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DPT 6150 PHYSIOLOGY > Week 2 Questions > Flashcards

Week 2 Questions Flashcards

1
Q
  1. What is the diffusion potential?
A

a. The potential difference generated across a membrane when an ion diffuses down its concentration gradient
b. Can only be generated if the membrane is permeable to that ion

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2
Q
  1. The ____ of the diffusion potential depends on the size of the concentration gradient.
A

a. Magnitude

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3
Q
  1. What is the equilibrium potential?
A

a. The diffusion potential that exactly balances or opposes the tendency for diffusion down the concentration gradient

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4
Q
  1. The electrochemical equilibrium occurs when the chemical and electrical driving forces acting on an ion are ___ and ___.
A

a. Equal and opposite

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5
Q
  1. How would we calculate the equilibrium potential?
A

a. Using the Nernst equation

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6
Q
  1. What is a membrane potential?
A

a. Arise when there is a difference in electrical change between both sides of a membrane

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7
Q
  1. The charge difference of the membrane potential, can result from what two things?
A

a. Passive ion diffusion– 90%
b. Electrogenic pumping– 10%
i. Sodium-potassium pump

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8
Q
  1. How does K+ maintain electroneutrality?
A

a. Leak channels

b. More permeable than Na+

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9
Q
  1. As K+ goes out of the cell it is losing positive charges and therefore the ____ becomes more positive.
A

a. Outside

i. Assuming the cell membrane is only permeable to K+

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10
Q
  1. As Na+ goes into the cell, the ____ becomes more positive.
A

a. Inside

i. Assuming the cell membrane is only permeable to Na+

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11
Q
  1. The resting membrane potential is closer to the equilibrium potential of K+ than it is to Na+. Why is this?
A

a. The membrane is more far more permeable to K+ than Na+

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12
Q
  1. What two processes allow for more K+ than Na+?
A

a. Sodium-potassium pump

b. K+ leak channels

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13
Q
  1. The Nernst Equation allows us to determine the equilibrium potential for each ion when..
A

a. We assume that the membrane is only permeable to that ion

b. We know the chemical concentrations across the membrane

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14
Q
  1. What does the Goldman Equation?
A

a. Can estimate the membrane potential for multiple ions

b. We have to know the permeability and concentration of the ions across the cell

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15
Q
  1. What three characteristics does diffusion potential depend on?
A

a. Polarity of each charge
b. Permeability of membrane to each ion
c. Concentration gradients

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16
Q
  1. The resting membrane potential is closest to the equilibrium potential for the ion with the highest ______.
A

a. Permeability

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17
Q
  1. What is the resting membrane potential?
A

a. -90mV

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18
Q
  1. What maintains the resting membrane potentials?
A

a. Passive Ion diffusion
b. Electrogenic pumping
i. Sodium-potassium pump

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19
Q
  1. What is an action potential?
A

a. Basic mechanism for transmission of information in the nervous system

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20
Q
  1. An action potential is the regeneration of depolarization of membrane potential that___ along an ___ membrane.
A

a. Propagates: conducted without decrement

b. Excitable: capable of generating action potentials

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21
Q
  1. What is the resting membrane potential?
A

a. -90 mV

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22
Q
  1. Depolarization is the process of making the membrane potential___ negative .
A

a. less

i. Moving closer to 0 mV

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23
Q
  1. Hyperpolarization is the process of making the membrane potential ___negative.
A

a. More negative

i. Moving farther away from 0 mv

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24
Q
  1. ____is when the membrane potential is moving back towards resting membrane potential.
A

a. Repolarization

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25
Q
  1. What is excitability?
A

a. The ability of the membrane to shift its polarization in response to stimuli from resting membrane potential to depolarized state and back

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26
Q
  1. What is threshold potential?
A

a. The membrane potential at which occurrence of the action potential is inevitable
b. -50mV

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27
Q
  1. The ___ is the flow of positive charge into the cell and causes the membrane potential to become ____.
A

a. Inward

b. Depolarize

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28
Q
  1. The ____ is the flow of positive charge out of the cell and causes the membrane potential to become ___.
A

a. Outward

b. Hyperpolarize

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29
Q
  1. What is the overshoot?
A

a. Also called polarize
b. The portion of the action potential where the membrane potential is positive
c. Pass 0 mV

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30
Q
  1. What does it mean to undershoot?
A

a. Also called hyperpolarization afterpotential
b. The portion of the action potential (following repolarization) where the membrane potential is actually more negative than at rest

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31
Q
  1. What is the refractory period?
A

a. A period during which another normal action potential CANNOT be elicited in an excitable cell
b. Can be absolute or relative

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32
Q
  1. Action potentials are an _____ event.
A

a. All-or-none

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33
Q
  1. Action potentials have constant___.
A

a. Amplitude

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34
Q
  1. True/false: action potentials can summate.
A

a. FALSE

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35
Q
  1. Action potentials are initiated by____.
A

a. Depolarization

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36
Q
  1. Action potentials involve changes in_____.
A

a. Permeability

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37
Q
  1. Action potentials rely on ____channels.
A

a. Voltage-gated

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38
Q
  1. If we have a stronger stimulus, will we have a stronger amplitude?
A

a. No

i. Constant amplitude

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39
Q
  1. Fibers with ___ diameter conduct faster than ___fibers.
A

a. Larger
i. More myelination
b. Small

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40
Q
  1. Why do voltage-gated sodium channels open when the membrane potential becomes less negative and reaches threshold?
A

a. The stimulus causes the membrane to become more positive (depolarization)
b. The voltage sensor repels the positive charges, causing the portion of the channel to slide up
c. This opens the inactivation gate and allows sodium to flow into the cell

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41
Q
  1. What does the resting membrane look like?
A

a. Approximately -90mV
b. High conductance/permeability of K+
c. Low conductance of Na+

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42
Q
  1. At resting membrane potential, the ____ gate is closed
A

a. Activation gate

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43
Q
  1. What causes the activation gate to open?
A

a. Depolarization of the membrane (-90 mV to +35 mV)

b. Reaches threshold

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44
Q
  1. What occurs during the upstroke of the action potential?
A

a. Influx of Na+ into the cell

b. Happens very quickly

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45
Q
  1. The same stimulus that opens the activation gate also closes the ___ gate and OPENS the ___ channels.
A

a. Inactivation
b. K+
i. These two are both delayed responses

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46
Q
  1. At some point the activation gate is ___ and the inactivation gate is open.
A

a. Closed

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47
Q
  1. The downstroke of the action potential is caused by what two factors?
A

a. Closure of the Na+ channels

b. Efflux of K+ out of the cell

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48
Q
  1. The efflux of K+ causes the cell to become____.
A

a. Hyperpolarized

i. More negative

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49
Q
  1. Why does the after hyperpolarization phase occur?
A

a. Because the delayed closure of the K+ channels

b. K+ I higher than at rest and the membrane potential is driven even close to the K+ equilibrium potential

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50
Q
  1. Is the after hyperpolarization phase always seen?
A

a. No

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51
Q
  1. What medications block voltage-gated Na+ channels?
A

a. Tetrodoxtoxin

b. Lidocaine

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52
Q
  1. What medications block voltage-gated K+ channels?
A

a. TEA– tetraethylammonium

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53
Q
  1. What are the three combinations of the gates’ positions?
A

a. Closed but available
i. Occurs at resting membrane potential
ii. Activation gate is closed
iii. Inactivation gate is opened
b. Open
i. Occurs during the upstroke of the action potential
ii. Both gates are briefly open
c. Inactivated
i. Occurs at the peak of the action potential
ii. Both gates are closed

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54
Q
  1. How do the Na+ channels return to the closed but available state?
A

a. During repolarization, the inactivation gate opens

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55
Q
  1. True/false: action potential propagations have specific direction.
A

a. False– they do not have a specific direction

i. Due to activation gates being shut– Refractory period

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56
Q
  1. What are refractory periods?
A

a. Excitable cells cannot produce normal action potentials

b. Difficult or impossible for another action potential to occur

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57
Q
  1. What are the two types of refractory periods?
A

a. Absolute

b. Relative

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58
Q
  1. What is the absolute refractory period?
A

a. Overlaps with almost the entire duration of the action potential

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59
Q
  1. What is the basis for the absolute refractory period?
A

a. The closure of the Na+ channels in response to depolarization

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60
Q
  1. What is relative refractory period?
A

a. Begins at the end of the absolute refractory period

b. Overlaps primarily with the period of the hyperpolarization afterpotential

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61
Q
  1. During which refractory period can an action potential be elicited?
A

a. Relative

i. Only if greater than usual depolarization current is applied

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62
Q
  1. What is accommodation?
A

a. When a nerve or muscle cell is depolarized slowly or is held at a depolarized level
b. May pass threshold without an action potential being fired

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63
Q
  1. If depolarization occurs slowly enough, the Na+ channels ___.
A

a. Remain closed

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64
Q
  1. What is hyperkalemia?
A

a. Example of accommodation
b. Elevated [K]
c. The cell is less likely to fire an action potential because the sustained depolarization closes the inactivation gates on the Na+ channels

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65
Q
  1. What surrounds the axons?
A

a. Myelin sheath

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66
Q
  1. ____ in the CNS surround the axon and are responsible for myelination.
A

a. Schwann cells

i. Produces myelination

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67
Q
  1. Breaks in the myelin sheath are called _____.
A

a. Nodes of ranvier

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68
Q
  1. Voltage-gated Na+ channels are localized near the ____.
A

a. Nodes of Ranvier

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69
Q
  1. What is saltatory conduction?
A

a. Where the current is amplified at the nodes of ranvier by voltage gated Na+ channels
i. Makes propagation much faster

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70
Q
  1. Is the conduction speed of action potentials faster on a myelinated or non-myelinated axons?
A

a. Myelinated
i. On non-myelinated axons the sodium channels are activated at each spot vs. on a myelinated axon the sodium channels are activated at the nodes of Ranvier

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71
Q
  1. _____ is an immune-mediated inflammatory demyelinating disease of the CNS.
A

a. Multiple sclerosis

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72
Q
  1. How does MS affect the CNS?
A

a. The action potential won’t be able to pass and the CNS won’t be able to provide normal functions

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73
Q
  1. Do the symptoms go away completely?
A

a. No

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74
Q
  1. What is conduction velocity?
A

a. The speed at which action potentials are conducted along a nerve/muscle fiber
b. Time/length constant

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75
Q
  1. What is the time constant?
A

a. Indicates how quickly a cell membrane depolarizes in response to an inward current or how quickly it hyperpolarizes in response to an outward current

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76
Q
  1. What are two factors that affect the time constant?
A

a. Membrane resistance

b. Membrane capacitance

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77
Q
  1. When the membrane resistance is high, the time constant ____.
A

a. Increased

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78
Q
  1. When the membrane capacitance (ability to store charge) is high, the time constant is ___.
A

a. Increased

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79
Q
  1. What are two mechanisms that increase conduction velocity along a nerve?
A

a. Increase nerve diameter
i. The larger the fiber, the lower the internal resistance
b. Myelination
i. Increases membrane resistance and decreases membrane capacitance

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80
Q
  1. What are synapses?
A

a. How cells communicate

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81
Q
  1. What are the two different types of synapses?
A

a. Electrical

b. Chemical

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82
Q
  1. What is an electrical synapse?
A

a. Allows current to flow from one excitable cell to the other via low resistance pathways called gap junctions

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83
Q
  1. Where are gap junctions found?
A

a. In cardiac muscles and some types of smooth muscle

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84
Q
  1. Transmission of information in the electrical synapses is___.
A

a. Bidirectional

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85
Q
  1. What are chemical synapses?
A

a. There is a gap between the presynaptic membrane and the postsynaptic membrane called the synaptic cleft

86
Q
  1. Information in the chemical synapses is transmitted via___.
A

a. Neurotransmitters

87
Q
  1. The change in potential on the _____ can either be ____ or ___.
A

a. Postsynaptic side

b. Excitatory or inhibitory

88
Q
  1. In which of the synapses is there a presence of a synaptic delay?
A

a. Chemical

i. No synaptic delay in the electrical synapse

89
Q
  1. In the chemical synapses, what causes this delay?
A

a. The multiple steps in chemical neurotransmission to occur

90
Q
  1. What is a motorneuron?
A

a. The nerves that innervate muscle fibers

91
Q
  1. What is a motor unit?
A

a. Comprises of a single motor neuron and the muscle fibers it innervates

92
Q
  1. What is the motor end plate?
A

a. Where the nerve innervates the muscle fiber

93
Q
  1. What is the importance of the invaginations?
A

a. Increase surface area available for receptors

b. Accept more neurotransmitter

94
Q
  1. What occurs at the NMJ?
A

a. An action potential travels down the end of the axon terminal
b. The action potential stimulates the opening of calcium channels
c. Calcium enters the cell
d. Once calcium enters the cell it stimulates the release of the vesicles to bind to the membrane
e. Once the vesicles bind to the membrane they release their neurotransmitters, in this case ACH
f. Ach enters the synaptic cleft and travels to the post synaptic membrane
g. Attach to the nicotinic receptors on the postsynaptic membrane
i. Only found in the muscle cells
h. Causes a conformational change that allows Na+ into the cell
i. Changes can be excitatory or inhibitory
i. Opens up voltage-gated Na+ channels
j. Action potential

95
Q
  1. ACH-channels are large enough to allow passage of Na+, K+, and Ca++, so why do more Na+ ions pass through?
A

a. The -ve potential inside the membrane attracts Na+ influx and prevents K+ efflux

96
Q
  1. What is the end-plate potential?
A

a. The local positive potential
b. Responsible for generation of the AP
c. Can increase resting potential by 50-75 mV

97
Q
  1. As long as ___ is present is continues to stimulate the motor-end plate.
A

a. ACH

98
Q
  1. What would happen if ACH was not removed from its receptor?
A

a. Contraction wouldn’t happen

99
Q
  1. What are the two ways ACH is removed?
A

a. ACH-esterase enzyme
i. 50%
b. Spillover of ACH
i. Spill into the synaptic cleft and away from the NMJ

100
Q
  1. What forms ACH?
A

a. Choline and acetyl CoA

101
Q
  1. What is the function of the T-tubules in excitation-contraction coupling?
A

a. Responsible for carrying depolarization from action potentials at the muscle cell surface to the interior of the fiber (deep myofibrils)

102
Q
  1. Where is the dihydropyridine receptor (DHPR) located?
A

a. The membrane of the t-tubule

103
Q
  1. Where is the ryanodine receptor located?
A

a. On the membrane of the SR

104
Q
  1. What is the function the DHPR?
A

a. Opens voltage-gated Ca+ channels once the signal comes down the t-tubule

105
Q
  1. Once the channels open the calcium flows from the inside of the cell to the outside of the cell, and then binds to the ____ receptors.
A

a. Ryanodine receptor (RyR)

106
Q
  1. The binding to the RyR causes a conformation change that then allows…
A

a. Ca+ stored in the SR to be released into the cytoplasm

107
Q
  1. What happens when there is a high amount of Ca++ in the cytoplasm?
A

a. Calcium attached to the troponin C
i. Myosin-actin binding
ii. Movement

108
Q
  1. How does Ca++ get transported from the cytoplasm back into the SR?
A

a. SERCA 2

109
Q
  1. What are the steps involved in pumping calcium back into the SR?
A

a. Action potentials come down the t-tubule
b. Activates voltage-gated Ca++ channels
c. Ca++ is released into the cytosol and binds to the RyR
d. Once the RyR is stimulated it releases Ca++ from the SR into the cytosol
e. Initiates muscle contraction
f. Ca++ is the pumped against its concentration gradient using ATP and SERCA2 back into the SR

110
Q
  1. What is this process called?
A

a. Calcium-induced calcium release (CICR)

111
Q
  1. What does SERCA stand for?
A

a. Sarcoplasmic Endoplasmic Reticulum Ca++ ATPase

112
Q
  1. Ca++ is accumulated in the SR by the pump action of ____.
A

a. SERCA

113
Q
  1. Ca++ in the SR binds to _____.
A

a. Calsequestrin

114
Q
  1. What happens once Ca++ is reaccumulated back into the SR?
A

a. Relaxation

115
Q
  1. What are the 5 sets of ion channels involved in neuromuscular transmission?
A

a. Voltage-gated Ca++ channels
b. ACH-receptors (nicotinic receptors)
c. Voltage-gated Na+ channels
d. DHPR
e. RyR

116
Q
  1. Steps of neuromuscular transmission
A

a. Nerve impulse depolarizes the axon terminal, and opens voltage-gated Ca++ channels. Ca++ rushes into the nerve axon stimulating the release of ___.
i. ACH
b. Ach binds to ____, causing a conformation change that opens the channel causing Na+ influx
i. Nicotinic receptors
c. The local depolarization causes opening of voltage-gated __ channels, allowing __ influx and self-propagation of AP.
i. Na+
d. Impulse reaches the _____, causes the voltage-sensitive ____ to open.
i. t-tubule
ii. DHPR
e. This stimulates the ___ release channel and activates the ___.
i. Ca++
ii. RyR
f. The RyR releases Ca++ from the ___ into the ___.
i. SR
ii. The muscle cytoplasm

117
Q
  1. Which agent blocks ACH release from the nerve terminal and could potential cause paralysis and eventually death from respiratory failure?
A

a. Botulinum

118
Q
  1. Which agent competes with ACH for its receptor?
A

a. Curare
i. Max doses cause paralysis and death
ii. Prevents ACH from binding

119
Q
  1. Which agent inhibits Na+ channels and is found in the Japanese puffer fish?
A

a. Tetrodotoxin

120
Q
  1. Which agent would cause long-lasting contractions?
A

a. Neostigmine

i. AChE inhibitor

121
Q
  1. Which agent would prevent action potentials from happening?
A

a. Tetrodotoxin

122
Q
  1. Which agent blocks choline reuptake, thus depleted ACH?
A

a. Hemicholinium

i. Premature fatigue

123
Q
  1. True/false: if these agents are given at any dosage, there is a chance for paralysis and eventually death.
A

a. False: they have to be given in proper dosages

124
Q
  1. Excitatory neurotransmitter___ the postsynaptic cell.
A

a. Depolarize

i. EPSP

125
Q
  1. What are some examples of EPSP?
A

a. ACH, norepinephrine, epinephrine, dopamine, glutamate, serotonin

126
Q
  1. Inhibitory neurotransmitters _____ by opening Cl- or K+ channels.
A

a. Hyperpolarize

127
Q
  1. What are some examples of IPSP?
A

a. GABA and glycine

128
Q
  1. Anatomy of a muscle from smallest to largest structure
A

a. filaments
b. Muscle fiber (cell)
c. Fascicle
d. Muscle

129
Q
  1. The ___ surrounds the muscle fibers.
A

a. Endomysium

130
Q
  1. The ____surrounds muscle fascicles.
A

a. Perimysium

131
Q
  1. The entire muscle is surrounded by the ___.
A

a. Epimysium

132
Q
  1. Blood vessels and nerves that supply the muscle fibers are found within the ____.
A

a. Perimysium

133
Q
  1. What is the sarcomere?
A

a. Portion of the myofibril that lies between 2 adjacent Z disks

134
Q
  1. The light bands, or the I bands, only contain ____.
A

a. Actin

135
Q
  1. The dark bands, or the A bands, contain ____.
A

a. Actin and myosin

136
Q
  1. The z disks run down the middle of the ___ band.
A

a. I

137
Q
  1. Where is the bare zone?
A

a. Also called the H zone
b. Located in the center of the sarcomere
c. Contains only thick filaments

138
Q
  1. Where is the M line?
A

a. In the middle of the bare zone

b. Links central portions of the thick filament together

139
Q
  1. What is the function of actin?
A

a. Not just present in muscles

b. Determines the shape of cell’s surface and are necessary for whole cell locomotion

140
Q
  1. How does actin play a role in whole cell locomotion?
A

a. Moves the cell by “treadmilling”
i. Actin has a plus end and a minus end
ii. The rate of polymerization if faster on the + end
iii. It can disassemble and reassemble very quickly
1. Reassembly occurs on the + end which moves actin

141
Q
  1. True/false: actin works alone.
A

a. False: actin has multiple assistants

142
Q
  1. Alpha-actin acts as an accessory protein that anchors actin with ____ which allows space for myosin to bind.
A

a. Lots of space

143
Q
  1. _____binds actin very tightly and prevents myosin from binding.
A

a. Fimbrin

144
Q
  1. _____nucleates assembly and remains associated with the growing plus end/
A

a. Formin

145
Q
  1. ____binds subunits, prevents assembly.
A

a. Thymosin

146
Q
  1. The _____ prevents assembly and disassembly at the plus end
A

a. Capping protein

147
Q
  1. ____stabilizes the actin filament.
A

a. Tropomyosin

148
Q
  1. ____ binds actin to the membrane.
A

a. Spectrin

149
Q
  1. The myosin superfamily is a membrane of a larger family of ___.
A

a. Motor proteins

150
Q
  1. Where did myosin II get its name from?
A

a. Two heads

151
Q
  1. Myosin is composed of __heavy chains and ___ light chains.
A

a. 2 heavy

b. 4 light

152
Q
  1. The protruding heads are called ____.
A

a. Cross-bridges

153
Q
  1. True/False: each myosin head is independent of each myosin head.
A

a. True– this is what makes muscle contractions smooth

154
Q
  1. Muscle contraction occurs by sliding of the myosin filament past the actin filament ____ any change in the length of either filament.
A

a. WITHOUT

155
Q
  1. This is called the _____.
A

a. Sliding filament theory

156
Q
  1. Cap Z binds to actin at the __ end.
A

a. Plus

157
Q
  1. Alpha-actin binds actin to the ___.
A

a. z-disk

158
Q
  1. Cap Z and alpha-actin together prevent ____.
A

a. Depolymerization

159
Q
  1. ____ acts as molecular rule and helps determine the exact length of each actin filament.
A

a. Nebulin

160
Q
  1. What caps the minus end and stabilized it?
A

a. Tropomolulin

161
Q
  1. What is the function of titin?
A

a. Acts as the molecular spring and allows the muscle fiber to recover after being overstretched

162
Q
  1. What are the steps of the walk-along theory?
A

a. Myosin and actin are attached– rigor conformation
b. ATP binds to the myosin head and decreases its affinity of actin and releases the actin filament
c. ATP becomes hydrolyzed (producing ADP and Pi), the myosin head is cocked into position
d. P is released from the myosin head and strengthens the bond between myosin and actin
e. Myosin binds again to the actin and ADP is released and allows myosin head to return to its original position
f. Myosin returning to its original position triggers the power stroke

163
Q
  1. At____ all the myosin cross-bridges are in contact with action.
A

a. Optimal length

164
Q
  1. What happens if the sarcomeres are too far apart?
A

a. Actin is pulled all the way out
b. No cross-bridge over lap
c. Zero tension

165
Q
  1. What happens is the sarcomeres are too close?
A

a. The Z disks bump into each other

b. Strength of contraction drops rapidly

166
Q
  1. What is passive tension?
A

a. The tension developed by simply stretching a muscle to different lengths

167
Q
  1. What produces passive tension?
A

a. Cytoskeleton (titin) and other connective tissue

168
Q
  1. When does the passive component come into play?
A

a. Only at longer lengths

169
Q
  1. What is total tension?
A

a. The tension developed when a muscle is stimulated to contract at different preloads
b. It is the sum of active tension developed by the cross-bridge cycling in the sarcomeres and the passive tension caused by stretching the muscle

170
Q
  1. What is active tension?
A

a. Represents the active force developed during cross-bridge cycling

171
Q
  1. How is active tension determined?
A

a. By subtracting the passive tension from the total tension

172
Q
  1. As the muscle is continuously stretched ___ tension decreases.
A

a. Active

173
Q
  1. As we stretch the muscle, ___ tension increases.
A

a. Passive

174
Q
  1. In the force-velocity relationship, if the load is increased, the velocity is___.
A

a. Decreased

i. Cross-bridges cannot cycle as rapidly against higher resistance

175
Q
  1. Why is the maximal velocity the same at all three initial muscle lengths?
A

a. When the load is at zero, the velocity of shortening will be at its max

176
Q
  1. Why is it that the maximum amount of force at a shorter length is only 2 kg (not much)?
A

a. The shorter the length (too short), less contraction, less force

177
Q
  1. The speed of contraction is determined by the ___ of myosin ATPase.
A

a. Vmax

178
Q
  1. _____ are fast and white.
A

a. High Vmax (think speed of light)

179
Q
  1. ____ are slow and red.
A

a. Low Vmax

180
Q
  1. Which type of fiber has a rapid rate of shortening?
A

a. High Vmax

181
Q
  1. Which type of fiber has a rapid cross bridge cycling?
A

a. High Vmax(fast)

182
Q
  1. Which type of fiber has slow cross bridge cyclinig?
A

a. Low Vmax (slow)

183
Q
  1. True/False: most muscles contain both fiber types but proportions differ.
A

a. True

184
Q
  1. True/False: all fibers in a particular motor unit will be of the same type.
A

a. True

185
Q
  1. Slow fibers are also known as ___.
A

a. Type I

186
Q
  1. Fast fibers are also known as ___.
A

a. Type II

187
Q
  1. Which type of fiber is glycolytic?
A

a. Fast twitch/ type II

188
Q
  1. Which type of fiber is oxidative?
A

a. Slow twitch/ type I

189
Q
  1. Which type of fiber has a high myoglobin content?
A

a. Slow twitch fibers

190
Q
  1. Which type of fiber has a low capillary density?
A

a. Fast twitch fibers

191
Q
  1. Which type of fiber does not have a lot of mitochondria?
A

a. Fast twitch

192
Q
  1. Which type of fiber has a low content of glycolytic enzymes?
A

a. Slow twitch

193
Q
  1. All fibers are ____ type in a given motor unit.
A

a. The same

194
Q
  1. Small motor units are used for?
A

a. Precise control

b. Rapid reacting

195
Q
  1. What are large motor units used for?
A

a. Coarse control

b. Slower reacting

196
Q
  1. Motor units overlap, which provides ____.
A

a. Coordination

197
Q
  1. What is force summation?
A

a. Increase in contraction intensity as a result of the additive effect on individual contractions
i. If we stimulate a muscle, we get a single twitchh
ii. If we keep stimulating the muscle at a faster rate– tetanization
iii. ONLY changing the rate of the stimulus which increases the force of contraction

198
Q
  1. What are two ways to increase the force of contraction with increase the amplitude of the stimulus?
A

a. Multiple fiber summation

b. Frequency summation

199
Q
  1. What is multiple fiber summation?
A

a. Results from an increase in the number of motor units contracting simultaneously (fiber recruitment)
i. Contributes to an increase in force contraction

200
Q
  1. What is the size principle?
A

a. The smaller motor units respond first and then the large motor units
i. The small motor units are more excitable and therefore respond first

201
Q
  1. What is the frequency summation?
A

a. Results from an increase in the frequency of contraction of a single motor unit

202
Q
  1. What is the staircase effect?
A

a. Increasing overall Ca++ availability in the myoplasm
i. If the muscle is stimulated before complete relaxation has occurred the new twitch will sum with the previous one
ii. If the action potential frequency is sufficiently high, the individual contractions are not resolved and a ‘fused tetanus’ contraction is recorded/

203
Q
  1. What is hypertrophy?
A

a. Caused by near maximal force development
b. Increase in actin and myosin
c. Myofibrils split
i. This is why we take protein after we workout

204
Q
  1. What is hyperplasia?
A

a. Very rare
b. Formation of new muscle fibers
c. Can be caused by endurance training

205
Q
  1. In both hypertrophy and hyperplasia, there in an increase in ____ but there I no change in ____ or _____ of contraction.
A

a. Force generation
b. Shortening capacity
c. Maximum velocity of contraction

206
Q
  1. During hypertrophy and hyperplasia the sarcomeres are added in ____.
A

a. parallel

207
Q
  1. In lengthening, there is no change in ____.
A

a. Force development

208
Q
  1. In lengthening, there is an increase in ___ and ____.
A

a. Shortening capacity

b. Maximum contraction velocity

209
Q
  1. What are the causes of atrophy?
A

a. Denervation/neuropathy
b. Tenotomy
i. Muscle is no longer attached to the bone
c. Sedentary life style
d. Plaster cast
e. Space flight (zero gravity)

210
Q
  1. What are the consequences to muscle performance?
A

a. Degeneration of contractile proteins
b. Decreased max force of contraction
c. Decreased velocity of contraction

DPT 6150 PHYSIOLOGY (3 decks)

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