Muscles Flashcards
(116 cards)
1
Q
What are the 2 categories of muscle?
A
Smooth and striated
2
Q
2 types of striated muscle
A
Skeletal (voluntary) and cardiac
3
Q
2 types of smooth muscle cell
A
Single or multi-unit
- has to do with how connected the cells are
4
Q
Muscle cell is also known as what other two things?
A
Muscle fiber and myocyte
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
6
Q
Muscle cells contain strands of…
A
Proteins called myofibrils
7
Q
Sarcomere
A
Subunit of myofibril
8
Q
I band
A
Distance between end of one thick filament and end of adjacent thick filament in another sarcomere
9
Q
A band
A
Distance of thick filament
10
Q
Z line/disc
A
Backbone of sarcomere
- Holds up the thin filaments
11
Q
H zone
A
Distance between thin filaments
12
Q
M line
A
Line that goes down the middle of the sarcomere (vertically)
13
Q
Titin
A
Large elastic protein that is made of titanium, and anchors the thick filaments to the thin filaments
14
Q
__ region is only thin filaments, while __ region is only thick filaments
A
I (band), H (zone)
15
Q
Draw two sarcomeres adjacently and label the I band, A band, Z lines, M line, H zone and titin
A
16
Q
In vertebrates, there’s _ thin to _ thick filament
A
2 thin to 1 thick filament
17
Q
Myosin heavy chain is composed of what 3 components?
A
Head, neck and tail
18
Q
The head on the myosin heavy chain contains what two things?
A
ATPase and an actin binding site
19
Q
The neck of the myosin heavy chain is…
A
Just the part where it bends
20
Q
Where is the essential myosin light chain located?
A
Just below the myosin head
21
Q
Where is the regulatory myosin light chain located?
A
At the neck of the myosin heavy chain
22
Q
True or false: myosin heavy chains are isolated
A
False; myosin heavy chains usually come in pairs
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
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
25
Actin monomers
- What do they contain?
g-actin, each contain a binding site for attachment with myosin cross bridge
26
Actin polymer
f-actin
27
Where is troponin located?
Scattered along the length of the thin filament
28
Where is tropomyosin located (and its general structure)?
Long strand-like protein
- sits on top of myosin binding sites by wrapping around actin filament
29
In f-actin alone, myosin binding site (is always/is not) available
Is always available
30
Thin filament is composed of which 3 things? What does this result in?
f-actin, tropomyosin and troponin
Results in regulated binding
31
Whole muscles are made of ______ which are packed with _____,which are packed with ______
Whole muscles are made of fascicles which are packed with muscle fibers, which are packed with myofibrils
32
What surround the fascicles and whole muscle? What is its composition?
Connective tissue sheaths around fascicles and whole muscle - stretchy (elastic)
33
How is muscle contraction defined?
When the cross-bridge cycle is occurring
34
Describe the cross-bridge cycle (6 steps)
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
35
What happens to muscles if there's Ca2+ present but no ATP?
Muscles seize up because ATP can't release the strong bond
- happens in rigor mortis, muscles seize up until protein decomposition occurs
36
TN-I function
Troponin I, acts as an anchor (attach troponin to g-actin)
37
TN-C function
Binds to Ca2+
38
TN-T function
Binds to tropomyosin
39
What happens to TN-I, TN-C, TN-T and TM "complex" upon Ca2+ binding to TN-C?
The chain straightens out, so TM does not bind to myosin binding site
40
During contraction, what happens to the Z lines?
The move toward each other
41
In a muscle fiber, contraction occurs in...
All sarcomeres simultanenously
42
During contraction, ____ and ____ both shorten
Sarcomeres and muscle fiber
- so cell is physically getting shorter
43
True or false: contraction and shortening are the same thing
False
- they are related, but they are not the same thing
44
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?
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
45
Assuming there is no ATP and no Ca2+ present, would you expect binding to occur in a mixture of thin filaments and myosin?
No
- myosin binding site on actin would be blocked by tropomyosin
46
During shortening, the A band (increases/decreases/stays the same length)
Stays the same length
47
During shortening, the I band (increases/decreases/stays the same length)
Decreases
48
During shortening, the H zone (increases/decreases/stays the same length)
Decreases
49
What are the 3 parts of a length-tension curve?
1. Ascending limb
2. Plateau
3. Descending limb
50
What causes the decrease in force (tension) at higher sarcomere lengths?
Decreased/no overlap between thin and thick filaments
51
Peak muscle force (tension) at the end of the plateau phase happens when?
Happens when all of the myosin heads overlap with the thin filaments
52
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?
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
What happens to the sarcomere band prior to the drop in tension at smaller sarcomere lengths?
A band compression -> A band is no longer a straight line in the sarcomere, which drastically decreases force (thin filaments getting distorted)
54
When thin filaments overlap, what happens to Ca2+ availability in the cytoplasm and the affinity of TN-C for Ca2+?
-less Ca2+ available in the cytoplasm
- TN-C will have lower affinity for Ca2+
55
What are the two types of synapses?
Electrical and chemical
56
Describe the contact between cells in electrical synapses
Direct contact between excitable cells
57
What links electrical synapses?
Channels called connexons
- permit many different ions to move through
58
Connexons are (unidirectional/bidirectional)
Bidirectional
59
Electrical synapses are (faster/slower) than chemical synapses
Faster (near synchronous signals)
60
Electrical synapses (sometimes/always) transmits signal
Always
61
What are two downsides of electrical synapses
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
What connects chemical synapses?
Chemical intermediates that cross the space (cleft) between cells
63
True or false: all chemical synapses are uniform
False
- Chemical synapses vary in type based on neurotransmitters and receptors
64
Chemical synapses are (unidirectional/bidirectional)
Unidirectional
65
True or false: chemical synapses can modulate signals and responses
True
66
What is a downside of chemical synapses?
There's more places for things to go wrong (because there's more parts to a chemical synapse)
67
Cells that surround axon terminal and provide support
Schwann cells (not the myelin Schwann cells, these Schwann cells just provide support)
68
Region of axon terminal where vesicles are
Active zone
69
Membrane of skeletal fiber in a neuromuscular junction is called...
Sarcolemma
70
Sarcolemma contains ______ folds, with what type of channels within these folds?
Junctional folds, containing ligand-gated ion channels specific to Ach (that lets Na+ into sarcolemma) and voltage-gated Na+ channels
71
Where are junctional folds located in the sarcolemma relative to the axon terminal in a neuromuscular junction?
Junctional folds located at each active zone
72
What channels are found on the axon terminal at the NMJ?
Voltage-gated Ca2+ channels
73
Where are SNAREs found in the NMJ? (2)
1. Found on vesicle
2. Found on axon terminal membrane in active zone
74
6 steps for stimulating a muscle at the neuromuscular junction
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
3 ways to classify chemical synapses
1. Fast vs. slow
2. Strong vs. weak
3. Excitatory vs. inhibitory
76
Receptor for fast chemical synapse
Ligand-gated ion channels
77
Receptor for slow chemical synapse
G-protein coupled receptors
78
Strong chemical synapse
1 EPSP is strong enough to reach threshold and trigger an action potential
79
Weak chemical synapse
Need multiple EPSPs to reach threshold and trigger an action potential
80
Excitatory vs inhibitory chemical synapses
Excitatory: depolarizes the cell
Inhibitory: hyperpolarizes the cell
81
Neuromuscular junction is a (fast/slow) chemical synapse
Fast
82
Neuromuscular junction is a (strong/weak) chemical synapse
Strong
83
Neuromuscular junction is a (excitatory/inhibitory) chemical synapse
Excitatory
84
How could signal transmission be disrupted on the presynaptic side of the NMJ? (4)
Disrupting SNAREs, disrupting voltage-gated Ca2+ channels, problem with neurotransmitter formation/packaging into vesicles, not enough vesicle formation
85
After an action potential is produced at the NMJ in the sarcolemma, how does the action potential get carried deep into the cell?
Travels down T-tubules
86
T-tubules contain...
A DHPR (type of receptor), which is voltage-sensitive
87
Sarcoplasmic reticulum contains...
A RyR (type of receptor), which is a Ca2+ channel
88
DHPR and RyR are...
Physically linked
89
Describe what happens after the action potential travels down the T-tubule (4 steps)
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
What would happen if you stimulate a muscle fiber repeatedly?
Continuously triggering opening of Ca2+ channels -> leads to continual contraction
91
Myasthenia gravis is an autoimmune disease where antibodies block or destroy AChRs. How would this disease impact muscular function?
Signal from NMJ no longer received -> muscle is paralyzed
92
What are two ways that the signal is stopped at the neuromuscular junction to end contraction?
1. Enzyme breaks ACh down
2. A little ACh diffuses out (but most ACh is degraded by acetylcholinesterases)
93
True or false: acetylcholinesterase is always running
True. It is always running but the enzyme gets overwhelmed by so much ACh that it can't keep up
94
How is Ca2+ removed from the cytoplasm after muscle contraction?
ATP-dependent pump constantly moves Ca2+ back into sarcoplasmic reticulum
95
What is latency?
The delay between muscle excitation and subsequent events
- Key idea: stuff takes time!
- Excitation, then Ca2+ release, then force, then shortening
96
Contraction vs. shortening
Contraction: Cross-bridge cycles are occurring
Shortening: The actual physical change in size of the sarcomere
97
Concentric contraction and example
Generating force and length is getting shorter
ex: shoulder muscle as you raise your arm to the side
98
Eccentric contraction and example
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
Isometric contraction and example
Generating force and no length change
ex: Quad muscle during a wall sit
100
Isometric vs. isotonic contraction
Isometric: constant length of muscle
Isotonic contraction: Constant force in muscle (can only occur in lab setting because force is typically a vector)
101
Draw the length-tension graph for sarcomeres, the elasticity of a muscle and the whole muscle
(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
What are the 4 sources of elasticity in a muscle?
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
Draw the force-velocity relationship in single myofibril, a single muscle fiber or a constant number of fibers
104
What does the boost in force come from when shortening velocity is negative?
Eccentric contraction, boost comes from elasticity
105
How are cross-bridges the source of the force/velocity trade-off? (2)
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
What is the source of the trade-off between force and velocity?
Cross-bridges are the source of this trade-off
106
Where is contraction force at its maximum on the force-velocity curve?
Starts at isometric contraction (y-intercept) and increases to a plateau for the eccentric contraction
107
True or false: the shape of relationship curves are the same in all species
False; exact shape of relationships vary across species.
108
What are three sources of the variation in the shape of relationships across species?
1. Length of filaments (invertebrates only)
2. Speed of ATPase in the myosin head
3. Affinity of troponin for Ca2+
109
What is the x-intercept on a force-velocity curve?
Vmax
110
When a sarcomere shortens at rate x, what happens to the Z lines, myofibril with 3 sarcomeres and the ends of this same myofibril?
- 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
Sarcomeres in _____ boost force
Parallel
- More sarcomeres in parallel means more myofibrils packed in which produces more force.
112
True or false: in strength training, we change the number of fibers and their arrangement
False
- in strength training, we make each fiber bigger in diameter by adding more myofibrils
113
What controls rotation around a joint? What does the load inlude?
- Skeletal muscle
- Load includes everything the muscle is moving (e.g. weight of forearm, bone, etc).
114
True or false: relaxation and lengthening mean the same thing
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
_____ muscles stretch muscles back to starting length
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.
