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Physio > Muscle > Flashcards

Muscle Flashcards

1
Q

Myofiber

A

Skeletal muscle cell / muscle fiber

Made of hundreds of myofibrils

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2
Q

Myofibers are multinucleated. T/F

A

True, they are derived embyrologically from hundreds of mesodermal cells

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3
Q

Myofibrils

A

Thread-like structures extending length of muscle fiber, hundreds of them make up myofiber

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4
Q

Skeletal muscles appear as striated or non-striated under a microscope?

A

Striated

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5
Q

Sarcolemma

A

Plasma membrane that surrounds the skeletal muscle cell

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6
Q

T-tubules function and structure

A

Transverse tubules
Invaginations of sarcolemma filled with extracellular fluid (high concentration of sodium and calcium), delivery system of electrical connection to deep regions of skeletal muscle cell

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7
Q

Triad

A

Two SR with a t-tubule

Allows for close coupling of action potential and calcium release

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8
Q

Sarcoplasmic reticulum

A

Stores calcium

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9
Q

Sarcomere

A

Contractile unit of skeletal muscle cell

An arrangement of thick myosin filaments and thin actin filaments allow contraction or sliding of actin along myosin

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10
Q

What is the thin filament of the sarcomere composed of?

A

Actin

G-actin arranged in double stranded helical structure of F-actin

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11
Q

What is the structure of the thick filament of the sarcomere?

A

300-400 myosin molecules bundled together

4 myosin chains: 2 heavy chains that form tail, neck, and head (golf club) and 2 light chains

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12
Q

What features does the thick filament of the sarcomere have that enable its function?

A

The myosin heads have an actin-binding site and ATPase enzymes
The heads also have an alkali light chain for structure and a regulatory myosin light chain to regulate the ATPase activity

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13
Q

What is the function of the alkali light chain on the thick myosin filament?

A

Structural role

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14
Q

What is the function of the regulatory myosin light chain on the thick myosin filament?

A

Regulates the ATPase activity of the myosin head

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15
Q

In order for a contraction to occur, there must be an increase in intracellular calcium. Where is this calcium coming from?

A

Sarcoplasmic reticulum

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16
Q

Tropomyosin

A

Lies in the groove of the actin double helix and covers the binding site for the myosin head

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17
Q

How far do tropomyosin molecules extend?

A

Every 7 G-actin molecules

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18
Q

Troponin subunits

A

TnC - binds calcium
TnT - binds tropomyosin
TnI - binds actin, inhibits actin and myosin from interacting

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19
Q

Troponin function

A

Calcium binds TnC subunit, causing a conformational change that allows tropomyosin to move out of actin groove, exposing the actin active sites for myosin

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20
Q

M line

A

center of sarcomere, where thick filaments are anchored by proteins

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21
Q

Z-discs

A

Anchor points for thin filaments, boundaries for sarcomere

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22
Q

A band

A

Entire length of thick filament

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23
Q

H zone

A

Non-overlapped portion of the thick filament

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24
Q

I band

A

Non-overlapped portion of the thin filament

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25
Q

What shape does a cross-section of sarcomeres have and what maintains this structure?

A

Hexagonal fiber shape with thin filaments around thick filaments, maintained by structural proteins

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26
Q

During skeletal muscle contraction, what happens to the length of the Z-disc to Z-disc?

A

Decreases

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27
Q

During skeletal muscle contraction, what happens to the length of the H zone?

A

Decreases

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28
Q

During skeletal muscle contraction, what happens to the length of the I band?

A

Decreases

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29
Q

During skeletal muscle contraction, what happens to the length of the A band?

A

Stays the same

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30
Q

During skeletal muscle contraction, what happens to the length of the myosin and actin filaments?

A

Stays the same

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31
Q

Skeletal muscle innervated by a what?

A

Alpha-motor neuron

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32
Q

Motor unit

A

The alpha-motor neuron and all of the skeletal muscle fibers that it innervates

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33
Q

The control of the movement of muscle fibers is dependent on the size of the motor unit. T/F

A

True, smaller motor units are capable of finer, more controlled movement while larger can generate more force/maintain posture

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34
Q

What are the steps of excitation-contraction coupling of the neuromuscular junction?

A
  1. AP spreads down alpha motor neuron, depolarizes end-bulb
  2. Depolarization opens voltage-gated calcium channels, calcium goes down gradient into cell
  3. Influx of calcium causes fusion of membrane-bound vesicles with plasma membrane at active zone, hundreds of quanta of ACh are released into synaptic cleft
  4. ACh binds to receptors at motor end-plate, opens ligand-gated cation channels
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35
Q

What type of receptors does the ACh bind to at the motor end plate?

A

Nicotinic, cholinergic receptors (somatic nervous system)

AKA non-specific/ligand-gated cation channels

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36
Q

ACh binding to the nicotinic, cholinergic receptors at the motor-end plate leads to the opening of ligand-gated cation channels, which depolarize the motor-end plate at spread an AP. T/F

A

False, the ligand-gated cation channels are the receptors and create the EPP

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37
Q

Where is the active zone at the neuromuscular junction?

A

The end-bulb of the alpha motor neuron where the ACh vesicles fuse to the plasma membrane and release ACh

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38
Q

How is ACh removed from the synaptic cleft?

A

ACh is enzymatically digested by acetylcholinesterase and the choline portion is transported back into the end bulb of the alpha motor neuron

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39
Q

How is an end-plate potential generated?

A

ACh binding to a receptor causes the opening of ligand-gated cation channels at the motor end-plate. The sodium influx is greater than the potassium efflux, so the cell depolarizes, generating the EPP

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40
Q

The end-plate potential is an action potential. T/F

A

False, since there are no fast voltage-gated sodium channels in the end-plate, no action potential can be generated

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41
Q

What is the EPP an example of?

A

Excitatory post-synaptic potential (EPSP)

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42
Q

How does the EPP lead to skeletal muscle contraction if it does not generate an action potential at the end-plate?

A

The EPP is sent away from the motor end-plate and depolarizes the adjacent sarcolemma, which contains fast voltage-gated sodium channels that open once threshold is reached

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43
Q

What 3 electrical events need to occur for a muscle cell to be stimulated?

A
  1. The alpha motor neuron must generate an AP and release ACh
  2. ACh binds to its receptor on motor-end plate and opens ligand-gated cation channels, leads to EPP
  3. The EPP depolarizes the adjacent sarcolemma to threshold, opening fast voltage-gated sodium channels, which generates a muscle AP.
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44
Q

Is the slope of an action potential or an end-plate potential steeper? Why?

A

The slope of an AP is steeper due to the fast voltage-gated sodium channels of motor neurons and muscle fibers, while the motor-end plate has potassium efflux occurring at the same time as sodium influx in the ligand-gated cation channels

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45
Q

What is the cause of the miniature end-plate potentials ?

A

Periodic release of small quanta of ACh without electrical stimulation of AP or calcium release

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46
Q

The motor-end plate lacks a resting membrane potential. T/F

A

True, from the quantal release of ACh from terminal bouton

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47
Q

What is the function of the periodic release of small quanta of ACh from the terminal bouton?

A

To keep the acetylcholine receptors localized to the motor-end plate
Called Miniature end-plate potentials (MEPP)

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48
Q

What are the 3 safety factors to ensure neuromuscular transmission of an action potential in the muscle fiber?

A
  1. More ACh is released than needed
  2. More ACh receptors are present than needed
  3. The EPP is stronger than needed for depolarization of sarcolemma
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49
Q

It takes several EPPs to generate an action potential in the muscle fiber. T/F

A

False, EPPs are an exception for EPSPs, where it only takes one to depolarize the sarcolemma to threshold and generate an AP. This is a safety factor where the EPP is greater than it needs to be to ensure transmission of an AP in muscle fiber.

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50
Q

Cause+Effect:

An anti-acetylcholinesterase drug

A

Pro-longed postsynaptic response to ACh

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51
Q

Cause + Effect:

Blocking voltage-gated calcium channels in nerves

A

Prevents exocytosis of ACh

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52
Q

Cause + Effect:

Blocking voltage-gated K+ channels

A

Prevents repolarization of presynaptic membrane and increases release of ACh

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53
Q

Cause + Effect:

Blocking voltage-gated Na+ channels (tetrodotoxin)

A

Prevents nerve and muscle action potentials

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54
Q

Cause + Effect:

Blocking synaptic vesicle exocytosis in inhibitory neurons

A

Produces skeletal muscle spasms (lockjaw)

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55
Q

Cause + Effect:

Blocking the acetylcholine receptor

A

Produces flaccid paralysis

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56
Q

Calsequestrin

A

Calcium binding protein found in SR, lowers concentration of free calcium, makes overcoming gradient easier

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57
Q

Terminal cisterns

A

The Junctional SR regions that act as reservoirs for calcium

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58
Q

How does the action potential travel to all of the muscle fibers and initiate contraction?

A

Through the T-tubule, which contains extracellular fluid

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59
Q

Dihydropyridine receptors

A

Channels in the sarcolemma that act as voltage sensors and voltage-gated calcium channels
Remain open for a long time after stimulation by AP from T-tubule
AKA L-type calcium channels

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60
Q

What are the DHPR blocked by?

A

Dihydropyridine

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61
Q

What is another name for the dihydropyridine receptors?

A

L-type calcium channels

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62
Q

Ryanodine receptor

A

Calcium release channel in the membrane of the SR

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63
Q

CCICR

A

Calcium channel induced calcium release

DHPR stimulates the RYR to release calcium into the sarcoplasm, down its concentration gradient

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64
Q

Where is the DHPR located?

A

In the membrane of the sarcolemma

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65
Q

Where is the RYR located?

A

In the membrane of the SR

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66
Q

CICR

A

Calcium induced calcium release
Depolarization of the T-tubule stimulates the L-type calcium channels to open and calcium goes into the sarcoplasm down its concentration gradient. This calcium directly stimulates the RYR to open and the SR to release calcium

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67
Q

CICR is an essential process in the ___

A

Cardiac muscle

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68
Q

In skeletal muscle, DHPR acts primarily as ___

A

Voltage sensory for CCICR

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69
Q

What percentage of calcium in the sarcoplasm comes from the T-tubule in CICR?

A

20%

Calcium from the EC acts as a stimulus for the RYR to release calcium

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70
Q

Where are T-tubules located in relation to the sarcomere?

A

At the junction of the A and I bands

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71
Q

What happens to the calcium released into the sarcoplasm by the sarcoplasmic reticulum?

A

The calcium binds to troponin (TnC), which causes a conformational change and moves tropomyosin out of the active site of actin. The myosin head can bind to the actin filament and initiate contraction

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72
Q

What is the overall process for excitation/contraction coupling? (5 steps)

A
  1. The AP travels down the sarcolemma and into the T-tubules
  2. The AP activates the DHPR (L-type calcium channels)
  3. The DHPR stimulates the RYR in the SR to open
  4. The SR releases calcium down its gradient into the sarcoplasm
  5. Calcium binds to TnC subunit of troponin, causing a conformational change that moves tropomyosin out from the actin active sites, allowing the myosin heads to bind to the thin actin filaments and initiate contraction
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73
Q

What structure is responsible for the power stroke?

A

The myosin head of the thick filaments

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74
Q

What powers the movement of the myosin head?

A

The breakdown of ATP to ADP by the ATPase of the myosin head

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75
Q

What filament is moved during contraction? In what direction (in relation to the sarcomere)?

A

The thin actin filament is moved towards the M line

76
Q

How does the myosin head achieve the cocked state?

A

The breakdown of ATP to ADP (from ATPase ability of myosin head)

77
Q

When ADP is bound, the myosin has ___ affinity for the actin filament.

A

High

78
Q

In the cocked state, the myosin head is positioned ___ the M-line

A

Away from

79
Q

For the cross-bridge formation, what is necessary?

A

High intracellular concentration of calcium (for tropomyosin to be released from actin active site)

80
Q

Cross-bridge state

A

When the myosin head binds to the actin filament, bridging the filaments
Occurs with high intracellular calcium concentration and tropomyosin removed from actin groove

81
Q

How does the myosin head achieve the power stroke?

A

Release of ADP and inorganic phosphate from the myosin head

Head moves from 90 to 45 degree angle, moves actin filament towards the M line

82
Q

Why does Rigor mortis occur after death?

A

After death, ATP levels in the body deplete, while calcium leaks into the sarcoplasm, leaving the myosin head attached to the thin actin filament in contraction, but without means to release

83
Q

When ATP is bound to the myosin head, the head has a ___ affinity for the actin filament.

A

Low

84
Q

What causes the myosin head to release the actin filament?

A

The binding of ATP to the myosin head

85
Q

Each of the myofilaments act synchronously in contraction. T/F

A

False, the myosin filaments act asynchronously, allowing for smooth contractions rather than jerky ones

86
Q

What allows for smooth contractions rather than jerky ones?

A

The fact that the many myosin heads of a muscle fiber are in different stages of the cross-bridge cycle at one time

87
Q

SERCA pump

A

Sarcoplasmic/endoplasmic reticulum caclium ATPase pump
Uses primary active transport to move calcium against its concentration gradient from sarcoplasm into the SR
Activity of SERCA pump is increased by the phosphorylation of phospholamben

88
Q

How does phospholamben help in muscle relaxation?

A

When phosphorylated, phospholamben increases the activity of the SERCA pump, resequestering more calcium into the SR

89
Q

How does calsequestrin help in muscle relaxation?

A

Binds calcium in SR, lowers concentration of free calcium, makes overcoming gradient easier for SERCA pumps

90
Q

Besides helping to terminate muscle contraction, what is another function of calsequestrin?

A

To localize the calcium in the Junctional SR, for easy release

91
Q

During a skeletal muscle contraction in which the sarcomere shortens, the length of the I band decreases. T/F

A

True

92
Q

In the neuromuscular junction, acetylcholine binds to

nicotinic, cholinergic receptors at the motor end plate. T/F

A

True

93
Q

During an end-plate potential, an influx of ___ through ___-gated, non-specific ___ channels leads to depolarization.

A

Sodium, ligand, cation

94
Q

In order for a skeletal muscle contraction to occur, there must be an increase in sarcoplasmic ___?

A

Calcium

95
Q

Which of the following composes the “triad” found in skeletal muscle?

A

A T-tubule and 2 Junctional SR

96
Q

In skeletal muscle, what is the primary source of sarcoplasmic calcium?

A

Release from the SR via ryanodine receptors

97
Q

The magnitude of a miniature end-plate potential is 3-4 times greater than required to initiate depolarization of the sarcolemma to threshold. T/F

A

False

98
Q

Muscle twitch

A

One muscular contraction and relaxation cycle

99
Q

What are the three phases of a muscle twitch?

A

The latent period, contraction period, and relaxation period

100
Q

Latent period of muscle twitch

A

Between electrical stimulus and generation of muscle tension

101
Q

What is happening during the latent period of a muscle twitch?

A

AP spreads down sarcolemma, RYR opens, calcium influx from SR, binds to TnC and tropomyosin moves from actin groove

102
Q

Contraction period

A

When muscle is generating tension

103
Q

Relaxation period

A

When muscle is releasing tension

104
Q

Optimal length of sarcomere for skeletal muscle

A

2.2 microns

105
Q

Preload

A

The length of the muscle prior to contraction

106
Q

The ability of the sarcomere to generate tension is dependent on?

A

The sarcomere initial length prior to contraction (preload)

107
Q

Recruitment

A

When the load is large enough, additional motor units need to be recruited
AKA synchronous summation or spatial summation

108
Q

Asynchronous motor unit summation

A

The activity of different motor units at different times for sustained contraction (posture)

109
Q

Tetanus

A

Fused muscle contraction

110
Q

What is the cause of tetanus?

A

The same motor unit repeatedly stimulated in quick succession (temporal summation)

111
Q

Isometric twitch

A

No shortening of the anatomical muscle length as the tension generated doesn’t move the large load
The sarcomeres shorten (actin and myosin form crossbridges) and the elastic elements stretch

112
Q

Isotonic twitch

A

Muscle first contracts isometrically until the tension generated can move the load, then muscle shortens and tension stays constant during contraction and relaxation

113
Q

Which contraction type allows for more overall tension to be generated?

A

Isometric

114
Q

Which contraction type allows for more muscle building?

A

Isotonic

115
Q

Sarcomeres shorten in both isometric and isotonic contractions. T/F

A

True, but the entire anatomical length doesn’t change in isometric

116
Q

During isometric contraction, the ___ stays the same while the ___ shorten.

A

Anatomical muscle length, sarcomere

117
Q

Muscle fatigue

A

Caused by diminished energy stores or ACh in nerve terminals

118
Q

Hypertrophy

A

When muscles are required to contract repeatedly against heavy loads, building the cells and muscles with new sarcomeres, vessels, and mitochondria

119
Q

Hyperplasia

A

An increase in the number of muscle fibers, very rare

120
Q

Atrophy

A

Cell and muscle size decrease from lack of use

121
Q

3 energy sources for muscle cells

A

Creatine phosphate, glycolysis, and cellular respiration

122
Q

Creatine phosphate

A

Short term supply of energy that powers contraction for 10 seconds (gives phosphate to ADP to make ATP)

123
Q

Glycolysis

A

Glycogen stored in muscle is broken down into glucose, which enters glycolysis (enzyme cascade) in cytoplasm that produces 2 ATP
Doesn’t use oxygen

124
Q

Cellular respiration

A

End products of glycolysis undergo respiration in mitochondria, yields 32 ATP
Uses oxygen as final electron acceptor

125
Q

Type 1 slow muscles

A

Generate contraction for long periods of time for endurance, use cellular respiration to produce energy
Red

126
Q

Type 2 fast muscles

A

Capable of rapid contraction, but can’t endure period of sustained contraction, depend on glycolytic processes for energy
White

127
Q

A motor unit can be mixed with fast and slow muscle fibers. T/F

A

False, all the muscle fibers in one motor unit are the same type

128
Q

A given muscle may contain a mix of both slow and fast fibers. T/F

A

True

129
Q

Motor unit muscle types can be modified over time. T/F

A

True, can transition from one muscle fiber type to another with training

130
Q

___ muscles depend on cellular respiration, while ___ muscles rely heavily on glycolytic processes.

A

Type 1 slow, type 2 fast

131
Q

___ muscles are capable of rapid contraction for sprints, while ___ muscles are able to generate contractions for extended periods of time for endurance.

A

Type 2, type 1

132
Q

Type 1 slow muscle characteristics

A

Lots of myoglobin and mitochondria, dense capillary network, and slow ATPase and SERCA

133
Q

Type 2 fast muscle characteristics

A

Little myoglobin and mitochondria, fast ATPase and SERCA

134
Q

Which muscle type is more vascular? Why?

A

Type I because it depends on cellular respiration to produce energy, which uses oxygen

135
Q

Cardiac muscle anatomy

A 
Branched fibers (Z shape) 
Central nuclei (1-2)
Intercalated discs made of desmosomes (tightly anchor cells) and gap junctions (electrically connect cells) 
Sarcomeres (striated appearance) 
Dyad (1 T-tubule and 1 Junctional SR)
136
Q

What are intercalated discs composed of?

A

Desmosomes and gap junctions

137
Q

What is the function of gap junctions in cardiac muscles?

A

Allow ions to flow easily from cardiac cell to cell, electrically connecting them, allowing electrical syncytium

138
Q

Electrical syncytium

A

The ability of the heart to beat as one unit due to gap junctions

139
Q

What anchors the cardiac cells together to prevent separation during contraction?

A

Desmosomes of intercalated discs

140
Q

The T-tubule and Junctional SR form a ___ in skeletal muscle and a ___ in cardiac muscle.

A

Triad, dyad

141
Q

The DHPR and RYR are closely associated in both skeletal muscle and cardiac muscle. T/F

A

False, they are not closely associated in cardiac muscle

142
Q

How are heart action potentials generated intrinsically?

A

The SA node can self-depolarize due to an unstable resting membrane potential

143
Q

Does the cardiac muscle use CCICR or CCIR for muscle excitation?

A

Both. Cardiac muscle uses CCICR but must have an influx of extracellular calcium through DHPR for CICR

144
Q

How much of sarcoplasmic calcium comes from extracellular sources?

A

20% is from influx through DHPR of CICR

145
Q

What are the 3 methods for resequestering calcium during relaxation of cardiac muscle?

A
  • -SERCA pumps bring calcium back into SR
  • -Sodium calcium exchanger uses secondary active transport to move calcium back into ECF across the sarcolemma
  • -Sarcolemmal calcium pump actively transports calcium back into ECF
146
Q

What locations is calcium resequestered back into during relaxation of cardiac muscle? Why?

A

SR (SERCA pump) and ECF (sodium/calcium exchanger & sarcolemmal pump)
Calcium needs to return to those areas because it came from both of those areas due to CCICR and CICR

147
Q

At the motor end-plate, ACh binds to ___-gated, non-specific cation channels

A

Ligand

148
Q

___ end-plate potentials occur due to quantal release of ACh from the terminal bouton. This occurs without the electrical stimulus of an action potential.

A

Miniature

149
Q

T-tubules contain ___

A

ECF

150
Q

___ is a synonym for cytoplasm in muscle cells.

A

Sarcoplasm

151
Q

Sarcomeres shorten during isometric contraction. T/F

A

True

152
Q

Cardiac muscle contains ___ composed of one T-tubule and one junctional SR

A

dyad

153
Q

Smooth muscle anatomy

A 
Smaller, spindle-like / fusiform 
Have caveolae (small indentations) instead of T-tubules  where calcium enters the cells 
Actin attached to plasma membrane and dense bodies in cytoplasm (not arranged in sarcomeres)
154
Q

Smooth muscle contain T-tubules. T/F

A

False, smooth muscle has caveolae instead

155
Q

Unitary smooth muscle

A

Connected by gap junctions, contract as unit, capable of self-depolarization (produce slow waves)
Found in GI, bladder, uterus, common throughout body

156
Q

Multi-unit smooth muscle

A

Myofibers acts separately, innervated by ANS, found in eye and vas deferens

157
Q

Smooth muscle is dependent on ___ for contraction.

A

Calcium

158
Q

The depolarization of smooth muscle is due to fast sodium channels. T/F

A

False, it is due to an increase in intracellular calcium

159
Q

What are the 6 ways intracellular calcium can be increased during smooth muscle excitation?

A
  1. Voltage-gated calcium channels
  2. CICR
  3. Ligand-gated calcium channels
  4. IP3 mediated release
  5. Store-operated channels
  6. Stretch-operated channels
160
Q

Smooth muscle: voltage-gated calcium channels

A

Channels in plasma membrane open due to electrical signal

161
Q

Smooth muscle: CICR

A

Increase in intracellular calcium triggers opening of RYR channels of SR

162
Q

Smooth muscle: ligand-gated calcium channels

A

Angiotensin II / NoEP bind and allow calcium influx from ECF

163
Q

Smooth muscle: IP3 mediated release

A

EC ligands bind to G-protein coupled receptors, cause release of intracellular IP3, which leads to calcium release from SR

164
Q

Smooth muscle: store-operated calcium channels

A

When SR calcium gets low, these channels in plasma membrane replenish calcium

165
Q

Smooth muscle: stretch-operated calcium channels

A

Channels in plasma membrane open when smooth muscle cell is stretched

166
Q

Smooth muscle uses troponin to regulate contraction. T/F

A

False, smooth muscle uses calcium-calmodulin to activate the myosin light chain kinase to phosphorylate the light chain on the myosin head, allowing cross-bridge cycle to occur

167
Q

Where is regulation of contraction done for smooth muscle?

A

At the thick filament

168
Q

Calmodulin

A

Binds calcium in the cytosol, forms calcium-calmodulin complex that activates myosin light chain kinase (MLCK)

169
Q

Myosin light chain kinase (MLCK)

A

Activated by calcium-calmodulin complex, phosphorylates the regulatory light chain on the myosin head, allowing cross-bridge formation

170
Q

The mechanism to regulate smooth muscle contraction also functions to control the strength of contraction in cardiac tissue. T/F

A

True

171
Q

The cross-bridge cycle in smooth muscle is the same as in skeletal muscle. T/F

A

True

172
Q

What are the 3 processes for smooth muscle relaxation?

A
  1. Intracellular calcium decreased via sequestration in SR or removal through plasma membrane
  2. MLCK inactivated to prevent further phosphorylation of myosin heads
  3. Myosin light chain phosphatase (MLCP) removes phosphate groups from myosin regulatory light chain
173
Q

Myosin light chain phosphatase (MLCP)

A

Removes phosphate from the myosin regulatory light chain in smooth muscle relaxation
Can also remove the phosphate while the myosin head is still bound to actin, causing muscle to remain in latch state (continued contraction)

174
Q

___ is responsible for the latched state.

A

Myosin light chain phosphatase

175
Q

Latch state

A

A state of continued contraction with low energy expenditure in smooth muscle
Caused by MLCP removing phosphate from myosin head while attached to actin

176
Q

Only skeletal muscle can contain multiple nuclei (>2). T/F

A

True

177
Q

Only skeletal and smooth muscle are striated. T/F

A

False

178
Q

Only cardiac muscle fibers are branched. T/F

A

True

179
Q

Only cardiac and smooth muscle fibers are spindle-shaped. T/F

A

False, only smooth muscle

180
Q

All 3 muscle type contain T-Tubules. T/F

A

False, smooth muscle has caveolae

181
Q

Only cardiac and smooth muscle are electrically coupled via gap junctions. T/F

A

True

182
Q

Only skeletal muscle and smooth muscle contain sarcomeres. T/F

A

False, cardiac muscle contains sarcomeres but smooth muscle does not

183
Q

Only skeletal and cardiac muscle have cross-bridge formation by binding calcium to troponin. T/F

A

True

184
Q

In only skeletal and cardiac muscle, the tension generated varies with filament overlap. T/F

A

False, smooth muscle too

185
Q

Only in smooth muscle is the force of primary contraction influenced by MLCK activation. T/F

A

False, cardiac muscle also is regulated by MLCK

Physio (8 decks)

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