really stiff rubber band
103
Q

Draw the force-velocity relationship in single myofibril, a single muscle fiber or a constant number of fibers

A
104
Q

What does the boost in force come from when shortening velocity is negative?

A

Eccentric contraction, boost comes from elasticity

105
Q

How are cross-bridges the source of the force/velocity trade-off? (2)

A
  1. Fewer cross-bridges are able to attach at any given time at higher shortening velocities, reducing the force the muscle can produce.
  2. Cross-bridges don’t detach fast enough at higher shortening velocities to maintain force.
105
Q

What is the source of the trade-off between force and velocity?

A

Cross-bridges are the source of this trade-off

106
Q

Where is contraction force at its maximum on the force-velocity curve?

A

Starts at isometric contraction (y-intercept) and increases to a plateau for the eccentric contraction

107
Q

True or false: the shape of relationship curves are the same in all species

A

False; exact shape of relationships vary across species.

108
Q

What are three sources of the variation in the shape of relationships across species?

A
  1. Length of filaments (invertebrates only)
  2. Speed of ATPase in the myosin head
  3. Affinity of troponin for Ca2+
109
Q

What is the x-intercept on a force-velocity curve?

A

Vmax

110
Q

When a sarcomere shortens at rate x, what happens to the Z lines, myofibril with 3 sarcomeres and the ends of this same myofibril?

A
  • One sarcomere: Z-lines move toward each other at rate X
  • Myofibril: individual sarcomeres each shorten at rate x
  • Ends of myofibril get closer at rate of 3x (so there is a boost in shortening velocity by having a longer myofibril)
111
Q

Sarcomeres in _____ boost force

A

Parallel
- More sarcomeres in parallel means more myofibrils packed in which produces more force.

112
Q

True or false: in strength training, we change the number of fibers and their arrangement

A

False
- in strength training, we make each fiber bigger in diameter by adding more myofibrils

113
Q

What controls rotation around a joint? What does the load inlude?

A
  • Skeletal muscle
  • Load includes everything the muscle is moving (e.g. weight of forearm, bone, etc).
114
Q

True or false: relaxation and lengthening mean the same thing

A

False
- Relaxation means we are not contracting (cross-bridges are not happening)
- Lengthening means we are getting bigger). This needs some external factor lengthening the muscle.

115
Q

_____ muscles stretch muscles back to starting length

A

Opposing
- Muscles cannot “push” themselves back to their lengthened state on their own. Opposing (antagonistic) muscles provide the necessary force to stretch the muscle that just contracted, restoring it to its original length and preparing it for the next contraction.

ZOOL 461 (11 decks)

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