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HLSC120: Physiology > Chapter 8: Muscle Physiology > Flashcards

Chapter 8: Muscle Physiology Flashcards

1
Q

skeletal muscle

A
  • striated
  • voluntary
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2
Q

muscle fiber

A
  • single muscle cell
  • relavitly large, elongated and cylinder shape
  • formed during embronic development by fusion of smaller muscles called myoblasts
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3
Q

myoblasts

A
  • formed during embronic developments
    Features;
  • multiple nuclei in a single cell
  • abundance of mitochondria
  • specialized contractile elements
  • 80% volume of muscle fibers
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4
Q

myoblast are composed to

A
  • thick filaments
  • thin filaments
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5
Q

thick filaments

A
  • special assemblys of myosin
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6
Q

thin filaments

A
  • primary made up of actin
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7
Q

Level of organization: muscles

A
  • whole muscle (an organ)
  • muscle fiber (cell)
  • myofribril (specialized intercellular structure)
  • thick and thin filaments (cytoskeleton)
  • myosin and actin (protein molecules)
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8
Q

muscle covering layer

A
  • epimysium
  • perimysium
  • endomysium
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9
Q

epimysum

A

covers the whole muscle

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10
Q

perimysium

A

divides the muscle fibers into bundles of fascicles

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11
Q

endomysium

A

innermost layer
- cover each muscle fober or cell contractile components
- transfer for to connective tissue shealths, then to the tendon, then the bone

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12
Q

a band

A

Dark band
– thick and thin filaments overlap

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13
Q

H zone

A
  • central portions of the thick filament
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14
Q

m line

A
  • holds thick filaments together vertically
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15
Q

i band

A

Light band
- contains only thin filaments

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16
Q

z line

A
  • verticle
  • flat, cytoskeleton disc that connects the adjacent sacromeres
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17
Q

sacromeres

A

functional unit of the skeleton muscle

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18
Q

titin

A
  • along with the m line and z line it help stabalize filaments
  • responsible for muscle elasticity and recoil
  • largest protein
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19
Q

cross bridges

A
  • myosin heads
  • extend from thick filaments towards thin filaments
  • interaction between actin and myosin bring about muscle contraction by means of the sliding filament mechanism
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20
Q

myosin

A
  • motor protein
  • responsible for the action-baded mobility
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21
Q

myosin heads

A

form cross bridges

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22
Q

Actin

A
  • thin filament
  • spherical
  • contractile protein
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23
Q

tropomyosin

A
  • threadlike proteins
  • conversatins binding sites that bind with cross bridges
  • hides actin binding sites
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24
Q

troponin

A
  • made up of three polypeptides
  • binds to tropomyosin, actin, and calcium –. result: exposes binding sites
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25
Q

reglatory proteins

A

prevent / premit contraction
- tropomyosin
- troponin

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26
Q

rigor mortis

A
  • “stiffness is dealth”
  • lacking in place of skeletal muscles that begins 3-4 hours after dealth
  • no ATP
  • no Ca
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27
Q

Sacroplasmic reticulum

A
  • modified endoplasmic reticulum
  • Sr in lateral sacs stores calcium
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28
Q

t tubules

A
  • action potentials spread down t-tubules trigger the release of ca
  • voltage gated receptors
  • dihydropridine receptors
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29
Q

features of skeletal muscles

A
  • sacrolemma
  • own nucleus
  • lots of mitochondria
  • lots of glycogen reserves
  • SR
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30
Q

nebulin

A
  • stabalizes
31
Q

ryanodine receptors

A

“foot proteins”
- calcium release channels

32
Q

dihydropyridine receptors

A
  • t tubules
  • causes the release of calcium –> troponin binds to ca ions –> tropomyosin is removed –> exposes binding sites –> action and myosin (crossbridges are formed)
33
Q

power stroke

A

ATP bereaks down into ADP+P

34
Q

sliding filament

A
  • z lines come closer together
  • I bands become shorter
  • m-line doesnt change
  • A band width doesnt change
  • H band becomes shorter
35
Q

relaxation

A
  • Acetylcholinesterase breaks down ACh at the neuromuscular junction
  • calcium returened to the neuromuscular junction
  • action potential stops
  • troponin and tropomyosin slips back into place
  • actin and myosin can no longer bind at crossbridges
36
Q

McArdle Disease

A
  • absense of enzyme phophorylase ( breaks down glycogen to glucosse for ATP production)
  • glycogen accumulates in the muscles
    SYMPTOMS: muscle weakness, legs lacking, living rigor mortis
37
Q

Temporal summation

A
  • results for sustained elevation of cyostolic calcium
38
Q

muscle tetnus

A
  • sustained contractile activity
  • flat region
  • result of temporal summation
39
Q

tetnus infection

A
  • caused by clastridum tensi
  • blacks GABA
    RESULT: spasms
40
Q

single action potental produces

A

a twitch

41
Q

muscle tension factors

A
  • frequency of stimulation
  • lenght of the fiber at the onset of contraction
  • extent of fatigue
  • thickness of fiber
42
Q

energy sources for contration

A
  • creatine phosphate
  • glycolysis
  • fatty acids
43
Q

Creatine phosphate break down

A
  • breaks down into creatine kinase which breaks down into creatine and ATP
44
Q

creatine phosphase as a supplement

A
  • causes GI disterbances
  • weight gian
  • dehydration
45
Q

creatine phosphate is used in

A

sphincters

46
Q

fatty acids

A

enter the krebs cycle directly

47
Q

isotonic contractions

A

equal stretch; creates force and movement
- concentric
- eccentric

48
Q

concentric

A

towards the center of the body
EXAMPLE: shortening of the biceps

49
Q

eccentric

A
  • away from the center of the body
  • most common cause of injury
50
Q
A
51
Q

types of contractions

A
  • isotonic
  • isometric
52
Q

isometric

A
  • equal movement
  • force but no movement
    EXAMPLE: yoga, planks, pilates
53
Q

twitch fiber types

A
  • fast
  • slaw
54
Q

slow twitch fibers

A
  • slower
  • uses ATP slower
  • slower relase of calcium
  • frequently used for daily acivities
  • twitch sustained for longer
    Example: posture, wlaking
55
Q

fast twitch fibers

A
  • 2-3x faster
  • slits ATP faster
  • calicum is released faster
  • used occasionally
  • twitch is sustained for shorter
    Example: violine, piano
56
Q

types of engergy uses

A
  • oxidative
  • glycolipid
57
Q

oxidative

A
  • uses oxegen, increase of myoglobin
  • goes through all three cycles
  • 36 ATP total
  • more mitochondria
  • increase bllod vessels
  • rich red color
    fatigues less
58
Q

glycolipid

A
  • does not need oxegen
  • produces 2 ATP
  • less mitochondria
  • fewer blood vessels
  • pale “white” fibers
  • fatiguee more
59
Q

muscle fatigue

A

occurs when muscles can no longer respond to stimulation with the same degree of muscle contraction

60
Q

types of muscle fatigue

A
  • central
  • peripheral
61
Q

Central muscle fatige

A
  • psychological
  • CNS
  • montonomy (continous activity; like assembly line workers)
  • somatic motor neuron
62
Q

peripheral motor fatigue

A

contibute to the vunrability of the neuromuscular junction
- calcium release
- SR and T tubule receptors
- decreased glucose
- lack of ATP

63
Q

solution ot muscle fatigue

A

E -excess
P - Post excersize
O - oxegen
C - consumption

64
Q

control of motor movement

A
  • spinal cord (reflexes)
  • brain stem (reticular formation)
  • Primary motor cortex
65
Q

Parkiinsons Disease

A
  • basal nuclei
  • tremors, reptilian stare, difficulty walking, confusion, afffected sleep, gait walking
66
Q

Duchennes Muscular Dystrophe

A
  • affects more males
  • genetic
  • carried in x chromosone
  • lack dystrophin (protein)
  • affects muscles of the hip and girdle
    Treatment: gene therapy
67
Q

muscle receptors

A

muscle spindles

68
Q

muscle spinals

A

monitor muscle stretch

69
Q

Alpha motor neuron

A

forms the neurmusclular junction

70
Q

intrafusal fibers

A

receptors

71
Q

Gama mtor neuron

A
  • flower spray ending in periphery in intrafusal fibers
  • annulospiril ending in enter of intrafusal fibers
72
Q

annulospiril ending

A

controls stretch

73
Q

extrafusal fibers

A

ordinary muscle fibers

74
Q

Golgi tendo organ

A
  • monitors force/tension
  • protects from injury (drop load)
  • collogen

HLSC120: Physiology (7 decks)

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