Lecture 21 & 22: Muscles I & II Flashcards

1
Q

Describe the composition of a muscle fiber.

A

Myofibrils covered by a cell membrane called the sarcolemma

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2
Q

What are T-tubules?

A

Invaginations of the sarcolemma

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3
Q

What is the terminal cisternae of the sarcoplasmic reticulum?

A

Part of the SR near the T-tubules

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4
Q

What is the sarcoplasmic reticulum? How is calcium bound inside?

A

ER of the muscle cells containing high calcium bound by calsequestrin (to keep concentration high in SR)

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5
Q

What triad is important for excitation contraction coupling?

A

2 terminal SR cisternae + 1 T-tubule

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6
Q

Describe the Na+ and K+ channels along the sarcolemma and its T-tubules.

A

They are all over the sarcolemma including down the T-tubules, but due to the limited spaces in the T-tubules the K+ is unable to clear during repolarization which temporarily inhibits repolarization and prevents hyperpolarization

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7
Q

What is the intracellular [K+] in muscle cells? Why?

A

It’s elevated because the due to the limited spaces in the T-tubules the K+ is unable to clear during repolarization

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8
Q

What helps compensate for the difficulty of the K+ to exit muscle cells during repolarization? How does this affect the RMP of muscle cells?

A

Leakage Cl- channels which are constantly active: lower RMP (-85/-90 mV)

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9
Q

Why is there no undershoot in repolarization of muscle cells?

A

Because of the accumulation of K+ in the T-tubules

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10
Q

Explains muscle fatigue? How can it be compensated for?

A

Caused by increase in extracellular K+ (making it harder for cells to repolarize) Lactic acid boosts Cl- leakage channels (allowing for repolarization)

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11
Q

What is myotonia?

A

Cl- leakage channels are defective

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12
Q

What is excitation-contraction coupling?

A

Process by which the AP in skeletal muscle causes calcium release from the SR to the intracellular space of the muscle fiber generates force (mechanical contraction)

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13
Q

What is the difference between excitation secretion coupling and excitation contraction coupling in skeletal muscle?

A

Excitation secretion coupling: happens in pre synaptic neuron and requires extracellular calcium Excitation contraction coupling: happens in the muscle cells and does not require extracellular calcium

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14
Q

Does excitation contraction coupling require EXTRACELLULAR calcium? Why?

A

Skeletal muscles: no (BUT the ryanodine receptor still needs to be activated) - because we’ve evolved to be able to react fast Smooth and cardia muscles: yes

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15
Q

What are the 2 important parts of the triad for excitation contraction coupling? Where is each located?

A

2 calcium channels to release calcium: 1. L-type channel = DHP receptor on T-tubule 2. Ryanodine receptor = calcium-release channel on SR (activated by calcium or activated DHP) THEY ARE CONNECTED

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16
Q

Describe the 3 steps of excitation contraction coupling. Is this pathway essential in skeletal muscle? How fast is it?

A
  1. Membrane depolarization causes L-type channel DHP receptor to be activated = conformational change 2. Mechanical coupling between L-type (ligand) and ryanodine receptor acitvation 3. Calcium exits the SR into the sarcoplasm and activates troponin C, leading to muscle contraction 4. Ca-ATPase on the SR pumps calcium back into SR
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17
Q

How can contraction happen with extracellular calcium coming into the sarcoplasm (in skeletal muscle)?

A
  1. Depolarization and activation of DHP receptors 2. Flow of extracellular calcium into sarcoplasm through DHP 4. Ryanodine receptors activated 5. Release of SR calcium into sarcoplasm
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18
Q

List the 15 steps to achieve muscle contraction in skeletal muscle.

A
  1. Terminal end of motor neuron takes up calcium after depolarization 2. ACh exocytosed 3. AChRs bind ACh in muscle fiber and produce EPP 4. EPP triggers AP and a depolarization wave is sent along the sarcolemma, down the T-tubules into the triads 5. Depolarization reaches DHP receptor and activates it 6. DHP activates ryanodine receptors 7. Calcium is released into sarcoplasm 8. Myosin hydrolyzes ATP recocking the myosin head for it to be perpendicular to actin = cross bridge release 9. Calcium binds to troponin (attached to tropomyosin) 10. Shift in tropomyosin= exposure of myosin binding sites on actin 11. Myosin (bound to ADP + Pi) binds to actin 12. Myosin releases ADP + Pi = contraction (crawling on actin filaments) 13. ATP binds to myosin= actin release 14. Calcium is resorbed by SR by Ca-ATPase 15. Tropomyosin hides myosin binding sites on actin = muscle relaxation
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19
Q

Skeletal muscle: multi or uninucleated?

A

Multi

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20
Q

What is the A band of the sarcomere?

A

Thick filaments in their entirety

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21
Q

What is the M line in the sarcomere?

A

Cuts the thick filaments in half

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22
Q

What is the I band of the sarcomere?

A

Thin filaments ONLY

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23
Q

What is the H zone of the sarcomere?

A

Thick filaments ONLY

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24
Q

Describe the sarcomere composition in skeletal muscle.

A

Thin filaments: actin, tropomyosin, and troponin Thick filaments: myosin

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25
Q

What part of the sarcomere moves during muscle contraction?

A

Thin filaments

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26
Q

What is the Z-line of the sarcomere?

A

Cuts the thin filaments in half (also where invagination of T-tubules occurs)

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27
Q

Describe the thin filaments in the sarcomere in skeletal muscle.

A

Two filamentous actin fibers of individual globular actin monomers intertwine. Attached at regulatory points is tropomyosin which hides the myosin binding sites. Troponin is attached at the ends of tropomyosin and can bind calcium.

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28
Q

What are the 3 subunits of troponin?

A
  1. Troponin T: tropomyosin binding site 2. Troponin I: locks tropomyosin in place to hide myosin binding sites on actin 3. Troponin C: 4 calcium binding sites: 2 low affinity and 2 high affinity (bound at all times)
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29
Q

Describe the thick filaments in the sarcomere. What do they allow?

A

2 chains of light meromyosin + 2 heads of heavy meromyosin (bind actin and ATPase) + 2 hinged regions Both connected by hinged regiond that allow the cross bridge to bend 45 degrees with respect to the backbone allowing for the cross bridge movement

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30
Q

How big is the angle motion of the myosin head?

A

45 degrees

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31
Q

How does ATP affect myosin’s affinity for actin?

A

ATP decreases its affinity for actin

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32
Q

By how much does the sarcomere shorten during contraction?

A

1 microm

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33
Q

What does the speed of the cross bridge cycle depend on? What is this theory called?

A

The speed of the ATPase on the myosin head The sliding filament theory

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34
Q

What does the strength of the cross bridge cycle depend on?

A

The amount of cross-bridges formed, which depends on the amount of calcium present

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35
Q

What happens if calcium concentration stays high in a muscle cell?

A

Cell death

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36
Q

What happens in rigor mortis?

A

Lack of ATP keeps myosin from unbinding actin so the muscles remain contracted without any action potential involved

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37
Q

What are the 3 major sources of ATP? Explain each one and how it potentially affects the cellular environment.

A
  1. Glycolysis: glycogen broken down by phosphorylase (myophosphorylase in muscles): cell acidosis because of lactic acid 2. Krebs cycle (oxidative phosphorylation) burning fatty acids with water and CO2 as byproducts (easily diffusible so no side effect) 3. Creatine phosphate: very low capacity emergency storafe
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38
Q

What are the 2 times ATP is used during muscle contraction?

A
  1. To dissociate myosin from actin 2. To remove calcium from sarcoplasm back into SR
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39
Q

Are the invaginations created by the T-tubules extracellular or intracellular?

A

Extracellular

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40
Q

How is maximal force (tension) of contraction of a sarcomere achieved?

A

Maximal overlap between actin and myosin to allow for maximal number of cross-bridges

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41
Q

What is contraction strength dependent on?

A

The number of cross-bridges

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42
Q

What is the resting length of the sarcomere?

A

The optimum position of myosin relative to actin

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43
Q

Would small deviations in sarcomere length affect strength of contraction? Why?

A

No because the resting length of the sarcomere is the optimum position of myosin relative to actin

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44
Q

How is the force of contraction controlled in cardiac muscle?

A

By altering the resting muscle length

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45
Q

What is the purpose of the T-tubules?

A

Plasma membrane wants to make sure the AP goes deep in the muscle cell to cause a contraction

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46
Q

What is special about the DHP receptor on skeletal muscle membranes not needing calcium entry for contraction?

A

Only place in physiology where ion flow is not required through an ion channel for activation

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47
Q

What is the hierarchy of the skeletal muscle?

A

Actin+myosin > sarcomeres in series > myofibril > myofiber > muscle bundle > muscle

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48
Q

What are the potassium, sodium, and calcium concentrations of the SR (high/low)?

A

K: High Na: Low Ca: High

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49
Q

What are the potassium, sodium, and calcium concentrations of the T-tubules (high/low)?

A

K: Low Na: High Ca: High

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50
Q

What are the potassium, sodium, and calcium concentrations of the sarcoplasm (high/low)?

A

K: High Na: Low Ca: Low

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51
Q

Which step is ATP dependent in excitation-contraction coupling?

A

The action of Ca-ATPase to pump Ca back into the SR

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52
Q

What does it mean for the RMP if [K+] out is higher than normal?

A

RMP is depolarized

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53
Q

Myofiber: poly or uninucleated?

A

Poly

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54
Q

Does the A band change in length?

A

No

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55
Q

Does the I band change in length?

A

Yes: shrinks

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56
Q

Which 2 proteins make stripes on striated muscles?

A

Actin and myosin

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57
Q

Which 2 proteins in skeletal muscle are the regulatory ones? What do they form?

A

Tropomyosin and troponin = regulatory protein complex

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58
Q

What distinguishes the red and white muscles?

A

Different types of myosin based on the speed of their myosin ATPase (and their myoglobin content): white: fast and red: slow

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59
Q

How many heads on myosin?

A

2

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60
Q

What does the number of cross bridges cycling depend on?

A

Calcium concentration

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61
Q

What causes cramps?

A

ATP not attaching to myosin so that it releases actin so the muscles remain contracted

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62
Q

What does the curve of intracellular [Ca] vs the force of the ATPase activity on myosin look like? Why?

A

Sigmoidal because it takes a certain amount of calcium to expose myosin binding sites on actin (slow start) and then it goes fast and then it reaches a plateau

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63
Q

At what intracellular [Ca] is contraction maximal?

A

10 microM

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64
Q

What is the minimal intracellular [Ca] for contraction?

A

100 nM

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65
Q

How can you measure the force of contraction biochemically?

A

ATPase activity

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66
Q

What is relaxation of skeletal muscle after a contraction controlled by?

A

The uptake of calcium by the SR Ca-ATPase

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67
Q

What “charges” the power stroke?

A

Hydrolysis of ATP

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68
Q

“The cell has a larger resting potential”: what does this mean?

A

MORE NEGATIVE RMP!

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69
Q

What would be the effect on the RPM if the plasma concentration of K+ was lower than normal (but same inside the cell)?

A

RPM would be hyperpolarized = larger

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70
Q

What is different about the action potential of a skeletal muscle cell instead of a nerve? Why? 3 things.

A
  1. There is a hump during the repolarization because the K+ is getting stuck in the T-tubules and so the Cl- leakage channels will be driven by the positive charge and take over to help repolarize 2. No undershoot 3. RMP is lower in muscle cells
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71
Q

What does the maximum velocity of the shortening of the cross-bridge depend on?

A

Type of ATPase: fast and slow

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72
Q

What does the maximum tension of the cross-bridge depend on?

A

The degree of overlap of the cross-bridge

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73
Q

What is 1 cross-bridge?

A

The attachment of myosin with actin within the muscle cell

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74
Q

What is an isometric contraction? 2 examples?

A

The muscle tension developed is less than its opposite load so it generates force without changing the length of the muscle. The muscle cannot change from a prefixed length but the tone changes. For example you are pushing against a wall or muscles pulling on tendons

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75
Q

What is an isotonic contraction? Example? 2 types?

A

Generates force by changing the length of the muscle meaning the muscle tension developed is greater than its opposing load (lifting). The muscle tone (strength) therefore remains the same, but the length changes. For example Kate lifting hamsters (that are a constant weight) at the gym. My muscles will not change their strength but I will decrease the length of my muscles as I move the hamsters up and down. Two types of isotonic contraction: i. Concentric- muscle shortening ii. Eccentric- muscle lengthening

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76
Q

What is a tetany? What is it responsible for?

A

The muscle response to multiple APs at high frequency to generate a greater force of contraction due to the fact that the calcium does not have time to be reuptake into the SR Responsible fora high, sustained maximal force

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77
Q

What is the shortening velocity of an isotonic contraction dependent on?

A

Inversely proportional to the magnitude of the load

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78
Q

Are heart muscles cells performing isometric or isotonic contractions?

A

Isotonic contractions

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79
Q

With what types of contractions is the force-velocity relationship shown? What do they show?

A

Isotonic contractions They show that as the load decreases, the contraction velocity increases

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80
Q

What type of muscle contractions are movements made of?

A

First isometric and then isotonic when the load is greater than the tension

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81
Q

What are the 2 ways to regulate contraction speed?

A
  1. ATPase activity 2. Changing the force on the muscle
82
Q

What are the 4 ways to control muscle force?

A
  1. Length/tension relationships 2. Hypertrophy 3. Number of stimuli 4. Increasing the # and type of motor units involved
83
Q

What is the active tension of a muscle?

A

Tension seen for normal sarcomere contraction (specific length of sarcomere gets max force from max overlap)

84
Q

What is the passive tension of a muscle?

A

Intrinsic tension due to the elasticity of the muscle components = tendency of tendons, sarcomeres, etc to return to their normal shape

85
Q

What is the passive tension of a muscle also called? Why?

A

The parallel elastic element because it is synergistic with the active component of muscle tension

86
Q

Is the length tension relationship in a whole muscle the same than in a myofiber? Why/Why not?

A

NOPE because in the whole muscle you also have to consider passive tension whereas in a single sarcomere you do not

87
Q

What is the total tension of a whole muscle?

A

Sum of the forces of its active and passive elements

88
Q

What is the series elastic element of muscle contraction? What does it explain?

A

A slack of the tendons, tissue, and muscle fibers that must be taken up before contraction can occur. It causes a delay between calcium release in sarcoplasm and contraction and explains why a single twitch cannot cause maximum tension because it does not provide enough tension to take up the slack = its max tension happens when calcium concentrations have been decreasing

89
Q

Which delay is longer: AP and Ca release or Ca release and muscle contraction?

A

Calcium release and muscle contraction

90
Q

What is a motor unit?

A

Ensemble of muscle fibers receiving innervation by the same alpha neuron

91
Q

What will the strength of the motor unit depend on?

A

The number of fibers innervated by the alpha motor neuron

92
Q

What does the brain do to be able to perform a more strenuous task? 3 ways

A
  1. It will recruit more motor units 2. It will recruit bigger motor units 3. It will change the type of motor unit firing
93
Q

What are the 3 types of motor units? What type of muscle fibers does each have?

A
  1. Type I: Red 2. Type IIX: White 3. Type IIA: Red
94
Q

What type of motor units does anaerobic exercise (quick bursts) use? What does this explain?

A

Type 2, which use glycolytic metabolism producing lactic acid as a by-product which explains muscle soreness

95
Q

Describe the nerves of the Type 1 motor units.

A

High excitability and innervate few fibers (20-35)

96
Q

How fast is the contractibility velocity speed of Type 1 motor units?

A

Moderate contraction velocity speed

97
Q

What kind of metabolism do Type 1 motor units use?

A

Oxidative metabolism (burning fat)

98
Q

Which have a higher threshold for fatigue resistance: Type 1 or Type 2 motor units?

A

Type 1

99
Q

Describe the metabolic properties of the red fibers in Type 1 motor units.

A

High myoglobin (necessary for ETC) High concentration of mitochondra Low glycogen

100
Q

What kinds of activities do we use Type 1 motor units for?

A

Activities requiring endurance (running a marathon or maintaining posture)

101
Q

Describe the nerves of the Type 2 motor units.

A

Low excitability and innervate many fibers (100-150)

102
Q

How fast is the contractibility velocity speed of Type 2 motor units?

A

Very fast

103
Q

What kind of metabolism do Type 2 motor units use?

A

Glycolytic metabolism (burning glycogen)

104
Q

Describe the metabolic properties of the white fibers in Type 2 motor units.

A

High glycogen Low concentration of mitochondria Lack of myoglobin

105
Q

What kinds of activities do we use Type 1 motor units for?

A

Intense but short activities

106
Q

What are Type 2a motor units? What is another name for them? What fibers do they have?

A

Hybrid between Type 1 and Type 2 Fast oxidative-glycolytic motor units with red fibers

107
Q

Type 1 motor unit: describe the diameter of nerves and of muscle cells.

A

Nerves: small Muscle cell: moderate

108
Q

Type 2 motor unit: describe the diameter of nerves and of muscle cells.

A

Nerves: large Muscle cell: large

109
Q

What is Type IIB?

A

Type IIX in mice

110
Q

How does high-intensity resistance training affect our muscle fibers?

A

Hypertrophy of Type II fibers

111
Q

How does cardio training affect our muscle fibers?

A

Promotes improved oxidative capacity in oxidative fibers (using O2 more efficiently)

112
Q

Which muscle fiber is the least desirable? Does the switch to this type ever happen? How?

A

Type IIX Yes, through disuse atrophy

113
Q

What can muscle fiber atrophy be due to?

A

Disuse or denervation

114
Q

Describe the capacity for repair of muscle fibers.

A

Limited

115
Q

What are the 2 types of smooth muscle?

A
  1. Multiunit 2. Unitary
116
Q

Where are multiunit smooth muscles found?

A

In areas that require fine motor movement: iris, pili erector, ciliary muscle

117
Q

Describe the cell membranes of multiunit smooth muscles. What does this allow?

A

They are electrically isolated to allow for finer muscle control.

118
Q

Why are smooth muscles unstriated?

A

Because their myosin and actin are not organized the same way as in skeletal muscle

119
Q

What is force used for in smooth muscles? 4 things. Example for each?

A
  1. Motion (eg: pilomotor and nictitating membrane in cats’ eyes) 2. Expelling content of hollow organs (eg: uterus) 3. Changing cross-sectional dimension of tubular organs (eg: alveoli) 4. Changing dimension of passive organs (eg: ciliary muscles in lens)
120
Q

Describe the size of smooth muscles.

A

They are small.

121
Q

Do smooth muscles include the heart?

A

NOPE

122
Q

What does it mean for multiunit smooth muscle cells to be neurogenic?

A

They have few muscle fibers/cells per neuron

123
Q

What is muscle fiber synonymous with?

A

Muscle cell

124
Q

Other than nerves, what else can control multiunit smooth muscle cells?

A

Hormones

125
Q

What do unitary smooth muscle cells form?

A

Syncytium = functional group of interconnected cells

126
Q

What is the activity of unitary smooth muscle cells like? What is it generated by (3 possibilities)?

A

Myogenic activity generated by a self-excitable spontaneous pacemaker potential (one or more of the cells of the syncytium) OR automatic shifts in ion concentrations in the ECF and ICF OR sudden mechanical stretch allowing Na+ to enter the cell that allows for the AP to travel through gap junctions yielding a slow wave throughout the whole group

127
Q

What is peristalsis due to?

A

The myogenic activity being communicated through gap junctions between unitary smooth muscle cells of the syncytium

128
Q

Which smooth muscles have more precision: unitary or multiunit?

A

Multiunit

129
Q

Which smooth muscles have a higher innervation ratio: unitary or multiunit?

A

Multiunit

130
Q

Can unitary smooth muscles be innervated by the autonomic nervous system as well?

A

Yup

131
Q

Describe the 4 different action potentials that go through smooth muscle cells. What is each caused by? For what type of smooth muscle does each happen?

A
  1. Single spike: electrical stimulation, hormone, or stretch 2. Plateau: due to L-type calcium channels that innactivate poorly 3. Slow wave: much slower, below threshold and due to intracellular calcium: unitary 4. Pacemaker potentials: rate of AP firing controlled by temperature, hormones, NTs, stretch, pO2, pCO2
132
Q

What is another name for smooth muscles?

A

Visceral muscles

133
Q

What is the plateau AP responsible for?

A

Prolonged contractions in the bladder and uterus

134
Q

What do smooth muscles have instead of T-tubules? What is found in these?

A

Caveoli with voltage-gated calcium channels

135
Q

What are the 4 pathways for calcium entry in the smooth muscle cells? How is each activated?

A
  1. Voltage-gated L-type calcium channels on the calveoli: AP on smooth muscle membrane 2. IP3-gated calcium channels on the SR: IP3 OR CALCIUM binding to SR channel 3. Calcium-induced calcium release channels on the SR: calcium binding to SR channel 4. Store-operated channels on the smooth muscle cell membrane: activated when SR calcium is depleted
136
Q

What do smooth muscles use to align the actin and myosin filaments? What does this replace compared to skeletal muscles?

A

Dense bodies scattered throughout replacing the Z-line of skeletal muscles

137
Q

What are unitary smooth muscle cells connected by?

A

Gap junctions

138
Q

Do smooth muscle cells have parallel elastic elements?

A

NOPE

139
Q

Which smooth muscles generated longer APs: unitary or multiunit?

A

Unitary

140
Q

Describe the thin and thick filaments in smooth muscles.

A

Actin, but no tropomyosin or troponin Myosin is just as thin as actin

141
Q

Describe the 7 steps for muscle contraction in smooth muscles.

A
  1. Calcium is released into sarcoplasm 2. Calmodulin binds calcium for Ca2+-CAM 3. Ca2+-CAM binds and activates myosin light chain kinase (MLCK) 4. Myosin hydrolyzes ATP recocking the myosin head for it to be perpendicular to actin = cross bridge release 5. MLCK phosphorylates the myosin head activating it 6. Myosin (bound to ADP + Pi) binds to actin 7. Myosin releases ADP + Pi = contraction (crawling on actin filaments) 8. ATP binds to myosin= actin release 9. Myosin light chain phosphatase (MLCP) dephosphorylates myosin, inactivating it 10. Calcium is resorbed by SR/sarcolemma by Ca-ATPase
142
Q

How does muscle contraction in smooth muscle compare to that in skeletal muscle?

A

Process is much slower because of series of reactions and decreased myosin ATPase activity

143
Q

What can smooth muscle utilize to generate a stronger and longer contraction? What is the mechanism? What is this similar to? Example?

A

The latch mode: dephosphorylation of myosin by MLCP while it has formed a cross-bridge with actin to allow for less ATP consumed and contraction maintained Similar to rigor mortis Eg: bladder remains contracted so we don’t pee ourselves without using too much energy

144
Q

What is incomplete tetanus due to?

A

Intermediate stimulation frequency

145
Q

What is the most efficient way to regulate muscle strength?

A

Repetitive APs!

146
Q

What is the innervation ratio?

A

The ratio of muscle fibers to nerve fibers in a motor unit

147
Q

What are finnesses of movement a function of?

A

The innervation ratio

148
Q

Which motor unit has more muscle fibers: Type I or Type II?

A

Type II

149
Q

What kind of fiber types do we have at birth? How does this change as we age?

A

All types: equal amounts Type II increase with age

150
Q

What does histological fiber grouping represent?

A

Denervation with successful re-innervation

151
Q

What is testosterone’s role on muscle fibers?

A

It causes hypertrophy of Type II muscle fibers by synthesizing proteins for increasing diameter

152
Q

What can cause a conversion of one muscle fiber type to another?

A

Weight training

153
Q

What does the length-tension relationship represent for skeletal muscle?

A

The effect of crossbridge formation on muscle tension

154
Q

During isometric contraction, what is the tension developed during a twitch used for?

A

The stretch the series elastic element

155
Q

Why can greater amounts of tension be measured during tetany compared to twitch?

A

Because any series elastic elements are maximally stretched during the first few stimuli

156
Q

What NS controls smooth muscles?

A

Autonomic NS

157
Q

Describe the properties of the multiunit smooth muscles.

A

Partway between unitary and skeletal

158
Q

Describe how cytosol calcium concentrations affect unitary smooth muscle contraction.

A

Extracellular calcium controls the contraction strength, which can be influenced by ANS, hormones, drugs, metabolites, etc.

159
Q

What calcium does the heart use to contract?

A

Extracellular calcium

160
Q

What is tone in a smooth muscle cell?

A

Low level of tension caused by baseline level of calcium in the cytosol of smooth muscle cells

161
Q

Which is more primitive: cross-bridge formation in smooth or skeletal muscle?

A

Smooth

162
Q

In what animal can the latch mode be observed?

A

Clams and mussels

163
Q

Can skeletal muscle contract with electrical stimulation and no extracellular calcium?

A

Yes because DHP receptors will be stimulated and activate ryanodine receptors on the SR

164
Q

Can smooth muscle contract with electrical stimulation and no extracellular calcium?

A

No because the electrically stimulatable receptors are on the plasma membrane

165
Q

Can smooth muscle contract with chemical stimulation and no extracellular calcium?

A

Yes because IP3 receptors on SR membrane will be activated (not as much calcium in smooth muscle SR though)

166
Q

Can cardiac muscle contract without extracellular calcium?

A

No because the electrically stimulatable receptors are on the plasma membrane

167
Q

Can skeletal muscle contraction be affected by hormones?

A

A little

168
Q

On what types of muscles can nerve stimulation cause inhibition?

A

Smooth and cardiac

169
Q

What does electrical coupling mean for muscle cells?

A

Gap junctions between them

170
Q

Are there gap junctions in multiunit and cardiac muscle?

A

Some

171
Q

How is the speed of contraction in all muscle types?

A

Skeletal: fast and slow Cardiac: slow Smooth: very slow

172
Q

How do skeletal muscles produce antagonistic movements?

A

Antagonistic muscles

173
Q

Describe innervation is skeletal muscle.

A

Each muscle cell is innervated

174
Q

Describe innervation is cardiac muscle.

A

Variable

175
Q

In which muscle types is spontaneous electrical activity seen?

A

Cardiac and unitary smooth muscle

176
Q

What is a major drive for the chloride to leave the muscle cytoplasm?

A

The myoplasm is positively charged because of all of the calcium in it!

177
Q

Does the sarcomere contract during an isometric contraction?

A

NOPE

178
Q

How are active and passive tensions used as length of the muscle increases? What does this mean for total tension?

A

As length increases active tension decreases and passive tension increases Total tension is relatively constant

179
Q

When does the maximum force of a twitch happen in relation to the curve of intracellular [Ca]?

A

When the concentration has already started decreasing

180
Q

What does the strength of a movement depend on?

A

The size, number, and type of motor units recruited

181
Q

What is the major factor in the moment to moment regulation of skeletal muscle tension?

A

Recruitment of motor units

182
Q

Which produces a large increase in tension when added: Type 1 or Type 2 motor units?

A

Type 2

183
Q

In what order are Type 1 and Type 2 motor units used?

A

First Type 1 and then Type 2

184
Q

Is there a point on the force-velocity curve that corresponds to an isometric contraction?

A

Yes, the point of 0 velocity

185
Q

How is unitary smooth muscle mechanically coupled?

A

By special connective tissue fibers and dense membrane patches

186
Q

How is sustained contraction in smooth muscle obtained?

A

Low ATP utilization: latch-mode

187
Q

What remains constant during an isotonic contraction?

A

Tension!

188
Q

What is the region between two Z lines?

A

A sarcomere

189
Q

Where are Z-lines on the muscle cell?

A

T-tubules

190
Q

What is the smooth muscle plateau AP due to?

A

Poor inactivation of L-type calcium channels on muscle membrane

191
Q

What are the fast and slow calcium releases due to?

A

Fast: DHP receptor (voltage sensor in T-tubule) Slow: calcium-activated calcium release

192
Q

Describe the length-tension relationship in skeletal muscle vs in smooth/cardiac muscle.

A

The length-tension relationship cannot be used to regulate tension in skeletal muscle, but is important in smooth and cardiac muscle.

193
Q

How does active tension change as the length of a muscle increases? How is this compensated for?

A

Active tension is always decreased when you stretch a muscle. Passive tension compensates for this.

194
Q

Does the series elastic element affect both isotonic and isometric contractions? How come?

A

YUP because the isotonic contraction has an isometric component at first

195
Q

Are gap junctions selectively permeable to ions?

A

NOPE

196
Q

Are blood vessels unitary or multiunit smooth muscles?

A

Large vessels: multiunit Small vessels: unitary

197
Q

Which band of the sarcomere is asinotropic? What does this mean?

A

The A band: because in a polarizing light microscope, the dark bands are birefringent

198
Q

Which band of the sarcomere is inotropic? What does this mean?

A

The I band: because in a polarising microscope, these bands are much less birefringent than the A bands

199
Q

What is the structural equivalent of skeletal muscle Z-line in smooth muscle?

A

DENSE BODIES: connect thin filament (actin) to plasma membrane

200
Q

What is this?

A

APs created by pacemaker potentials