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Physiology > BIOL 0800 Reading- Chapter 9 > Flashcards

BIOL 0800 Reading- Chapter 9 Flashcards

1
Q

What is a myoblast?

A

Undifferentiated, mononucleated cells that formed into a single cylindrical and multinucleated cell

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2
Q

What are satellite cells?

A

Undifferentiated stem cells that repair muscle in response to strain or injury

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3
Q

What are tendons?

A

Attach muscles to bones; bundles of collagen fibers

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4
Q

What are myofibrils?

A

Filaments that are part of small cylindrical bundles that make up striations

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5
Q

What are thick filaments of the sarcomere?

A

Made of myosin

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6
Q

What are the thin filaments of the sarcomere?

A

Composed mostly of actin, troponin, and tropomyosin

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7
Q

What is the A band?

A

The wide, dark band produced by thick filamins in the middle of the sarcomere

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8
Q

What is the Z line?

A

Where the thin filament is anchored to interconnecting proteins

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9
Q

What defines the limits of one sarcomere?

A

To adjacent Z lines

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10
Q

What is the I band?

A

The light band that’s between the A bands of adjacent sarcomeres that results from thin filaments and interconnecting proteins, but no overlapping thick filaments

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11
Q

What’s the H zone?

A

The narrow, light band in the middle of the A band, where the two thin filament sets don’t overlap

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12
Q

What’s the M line?

A

The proteins that link together the central region of adjacent thick filaments, in the center of the H zone

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13
Q

What is titin?

A

The elastic protein that extends from the Z line to the M line (interconnecting)

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14
Q

How are thin and thick filaments arrange?

A

Hexagonal thin around one thick; triangular thick around one thin

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15
Q

What are crossbridges?

A

Projections that bridge the space between overlapping thick and thin filaments; part of the myosin molecules on the thick filaments; the velcro heads

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16
Q

What is the sliding-filament mechanism of contraction?

A

When the overlapping thick and thin filaments in each sarcomere move past each other, propelled by crossbridge movement: shortens the sarcomere

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17
Q

What does the ability of a muscle fiver to generate force and movement depend on?

A

Interaction of the contractile proteins actin and myosin

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18
Q

What comprises the myosin molecule?

A

Two heavy chains and four light chains: produces two globular heads and a long tail

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19
Q

How are myosin molecules oriented in the thick filament?

A

Opposite directions, so tails point in, so that when the heads swivel, they drag the thin filaments in towards the center

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20
Q

What is the crossbridge cycle?

A

Attachment of crossbridge to thin filament, movement of crossbridges to produce tension, detachment of crossbridge from thin filament, energizing the crossbridge so it can attach to a thin filament again and repeat the cycle

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21
Q

What initiates crossbridge cycling?

A

Entry of calcium into the cytoplasm

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22
Q

What happens when the energized myosin binds to actin?

A

The strained conformation is released, to produce movement of the bound crossbridge and the release of a phosphate and ADP

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23
Q

How is the analogy of energy storage/release in myosin like a mousetrap?

A

Cock the spring (ATP hydrolysis), and spring the trap (bind to actin)

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24
Q

Why is ATP needed a second time when actin and myosin are bound?

A

To break the crossbridge bond to reenergize the crossbridge and start the cycle all over again

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25
Q

What role does ATP play when it breaks the bond between the bridged crossbridge and actin?

A

Allosteric modulator, NOT an energy source: allosterically modulates the myosin head to weaken the binding of myosin to actin

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26
Q

What happens after ATP allosterically modulates the myosin head?

A

It gets hydrolyzed into ADP and a phosphate, which reenergizes the myosin so that it can continue the crossbridge cycle

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27
Q

What are the two distinct roles for ATP in the crossbridge cycle?

A

1) energy release during hydrolysis to move the crossbridge, and 2) binding to allosterically modify myosin to release actin and reenergize the cycle

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28
Q

How do troponin and tropomyosin work?

A

Tropomyosin cover the myosin binding sites, held by troponin, until Ca binds to the troponin and changes it shape, allowing the tropomyosin to move away from the binding sites

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29
Q

What determines the number of actin sites available for crossbridge binding?

A

The cytosolic Ca concentration

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30
Q

What is excitation-contraction coupling?

A

How an action potential leads to crossbridge activity

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31
Q

What is the source for increased cytosolic Ca in a muscle fiber?

A

The sarcoplasmic reticulum

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32
Q

What are lateral sacs?

A

The enlarged regions of the SR, connected by tubes

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33
Q

What is the transverse tubule?

A

T-tubule: separate from SR, but associated with lateral sacs of SR: surround myofibrils where the A bands and I bands meet

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34
Q

How Is the action potential propagated to the sarcomeres?

A

The membrane of the T tubule can propagate the action potential, and the lumen of the T tubule is continuous with the ECF around the muscle fiber

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35
Q

What are the junctional feet?

A

Where the T-tubules contact the lateral sacs of the SR, using two integral membrane proteins

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36
Q

What are the two integral membrane proteins in the junctional feet between the lateral sacs of the SR and the T-tubules?

A

The DHP receptor (modified voltage sensitive Ca channel) and the ryanodine receptor (includes foot process and the calcium channel)

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37
Q

What happens during an T-tubule action potential?

A

Charged amino acid residues in the DHP receptor protein induce conformational change, using the foot process to open the ryanodine receptor channel, so Ca goes from the lateral sacs of the SR into the cytosol, activating crossbridge cycling

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38
Q

How is contraction terminated?

A

When Ca is removed from troponin and the tropomyosin slides back into place

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39
Q

Why does contraction continue even after the action potential is over?

A

It takes longer to get all the calcium back into the SR through active transport, so cytosolic Ca concentration is still elevated

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40
Q

What is the neuromuscular junction?

A

Where the motor neuron connects with the effector organ, the muscle

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41
Q

What’s the difference between motor neurons and somatic efferent neurons?

A

There is none! They’re the same! Such magical!

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42
Q

What are the largest diameter axons in the body?

A

Motor neurons

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43
Q

What happens when the axon of a motor neuron reaches the muscle?

A

It divides into a bunch of junctions with the muscle fiber: each muscle fiber is controlled by a branch from only one motor neuron

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44
Q

What is a motor unit?

A

A motor neuron and the muscle fibers it innervates

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45
Q

What is the motor end plate?

A

The region of the muscle fiber plasma membrane that lies directly under the terminal portion of the axon

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46
Q

What is the junction of an axon terminal with the motor end plate?

A

The neuromuscular junction!

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47
Q

What neurotransmitter is contained in the vesicles found at the axon terminals of a motor neuron?

A

ACh

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48
Q

What kind of receptors does the ACh released by the axon terminal of motor neurons bind to?

A

Ionotropic (nicotinic type)

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49
Q

What is an end plate potential?

A

When the binding of ACh to the ionotropic/nicotinic receptors on the muscle fiber opens ion channels to cause a local depolarization

50
Q

What kind of neuron-neuron synapse potential is EPP analogous to?

A

An EPSP

51
Q

Which has a larger magnitude, an EPSP or an EPP? Why?

A

And EPP, because neurotransmitter is released over a larger surface area, binds to more receptors, and opens more ions channels

52
Q

True or false: every action potential in a motor neuron niormally produces an aciton potential in each muscle fiber in its motor unit

A

True!

53
Q

True of false: neuromuscular junctions can be excitatory or inhibitory.

A

False! NO NO NO! ONLY EXCITATORY!

54
Q

How is ACh removed from the synaptic junction?

A

Broken down by acetylcholinesterase

55
Q

What happens when receptors are occupied by curare, in the motor end plate?

A

ACh can’t bind to the receptor, and there’s no EPP and no contractioin (even though mtor neurons could still conduct normal action potentials and release ACh, because curare doesn’t open the ion channels and It’s not destroyed by acetylcholinesterase

56
Q

How does inactivating acetylcholinesterase inhibit muscle function?

A

The ion channels in the end plate remain open, maintaining depolarization, so no action potentials can be generated because the voltage-gated Na channels are inactivated, which requires repolarization to reverse, and then the receptors on the motor end plate become desensitized to ACh and don’t EVER depolarize after that unless you reactivate acetylcholinesterase or provide an antagonist

57
Q

Muscle tension

A

Load

58
Q

What is the difference between muscle tension and load?

A

The force exerted on an object by the contracting muscle, or the force exerted on the muscle by the object

59
Q

What does the shortening of a muscle fiber depend on?

A

Whether muscle tension is greater than the opposing load

60
Q

What is an isotonic contraction?

A

When the muscle changes length while the load on the muscle remains constant

61
Q

What is an isometirc contraction?

A

When the muscle develops tension but doesn’t shorten or length: like supporting a load in a constant position or moving a supported load where the tension is less than the load

62
Q

What is concentric contraction?

A

When tension exceeds the load and the muscle fiber shortens

63
Q

Wjat is eccentric contraction?

A

When the unsupported load is greater than the tension generated by crossbridges; lengthening: the load pulls the muscle to a longer length in spite of the opposing force produced by the cross bridges

64
Q

When does eccentric contraction occur?

A

When an object being supported by muscle contraction is lowered, like when the knee extensor in your thighs lower you to a seat from a standing position

65
Q

Which is the only step of crossbridge cycling that differs between concentric and isometric contraction?

A

Step 2, when the crossbridges bound to actin rotate through their power stroke: in concentric, the crossbridges rotate and shorten the fiber, BUT in isometric, they can’t swivel, so the filaments don’t slide and the rotation force is absorbed into the crossbridge structure

66
Q

What happens to the crossbridges during step 2 of the crossbridge cycle for an isometric eccentric contraction?

A

The crossbridges repeatedly bind to the same actin, while the load pulls them further back toward the Z lines, resulting in a lengthening

67
Q

What determines whether muscle fibers shorten, lengthen, or stay the same length?

A

The magnitude of the muscle load

68
Q

What is twitch?

A

The mechanical response of a muscle fiber to a single action potential

69
Q

What happens during isometric twitch?

A

The latent period occurs, before the tension increases, and excitation-coupling processes start to occur: this last for as long as the “contraction time,” which depends on low long it takes fro cross bridges to complete their cycle and detach once Ca has been removed from the cytosol

70
Q

Which has a longer latent period, isotonic twitch or isometric twitch?

A

Isotonic twitch, BUT the force generation duration is longer in isometric

71
Q

What happens to latent period length, velocity of shortening, duration of twitch, and distance shortened when there is a heavier load during isotonic twitch?

A

Latent period is longer, velocity of shortening if slower, duration of twitch is shorter, and distance is less.

72
Q

Why is latent period longer for isometric than isotonic twitch contraction?

A

Because in isotonic, the latent period includes the time for excitation-contraction coupling to start AND how long it takes to accumulate enough crossbridge connections to lift the load

73
Q

What is the difference between fused an unfused tetanus?

A

Unfused is when tension oscillates based on low stimulation frequency, but fused has no oscillations and is produced by higher stimulation frequencies

74
Q

What is tetanus?

A

A maintained contraction in response to a repetitive stimulation

75
Q

Why is tetanic tension greater than twitch tension?

A

In tetanic tension, successive action potentials release calcium from the SR before it can be pumped back into the SR, persistently elevating Ca levels and preventing a decline in the number of available binding sites: more crossbridges can then be bound

76
Q

What is optimal length?

A

The length at which the fiber develops the greatest isometric active tension

77
Q

Why does stretching a fiber well beyond its optimal length result in no tension?

A

Then there’s no overlap of thick and thin filaments, so nothing can hook onto each other

78
Q

What are the three ways muscle fibers create ATP?

A

1) phosphorylate ADP with creatine phosphate, 2) oxidative phosphorylation of ADP in mitochondria; 3) phosphorylation of ADP by glycolytic pathway in cytosol

79
Q

What happens to CP in the muscle fibers during periods of rest?

A

It builds up so that there’s plenty left to phosphorylate ATP once contraction begins

80
Q

To what extent are the three methods of ATP production used by muscle fibers?

A

CP is used initially until the concentration of CP runs out, but that gives enough time for oxidation and glycolysis to kick in; at moderate levels of muscular activity, mostly it’s oxidative phosphorylation in mitochondria, and then as intensity increases, glycolysis pitches in more and more

81
Q

Why do you continue to breath hard after exertion?

A

Because your body is repaying the oxygen debt that is needed to help restore the creatine phosphate and glycogen to the muscle fibers

82
Q

What is muscle fatigue?

A

When tension drops off even as stimulation continues

83
Q

Why does muscle fatigue occur after high intensity exercise?

A

Conduction failure, lactic acid buildup, inhibition of cross-bridge cycling

84
Q

How might conduction failure cause muscle fatigue?

A

If conduction fails, Ca isn’t released from the SR, and K+ builds up in the T-tubule during the repolarization of repetitive action potentials: leads to persistent depolarization, inability to conduct action potentials, and inactivated sodium channels

85
Q

What are fast fibers?

A

Fibers containing myosin with high ATPase activity; type II

86
Q

What are slow fibers?

A

Fibers containing myosin with lower ATPase activity, type I

87
Q

What are the two ways of classifying muscle fibers?

A

Maximal velocities of shortening, or major pathway they use to form ATP

88
Q

What are oxidative fibers?

A

Fibers that rely on mitochondria to provide oxidative phosphorylation to make ATP; dependent on blood flow for oxygen and fuel; contain a lot of myoglobin (oxygen binding protein)

89
Q

Why are oxidative fibers called red muscle fibers?

A

Contain a lot of myoglobin, which is red

90
Q

What are glycolytic fibers?

A

Have few mitochondria and rely on glycolytic enzymes and glycogen to produce ATP by glycolysis; no myoglobin, so called white muscle fibers

91
Q

What are the three principal types of muscle fibers?

A

Slow oxidative (type I), fast-oxidative-glycolytic (type IIa), and fast-glycolytic (type IIb)

92
Q

Which of the three types of muscle fibers fatigues most quickly?

A

Fast-glycolytic (type 2b)

93
Q

Which of the three types of muscle fibers has the largest diameter of fiber? Middle? Smallest?

A

Fast-glycolytic; then fast oxidative-glycolytic; then slow-oxidative

94
Q

What does the total tension of a muscle depend on?

A

How much tension each fiber contributes, as well as how many fibers are contributing

95
Q

What size motor unit is responsible for fine movements?

A

Small motor units, like in the eye

96
Q

What does the number of fibers contracting depend on?

A

The number of fibers in each motor unit, and the number of active motor units

97
Q

What is the relationship between fiber size and force generated?

A

Greater diameter means greater force

98
Q

What is recruitment?

A

The process of increasing the number of motor units that are active in a muscle at any given time: activate the excitatory synaptic inputs to more motor neurons

99
Q

Why are the slow-oxidative fibers recruited first?

A

Because they’re activated by small motor neurons, which are activated before larger motor neurons because the depolarize faster and at a lower level of synaptic input, since the depolarization is distributed over a smaller surface area, leading to greater depolarization

100
Q

In what order are the three types of fiber recruited?

A

First slow oxidative, then fast oxidative glycolytic, then fast glycolytic

101
Q

What is hypocalcemic tetany?

A

Involuntary tetanic contraction of skeletal muscles when the extracellular calcium falls to 40% of its normal value

102
Q

What is hypocalcemia?

A

Low extracellular calcium

103
Q

What are costameres and what disorder are they related to?

A

Clusters of structural and regulatory proteins that link Z disks of outermost myofibrils; lack of/defect in leads to muscular dystrophy

104
Q

What causes myasthenia gravis?

A

Destruction of nicotinic ACh receptor proteins on the motor end plate because of an autoimmune problem

105
Q

Which muscle types can or cannot divide once they’ve differentiated?

A

Skeletal can’t, smooth can

106
Q

True or false: troponin is present in both skeletal and smooth muscle fibers.

A

False: troponin is not present in smooth muscle cells

107
Q

What are dense bodies?

A

Anchor the thin filaments to the plasma membrane in smooth muscle cells; functionally similar to Z lines

108
Q

How do the concentrations of actin and myosin compare in smooth to skeletal muscle fibers?

A

Less myosin, can be twice as much actin

109
Q

How is calcium modulated in smooth muscle cells, which differs from skeletal?

A

By phosphorylating the myosin, not by altering the binding sites on the actin filament

110
Q

What is the sequence of events following a rise in cytoplasmic Ca in smooth muscle?

A

Ca binds to calmodulin; the calcium-calmodulin complex binds to myosin light chain kinase; active myosin light chain kinase uses ATP to phosphorylate the myosin light chains on the heads; phosphorylation drives the crossbridges away and towards actin; the cycling continues as long as myosin light chains continue to be phosphorylated

111
Q

What is latch state?

A

When the stimulation is persistent and Ca concentrated is elevated, but the rate of ATP hydrolysis by crossbridges declines even as isometric contraction is maintained; in smooth muscle

112
Q

How does latch state occur?

A

When a phosphorylated crossbridge becomes dephosphorylated while still attached to actin

113
Q

What are the two sources of calcium ions to smooth muscle fibers?

A

Extracellular calcium ions and SR

114
Q

True or false: smooth muscle cells have just as much SR as skeletal, and also contain T-tubules.

A

FALSE! Neither.

115
Q

True or False: smooth muscle tension can be graded.

A

True: you can vary the cytosolic calcium concentration, which affects the number of crossbridges activated

116
Q

What is smooth muscle tone?

A

The activity when cytosolic calcium concentration is enough to maintain a low level of basal crossbridge activity without external stimuli

117
Q

What is pacemaker potential?

A

The membrane potential change occurring during the spontaneous depolarization to threshold

118
Q

What are slow waves?

A

The periodic fluctuation in membrane potential due to regular variation in ion flux

119
Q

What is the smooth muscle’s replacement of a motor end plate?

A

Varicosities

120
Q

How is excitation-contraction coupling different in cardiac cells?

A

Uses L-type Ca channels, which are modified DHP receptors that are usually used; these L-type Ca channels allow Ca influx after depolarization, but also trigger greater Ca influx from the SR

121
Q

True or false: cardiac muscle cannot undergo tetanic contractions.

A

True: the force generation lasts a lot longer, so the action potential and twitch are prolonged and extend the refractory period

Physiology (13 decks)

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