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A&P I (Fall 2022) > Skeletal Muscle Physiology pt.1 (Exam III) > Flashcards

Skeletal Muscle Physiology pt.1 (Exam III) Flashcards

1
Q

What organ system is the largest contributor to body weight and ICF volume in non-obese people?

In addition to fluid volume, what else does this body system store?

A

Skeletal Muscle System

Ions and proteins

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2
Q

What’s an example given in class of exceptionally fine motor control?

A

Voicebox Control

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3
Q

What organ system is the primary source of basal bodily temperature?
What is the prototypical basal body temperature?

A

Skeletal Muscle

37°C

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4
Q

What energy source is stored in skeletal muscle?

Describe the basic structure of these molecules?

A

Glycogen

Glycogen is essentially chains of glucose stuck together.

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5
Q

What type of glucose transporters do skeletal muscles use? Are these insulin-dependent or independent?

What is the relevance of this if a large dose of insulin is given?

A

Glut-4, Insulin Dependent transporters

↑ insulin dose = skeletal muscle absorbing excessive glucose from bloodstream.

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6
Q

How does the skeletal muscle contribute to body temperature when at rest?

A

Basal Resting Tone = Small, unnoticeable relaxations/contractions.

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7
Q

Describe the physiologic anatomy of a skeletal muscle all the way down to the cellular components.

A
  1. Muscle
  2. Fasciculous
  3. Muscle Fiber
  4. Myofibril
  5. Sarcomere
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8
Q

What are motor units?

A

Collection of muscle fibers that are innervated by a single A-α neuron.

verify that this is correct and a decent summary

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9
Q

Between small motor units and large motor units, which one is recruited for tasks first?

What does this allow for? What would be the result without this setup.

A

Small motor units

Precise movement and control. Without this we be clunky and do things like take notes using out biceps/triceps.

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10
Q

Which motor units uses smaller A-α neurons? Large A-α neurons?

A

Small motor units
Large motor units

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11
Q

Which type of skeletal muscle is characterized by increased levels of myoglobin and mitochondria?

Why is this muscle the color that it is?

How efficient is this muscle?

A

Type 1 - Red “slow” Muscle

Red due to the increased presence of Fe+ found in the myoglobin.

Very efficient

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12
Q

What type of skeletal muscle is characterized by very little myoglobin and fewer mitochondria?

Why is this muscle the color that it is?

How efficient is this muscle?

A

Type 2 - White “Fast-Twitch” Muscle.

Lack of myoglobin

Not as efficient, only used for short burst of movement.

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13
Q

Why does Myoglobin contain Fe+?

A

Fe+ in the myoglobin pulls O₂ from the blood into the skeletal muscle for use.

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14
Q

Why is red meat theorized to cause cancer?

How does this connect to men’s and women’s multivitamins?

A

Due to oxidizing effects of Fe+ over time.

Men’s multivitamins have no Fe+ while women’s generally do have some Fe+ due to monthly menstruation.

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15
Q

Give an example of a type 1 fiber muscle in humans?

Give an example of a type 2 fiber muscle in humans?

A
  • Soleus - supports body weight during long periods of standing.
  • Ocular muscles.
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16
Q

Between actin and myosin filaments, Which is considered “thinner”?

A
  • Actin = thin
  • Myosin = thick
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17
Q

What structure is denoted by 1 on the figure below?

What is this, essentially?

A
  • Sarcolemma
  • The cell wall of the muscle
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18
Q

What structure is denoted by 5 on the figure below?

A

Sarcoplasmic Reticulum

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19
Q

What 3 things should be known about our sarcoplasmic reticulum (SR)?

A
  1. SR replaces the ER in muscle cells
  2. Ca⁺⁺ storage
  3. ICF of cell (verify)
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20
Q

What structure is denoted by 6 on the figure below?

What purpose does this structure serve?

A

Transverse Tubule

Facilitates Action Potential Propagation

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21
Q

What structure is denoted by 15 on the figure below?

A

Myofibrils

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22
Q

What is the functional unit of skeletal muscle?

A

Sarcomere

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23
Q

Darker bands in the sarcomere are indicative of what cellular component?

A

myosin

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24
Q

What is the fluid inside a muscle cell called?

A

Sarcoplasm

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25
Q

What structure is denoted by 1 on the figure below?

A

Myosin

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26
Q

What structure is denoted by 2 on the figure below?

A

M-Line

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27
Q

What structure is denoted by 3 on the figure below?

What is the purpose of this structure?

A

Titin (made of Elastin)

Titin anchors the Myosin into the Z-disk.

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28
Q

What structure is denoted by 5 on the figure below?

A

Actin

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29
Q

What structure is denoted by 4 on the figure below?

A

Z-Disk

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30
Q

What comprises the I-Band?

A

Actin only

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31
Q

What comprises the A-band?

A

Actin and Myosin overlap

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32
Q

What comprises the H-band (H-zone)?

A

Myosin only

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33
Q

What demarcates the M-Line?

A

The very middle of the Myosin filament

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34
Q

What structure is denoted by 1 on the figure below?

A

Sarcomere

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35
Q

What Band is denoted by 2 on the figure below?

A

I-Band

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36
Q

What Band is denoted by 3 on the figure below?

What comprises this band?

A

A-Band

Myosin + Actin

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37
Q

What Band is denoted by 4 on the figure below?

What comprises this band?

What would the middle of this band be considered?

A

H-Band

Myosin Only

The M-Line

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38
Q

When talking about sarcomere bands, what occurs during contraction?

A

I-Band is pulled to A-Band

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39
Q

When may the I-band become unviewable?

A

During contraction as it is pulled into the A-Band.

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40
Q

What structure is by the cross-section denoted by 2 on the figure below? What makes up this cross-section?

A

I-Band cross-section

Actin Filaments

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41
Q

What structure is noted by the cross-section labeled 3 on the figure below? What makes up this cross-section?

A

H-Band cross-section

Myosin Filaments

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42
Q

What structure is by the cross-section denoted by 5 on the figure below? What makes up this cross-section?

A

A-Band cross-section

Myosin + Actin Filaments

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43
Q

Where specifically do myosin and actin bind to initiate pulling?

A

Myosin heads

44
Q

During skeletal muscle contraction, what occurs to the following:
1. A-Band
2. I-Band
3. H-Band
4. Z-Disk

A
  1. A-Band doesn’t change in width.
  2. I-Band’s shrink and may become masked
  3. H-Bands disappear
  4. Z-Disks move closer together
45
Q

Why do skeletal muscle cells have multiple nuclei?

A

Cell support for things such as mRNA protein synthesis.

46
Q

Skeletal muscles are often as long as neurons, what differentiates the two in terms of cellular homeostasis?

A

Neurons possess axonal transport system for movement of things such as proteins. Skeletal muscles do not and therefore have multiple nuclei to accomplish the same goal.

wordy

47
Q

Which two organelles does the skeletal sarcomere possess in greater quantities than most cells?

A

Mitochondria and Nuclei

48
Q

Which type of muscle fiber exhibits more inefficiency?

A

White “Fast Twitch” Type 2 Muscle Fibers

49
Q

What composes a myosin molecule?

Which sub-component of this molecule makes up the myosin head?

What do hundreds of these myosin molecules form when twisted together?

A

2 heavy chains and 4 light chains.

Myosin heads are composed of light chains.

Myosin Filament

50
Q

Myosin heads possess a high affinity for active sites on _________.

A

F-Actin

51
Q

Which part of the myosin filament cleaves ATP to do work?

A

Myosin heads

52
Q

What two structures, twisted together, form an Actin filament?

Which of these has active sites for binding with myosin?

A

Tropomyosin and F-actin.

F-actin possesses the active sites.

53
Q

In broad strokes, how are the active sites of an actin filament revealed for binding to myosin heads?

A
  1. Ca⁺⁺ interacts w/ Troponin C
  2. Troponin C → Troponin T and Troponin I to unwind Tropomyosin and F-actin.
  3. Binding site on F-actin revealed due to unwinding.
54
Q

Which component of an Actin filament “hides” the myosin head binding sites?

A

Tropomyosin hides active sites of the F-actin.

55
Q

Which troponin molecules is bound by Ca⁺⁺?

Which troponin molecule is bound to F-actin?

Which troponin molecule is bound to tropomyosin?

A

Troponin C

Troponin I

Troponin T

56
Q

What conditions characterize a myosin head at rest “cocked” state?

A

ADP and Phosphate attached to Myosin head

No connection to Actin

57
Q

What step occurs after the “cocked” state of cross-bridge cycling?

A

Weak Cross-Bridge State:

Myosin head with ADP and P is bound to active site of F-Actin.

58
Q

What characterizes the Strong Cross-Bridge State?

A

ADP attached to myosin head, phosphate has been sheared off.

Contraction occurs from this state (need to verify)

59
Q

When does phosphate leave the myosin head?

A

In-between the weak cross-bridge and the strong cross-bridge states.

60
Q

What phase follows myosin contraction?

A

Post-powerstroke phase

61
Q

What occurs between the post-powerstroke phase and the attached state?

A

ADP leaves the myosin head.

62
Q

What characterizes the attached state of cross-bridge cycling?

What is required to “unstick” the muscle so that it’s not frozen in the contracted state?

A

Myosin head with no ADP/ATP or phosphate attached to F-actin.

ATP has to attach to myosin head to free it from F-Actin sites.

63
Q

What occurs in the released state of cross-bridge cycling?

A

ATP is hydrolyzed (becoming ADP) leaving the myosin head in an at rest (stretched) state.

64
Q

What are the 6 phases of Cross-Bridge Cycling?

A
  1. Cocked
  2. Weak Cross-Bridge
  3. Strong Cross-Bridge
  4. Post-Powerstroke
  5. Attached
  6. Released
65
Q

What neurotransmitter is always used at the NMJ?

What receptor is used at NMJ’s?

A

ACh

Nicotinic ACh (nACh)

66
Q

What is used in the post-synaptic vesicle to increase surface area for ACh receptors?

A

Sub-Neural Clefts = “Invaginations” ~ pockets to ↑ cell surface area

67
Q

Why does a pathology like myasthenia gravis take a long time to become debilitating?

A

NMJ’s have excessive ACh and excessive ACh Receptors. This is a safety mechanism so we always have more neurotransmitters and receptors than necessary.

68
Q

How many nACh receptors are at each NMJ?

A

5 million

69
Q

How much of neurotransmitter and nACh capacity are typically utilized? How much does this leave in reserve?

A

10%

90% reserve.

70
Q

What is required for conformational change of an nACh receptors?

A

2 Acetylcholine molecules

71
Q

What are the subunits of an adult ACh receptor?

A

2 α subunits
1 β subunit
1 δ subunit (delta)
1 ε subunit (epsilon)

72
Q

Which subunits of a nACh receptor are bound by ACh?

A

The 2 α subunits

73
Q

Depolarization from a post-synaptic cell is called ____________.

What’s a good way to think of this depolarization?

A

End-Plate Depolarization

This is the depolarization needed to meet the threshold for an Action Potential.

74
Q

What primary ion comes through an nACh receptor when activated?

Can any other ions come through?

A

Na⁺

Ca⁺⁺ (much smaller amount) and K⁺ (no real movement)

75
Q

What structure helps facilitate rapid depolarization deep into muscle cells?

What type of channel is located in this structure to facilitate this effect?

A

Transverse “T”-Tubules

V-G Na⁺ channels

76
Q

What receptors are located along transverse tubules (and the cell wall) that open up the sarcoplasmic reticulum?

Does this structure become bound?

A

DHP (Dihydropyridine) Ca⁺⁺ Channel Receptor

No, this receptor is not bound, only activated by action potential.

77
Q

What structure is physically coupled to DHP receptors?

Where is this structure located?

A

Ca⁺⁺ Release Channel (RyR)

Located on Sarcoplasmic Reticulum

78
Q

During an action potential, by what process and from where does Ca⁺⁺ release intracellularly?

A
  1. AP activated DHP Receptor
  2. DHP receptor opens RyR Channel
  3. Ca⁺⁺ spills from SR to the ICF.
79
Q

Whats another name for the RyR receptor?

A

Ryanodine receptor

80
Q

How is Ca⁺⁺ reabsorbed back into the sarcoplasmic reticulum?

Is this through facilitated diffusion?

A

SERCA (SarcoEndoplasmic Reticulum Ca⁺⁺ ATPase Pump)

No, this process requires ATP due to steep Ca⁺⁺ gradient.

81
Q

By which two general methods is Ca⁺⁺ pumped across a concentration gradient?

A

Direct Ca⁺⁺ pump

Antiporter pump (3 Na⁺ for 1 Ca⁺⁺)

82
Q

What protein makes it possible for there to be massive Ca⁺⁺ stores in the sarcoplasmic reticulum?

A

Calsequestrin (binds many Ca⁺⁺ pumped in by SERCA’s)

83
Q

In a healthy adult how does the End-Plate Potential (EPP) generated by ACh binding, compare to the threshold needed for an action potential?

A

The EPP in a healthy adult is much greater than the threshold needed for an action potential.

84
Q

Where is AChEsterase produced?

A

Post-Synaptic Skeletal Muscle Cell of the NMJ

85
Q

What happens to ACh that ends up in the plasma?

A

Destroyed by PlasmaCholineEsterase (PlasmaChE)

86
Q

What was one possible used of AChE Inhibitors discussed in lecture?

What two side effects of AChE Inhibitors were very briefly discussed in lecture?

A

Treatment of Dementia (↑ ACh = ↑ Awareness)

↓ HR and ↑ Mucus production

87
Q

In the event of a tendon rupture (say Achilles Tendon) what would the function of this muscle be post-repair?

What type of repair would be better, suturing tendon portions back together, or pulling tendon taut and screwing it into the calcaneus?

A

Function would never be 100% again due to loss of optimal stretch.

Suturing would be the better option but 100% of function could not be returned to.

88
Q

In the depiction below, which letter(s) would be considered “optimal stretch”?

Which letter(s) would be considered overstretch?

Which letter(s) would be considered understretched?

With which letter(s) would be a contraction be possible?

A

Optimal Stretch = B & C (C is slightly better)

Overstretch = D

Understretched = A & E (A being worse)

Contraction possibility = E, B, & C (E sub-optimal)

89
Q

Describe in layman’s terms, the significance of the blue line below?

A

Blue Line = Passive tension of muscle at rest

90
Q

Describe in layman’s terms, the significance of the green line below?

A

Green Line = Active tension of muscle during contraction

91
Q

Describe in layman’s terms, the significance of the red line below?

A

Red Line = Active tension of muscle during contraction + passive tension of muscle at rest

92
Q

What drugs are given for reversal of -curare paralytics?

Why do these drugs have unintended side effects aside from paralysis reversal?

A

AChE Inhibitors (-stigmines)

AChE inhibition is not specific to NMJ and happens anywhere with ACh receptors.

93
Q

Describe the Load/Contraction Velocity Diagram’s basic premise

A

↑ Load = ↓ contraction speed.

Heavy things can’t be moved quickly.

94
Q

What are the “units” of hertz (Hz) regards to skeletal muscle?

A

Action Potentials / sec

95
Q

At what Hz would we expect to see complete recruitment of all motor units in a given area?

A

5 - 10 Hz

96
Q

What occurs in regards to muscle tension above 10-12 Hz?

A

Tension increases and more power is generated.

97
Q

What occurs in regards to intracellular Ca⁺⁺ around or above 10-12 Hz?

A

More Ca⁺⁺ is influxxing into cell than is being removed.

98
Q

At what Hz does force plateau?
Why does this occur?
What is this force plateau called?

A

~ 40Hz
- All Troponin C’s are bound w/ trigger Ca⁺⁺
- Tetanization

99
Q

Describe Quantal Summation vs Temporal Summation.

A
  • Quantal Summation: Nervous system activates small motor units 1st and then large motor units next.
  • Temporal Summation: Rapid muscle stimulation that modulates force production.
100
Q

What is muscular atrophy?

A
  • Shrinkage of the muscle myofibril size due to disuse.
101
Q

How does muscular denervation atrophy differ from muscular disuse atrophy?

Give an example of denervation atrophy.

A
  • Disuse Atrophy is technically reversible but takes work (no loss of basal resting tone).
  • Denervation Atrophy is mostly irreversible and is the result of losing your basal resting tone (ex. spinal cord injury)
102
Q

Can skeletal muscle denervation atrophy be avoided in the case of a spinal cord injury?

A

Yes with $.
- Direct muscular electrical stimulation therapy everyday can keep muscle innervated in the hopes of spinal cord therapy improving in the future.

103
Q

How are new muscle cells created in muscular hypertrophy?

A

Trick question. Existing myofibrils grow in size, new cells are not created.

104
Q

What occurs with the cardiovascular system alongside the process of hypertrophy?

A

Angiogenesis = ↑ blood vessel size for better blood delivery.

105
Q

How does muscular hyperplasia differ from hypertrophy?
What is required for muscular hyperplasia?

A
  • During muscular hyperplasia, new muscle cells actually develop in addition to hypertrophy.
  • Hyperplasia generally requires intense exercise & probably anabolic steroids.
106
Q

What general issue is noted with drugs that increase cell replication?

A

↑ cell replication = ↑ cancer.

A&P I (Fall 2022) (17 decks)

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