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Physio > muscle (skeletal, cardiac, and smooth) > Flashcards

muscle (skeletal, cardiac, and smooth) Flashcards

1
Q

from largest to smallest, list the organization/components of skeletal muscle

A
  1. whole muscle
  2. fascicle
  3. muscle fiber
  4. myofibril
  5. sarcomere
  6. filaments (thick and thin)
  7. protein
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2
Q

what is the structure of thin filaments

A

intertwined chains/strands of ACTIN molecules

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3
Q

tropomyosin vs troponin

A
  • tropomyosin covers the active sites/myosin binding sites on actin (looks like a strand)
  • troponin is bound periodically to tropomysosin and contains 3 subunits
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4
Q

what are the 3 subunits of troponin

A

TnC= ca2+ binding
TnT=binds to tropomyosin
TnI= inhibitory role

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5
Q

what is the structure of thick filaments

A

composed of myosin….with myosin heavy chains and myosin light chains. also contains the “cross-bridge”. there is an ATP binding site and an actin binding site

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6
Q

what is an isoform

A

same protein but slightly different a.a and still has similar fn

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7
Q

what is a sarcomere

A

functional unit of contractile muscle that can shorten to generate force

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8
Q

what is a sarcomere composed of (3)

A

thick and thin filaments are z-discs

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9
Q

I-band

A

composed of only thin filaments…changes length during a contraction

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10
Q

A-band

A

composed of thick and thin filaments (overlapping)

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11
Q

H-zone

A

only thick filaments…changes length during a contraction bc the thin filaments move in towards the m-line

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12
Q

what are titin filaments for

A

they have rigid compenent that are anchored at z-discs and at the m-line on thick filamens. they STABILIZE thick filaments in the center of the sarcomere

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13
Q

do the lengths of thick and thin filaments vary from different muscle fibers

A

thick filaments DONT…always 1.6 microns in all mm fibers

thin filaments can vary in length

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14
Q

what is nebulin

A

it is a protein within thin filaments to determine the length of the thin filament…it spans the whole length of the thin filament and is anchored at the z-line along with the thin filament

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15
Q

describe the “pseudo crystalin” structure of a myofibril

A
  • every thin filament surrounded by 3 thick filaments

- every thick filament surrounded by 6 think filaments

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16
Q

what is excitation-contraction coupling

A

mechanism by which AP (excitation) in sarcolemma (membrane) initiates a contraction

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17
Q

in excitation-contraction coupling there is a very large increase in what

A

rapid, large increase in the free Ca2+ within the muscle cell

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18
Q

what is the mechanism for excitation coupling

A
  1. a.p reaches the sarcolemma and enters the T-TUBULE
  2. this causes Ca2+ to be released from the LATERAL SACS of the sarcoplasmic reticulum out into the sarcoplasm
  3. Ca binds to TnC and removes the tropomyosin block on the actin active sites
  4. Ca2+ is removed from TnC (reblocking the actin active sites)
  5. Ca2+ is uptaken into the fenestrated collar of the sarcoplasmic reticulum= relaxation
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19
Q

uptake of Ca2+ into the fenestrated collar during muscle relaxation is what kind of transport

A

active transport…uses ATP via the Ca2+-ATPase pump in the s.r

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20
Q

free Ca2+ is stored where

A

lateral sacs of the sarcoplasmic reticulum

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21
Q

what does free Ca2+ bind to in order to be held in the lateral sacs

A

calsequestrin

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22
Q

what is the DHP receptor

A

receptor in the sarcolemma/t-tubule region of a muscle cell. contains 2 components:

  • Ca2+ channel that is INACTIVE
  • a voltage sensor that senses the a.p that reach the muscle cell
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23
Q

the DHP receptor voltage sensor contacts what other receptor

A

ryanodine receptor

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24
Q

what is the ryanodine receptor

A

a receptor located on the s.r membrane that is a Ca2+ channel that releases Ca from the lateral sac of the s.r

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25
Q

what is the latent period in skeletal muscle contraction

A

the time during which there is no change in muscle length….aka the mechanical event has not yet occurred (a.p is traveling along the sarcolemma–>t-tubule–>s.r–>Ca2+ released–>etc)

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26
Q

what is the sliding filament theory

A

muscle shortens by a relative sliding of thick and thin filaments, the filaments don’t change length. the thin filaments move inwards towards the m-line

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27
Q

what is the cross-bridge theory

A

thick and thin filaments are not connected at rest. cross bridges form when there is an increase in free Ca2+

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28
Q

what are the 4 stages of the cross bridge cycle

A
  1. (following an increase in Ca) ENERGIZED myosin binds to actin and (ADP and P are bound)
  2. power stroke in which ADP and P are released and the actin/thin filaments move inward
  3. ATP binds to UNENERGIZED myosin (at ATP binding site) and causes the cross-bridge to detach
  4. ATP hydrolysis occurs–> ADP + P to ENERGIZE myosin (no cross bridge exists still)
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29
Q

the amount of force generated is proportional to

A

the number of attached crossbridges

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30
Q

the rate of the cross-bridge cycle determines the rate of

A

muscle shortening/contraction

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31
Q

what is the source of energy for muscle contraction

A

ATP

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32
Q

the ATP inside the muscle cell does not change concentration during muscle contraction due to what

A

phosphocreatine (molecule in muscle cells) acts as a buffer. PCr and ADP combine to form ATP via the activity of creatine kinase

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33
Q

where is there the highest concentration of creatine kinase enzyme

A

at the m-line!

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34
Q

what are 3 sources of ATP in muscle cells

A
  1. phosphocreatine via creatine kinase
  2. oxidative phosphorylation (ETC)
  3. glycolysis
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35
Q

during muscle contraction/relaxation, what uses ATP

A
  • the myosin ATPase during contraction

- the Ca2+-ATPase during relaxation…when Ca is uptaken into the fenestrated collar

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36
Q

what is the length-tension relationship

A
  • reflects the arrangement AND the length of thick and thin filaments
  • the greater the length of the muscle/muscle fiber/sarcomere, the greater amount of force that can be generated (up to a certain extent)
  • the length of the sarcomere is depended upon the thin filament length which is different b/w different muscles due to the type of nebulin present
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37
Q

the amount of force generated is dependent on

A

the length of the muscle fiber/sarcomere…bell curve

38
Q

what is a motor unit

A

a single motor neuron and all the muscle fibers it innervates

39
Q

slow fibers vs fast fibers…. NMJ

A

smaller NMJs

40
Q

slow fibers vs fast fibers….diameter

A

smaller in diameter

41
Q

slow fibers vs fast fibers….isoforms

A

slow contain different sarcomere protein isoforms

42
Q

slow fibers vs fast fibers….contraction velocity

A

contract more slowly

43
Q

slow fibers vs fast fibers….fatigue

A

more fatigue resistant

44
Q

slow fibers vs fast fibers….glycolysis

A

less glycolysis. fast fibers are more glycolysis

45
Q

slow fibers vs fast fibers….oxidative phosphorylation

A

slow fibers have more oxidative phosphorylation and have more mitochondria

46
Q

fast fibers= type II fibers…what are the two types of type II fibers

A

IIa (fast oxidative) and IIb (fast glycolytic)

47
Q

type IIa vs type IIb…size

A

IIa is smaller

48
Q

type IIa vs type IIb…oxidative metabolism

A

IIa depend more on

49
Q

type IIa vs type IIb…fatigue

A

IIa less fatigable

50
Q

type IIa vs type IIb…contraction velocity

A

IIa contract slower

51
Q

type IIa vs type IIb…glycolytic metabolism

A

IIb depends more on

52
Q

type IIa vs type IIb…efficiency

A

type IIb (although faster and generate more power) are less efficient than IIa

53
Q

what skeletal fiber type is more efficient

A

type I…or slow fibers!

54
Q

muscles for posture have what predominant fiber type

A

type 1

55
Q

muscles for tasks that are rapid or require a lot of dexterity have what fiber type

A

type II

56
Q

is there nebulin in the heart

A

no…varying lengths of thin filaments found here

57
Q

what contractile proteins are found in cardiac sarcomeres and skeletal muscle sarcomeres

A

MHC-beta and TnC (which is in slow fibers but not fast)

58
Q

what contractile proteins are unique to cardiac sarcomeres

A

MHC-alpha and an isoform of TnI

59
Q

cardiac vs skeletal muscle cell size

A

cardiac=much smaller

60
Q

how are cardiac cells connected

A

end to end via intercalated discs

61
Q

what is the purpose of gap jns w/in the intercalated discs of cardiac cells

A

rapid and direct transmission of a.ps (electical synapses) b/w cardiac cells

62
Q

does skeletal muscle contain gap jns

A

no

63
Q

what is the significance of the LONG REFRACTORY PERIOD in cardiac muscle ventricular cells

A

makes sure that the cells can’t be stimulated at a high fq…this is a protective mechanism so that the ventricles can relax and allow for diastole/heart to fill with blood. prevents heart from undergoing tetanic contraction

64
Q

when does the ap in cardiac muscle end compared to its contractions

A

a.p lasts until the contraction is 50% relaxed

65
Q

during the phase 0 of a cardiac a.p what occurs

A

rapid depolarization, increase Na conductance as Na comes into the cell

66
Q

during phase 1 of a cardiac a.p what occurs

A

movement of Na has slowed due to electrical gradient, K flows out. so gNa decreases and gK increases

67
Q

during phase 2 of a cardiac a.p what occurs

A

plateau phase. gK decreases and leaves cell, but gCa increases and comes into cell. 2 cations being exchanged so you see a plateau phase

68
Q

during phase 3 of a cardiac a.p what occurs

A

gK increase and gCa decreases…see a rapid repolarization phase

69
Q

during phase 4 of a cardiac a.p what occurs

A

no net current flow….steady m.p at resting potential

70
Q

what are the 2 sources of Ca for the heart

A
  1. Ca can enter the cell from interstitial space via channels in the sarcolemma during the plateau phase (phase 2)
  2. the Ca from the interstitial space triggers Ca release from the s.r
71
Q

what is calcium-induced calcium release

A

Ca coming in from the interstitial space triggers the release of Ca from the s.r which can bind to TnC causing muscle activation

72
Q

mechanisms for Ca removal in cardiac muscle

A
  1. S.r is the primary mechanism (Ca-atpase pump)
  2. pump in the sarcolemma…a Ca-ATPase pump that moves Ca out of the cell
  3. Na/Ca exchanger
73
Q

what does the Na/Ca exchanger do

A

moves Na into the cell and Ca out.

74
Q

where does the Na/Ca exchanger get energy from

A

not ATP directly. uses the Na [ ] gradient…thus is secondary active transport. the Na/K, ATPase pump maintains the Na [ ] gradient

75
Q

the amount of Ca2+ that is removed by the Ca/ATPase exchanger (sarcolemma) and the Na/Ca exchanger, equals what

A

the Ca that moved in during the plateau phase of the cardiac a.p

76
Q

what component of smooth muscle is homologous to z-lines of striated muscle

A

dense bodies that thin filaments attach to

77
Q

is there troponin in smooth muscle

A

no

78
Q

where is smooth muscle innervation from

A

autonomic n.s= involuntary

79
Q

compare the cell lengths of smooth vs striated muscle

A

greater range of cell lengths in smooth to accomodate changes in volume of organs

80
Q

rate of ATP splitting in smooth vs striated

A

smooth is 10-100 times slower…no fatigue…force is the same as striated though …so greater economy

81
Q

excitation coupling in smooth muscle

A
  1. increase in Ca
  2. Ca binds to calmodulin
  3. Ca-calmodulin binds to myosin light chain KINASE to create an ACTIVE MLCK enzyme
  4. active MLCK phosphorylates relaxed myosin…myosin attaches to actin
  5. phosphatase (always active) removes the P from myosin to relax it
82
Q

what causes the myosin to detach from the actin

A

ATP causes dissociation of myosin from actin

83
Q

what is the purpose of the phosphatase

A

to prevent reattachment of myosin to actin

84
Q

how does smooth muscle maintain force with very little ATP consumption

A

myosin can remain attached to actin even when dephosphorylated to maintain the contraction without using ATP= high economy

85
Q

what are the 2 sources of Ca for smooth muscle contraction

A
  1. s.r

2. extracellular fluid via channels in membrane

86
Q

what initiates an a.p in smooth muscle

A

Ca2+ in the rising phase! rather than Na in striated muscle

87
Q

what are the 4 things that can activate smooth muscle

A
  1. cells that spontaneously generat a.ps…pacemaker potential
  2. ANS ending release n.t in vicinity of smooth muscle cells. NO NMJ IN SMOOTH MUSCLE
  3. hormones act as above
  4. local factors (pH, O2 level, etc)
88
Q

what are the 3 mechanisms of Ca removal in smooth muscle

A
  1. Ca pump in sarcolemma
  2. Na/Ca exchanger
  3. s.r
89
Q

what is single unit smooth muscle

A

muscle fns as single unit. uses electrical synapses (through gap jns). is spontaneously active (by pacemaker cells). stretch activated. innervation is by pacemaker cells)

90
Q

examples of single unit smooth muscle

A

uterus, intestines, small b.v

91
Q

what is multi unit smooth muscle

A

cells activated independently, not spontaneously activated, gap jns are rare

92
Q

examples of multi unit smooth muscle

A

large arteries, large airways

Physio (9 decks)

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