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Body logistics > Lecture 9- Muscle tissue introduction > Flashcards

Lecture 9- Muscle tissue introduction Flashcards

1
Q

‘myos’

A

muscle

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2
Q

myalgia

A

muscle pain

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3
Q

myasthenia

A

weakens the muscle

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4
Q

myocardium

A

muscular component of the heart

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5
Q

myopathy

A

any disease of the muscles

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6
Q

myoclonus

A

sudden muscle spasm

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7
Q

myoclonus

A

sudden muscle spasm

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8
Q

two types of muscle

A

striated and non-striated

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9
Q

striated

A

skeletal muscle

cardiac muscle

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10
Q

non-striated

A

smooth muscle

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11
Q

skeletal muscle is under

A

voluntary control

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12
Q

nerve muscle interactions in skeletal muscle

A

direct nerve-muscle communication

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13
Q

cardiac muscle is under

A

involuntary control

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14
Q

nerve-muscle interaction in cardiac muscle

A

indirect nerve-muscle communication

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15
Q

is myoglobin present in striated muscle

A

YES

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16
Q

is myoglobin present in non-striated muscle

A

NO

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17
Q

is smooth muscle under involuntary control

A

NO

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18
Q

nerve-muscle communication in smooth muscle

A

No direct nerve-muscle communication

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19
Q

myoglobin is a what colour protein

A

red

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20
Q

myoglobin is structural similar to

A

Hb (single unit)

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21
Q

myoglobin function

A

oxygen string molecule which provides oxygen to working striated muscle

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22
Q

at low pH Hb ..

A

gives up oxygen to myoglobin

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23
Q

when striated muscles dies (necrosis)

A

myoglobin is released onto the bloodstream

24
Q

what removes myoglobin from the blood

A

the kidneys

- excreted in the urine- myoglobinurea

25
excess myoglobin in the blood can
damage kidneys
26
sarcolemma
outer membrane of muscle cell
27
sarcoplasm
cytoplasm of a muscle cell
28
sarcosome
mitochondrion
29
sarcomere
contraction unit in striated muscle
30
sarcoplasm retioculum
smooth endoplasmic reticulum of a muscle cell 9high [Ca2+]
31
what is the contraction unit in striated muscle
the sarcomere
32
which types of muscle are under voluntary control
skeletal muscles
33
which types of muscle have dire nerve- muscle communication
skeletal
34
each muscle fibre contains
myofibrils
35
myofibrils are made up of
repeating subunits called sarcomeres
36
myofibrils are made up of which proteins
- actin - myosin - tropomyosin
37
thin filaments
composed of actin
38
thick filaments
composed of myosin
39
thin and thick filaments
partially overlap and form functional units called sarcomeres (why myofibrils ahem dark and light bands- striated)
40
how do myofibrils bring about muscle contraction
via the sliding-filament theory
41
the sarcomere A band
dark band composed of thick filaments and some thin filaments
42
the sarcomeres H band
centre of the A band- only thick filament present
43
I band
light bands composed of actin (thin) alone
44
Z band
found at the centre of I bands
45
Z bands are made of
alpha-actinin | - anchors actin filaments and acts as a boundary between sarcomere units
46
z to z=
width of sarcomere
47
contraction energy source
glycogen- glucose storage meolcile
48
what provides phosphate for ADP-ATP
creatine phosphate
49
glycogen is converted to ATP through
glycolysis and aerobic resp
50
contraction of sarcomere powered through
hydrolysis of ATP--> ADP and inorganic phosphate
51
when muscle are at rest
there is an incomplete overlap between the thick and thin filaments with some areas containing only one of the two types
52
when muscle are at rest the ATP molecule is attached to
globular myosin head on myosin filaments
53
when muscles are contracting
the sarcomeres shorten in length due to the thick and thin filaments sliding over each other resulting in greater overlap between the filaments and a narrowing of the H zones - the I bands will come closer together - Size of the A band will stay the same
54
MOA: muscles contraction
1. Ca2+ binds to troponin C on the actin filament (thin)- causing a conformational change in troponin 2. This causes Tropomyosin to move allowing interaction of actin and myosin (tropomyosin previously blocking myosin binding site on actin) 3. ATP molecule attached to myosin head is hydrolysed, changing its conformation 4. Myosin head binds actin and forms cross bridge and ‘power stroke occurs 5. Calcium is transported back to SR by (SERCA ATPase) and the muscle relaxes due to active site on actin being blocked by tropomyosin once again
55
outline Excitation-contraction coupling (long)
1. Action potential at NMJ causes Ach release at synaptic cleft- depolarises the sarcolemma 2. Action potential propagated down t-tubule of muscle 3. Depolarisation triggers conformation change in L-type channels which opens Ryanodine receptors 4. Ryanodine receptors open causing calcium from the SR to flood into the sarcoplasm 5. Ca2+ binds to troponin C on the actin filament (thin)- causing a conformational change in troponin 6. This causes Tropomyosin to move allowing interaction of actin and myosin (tropomyosin previously blocking myosin binding site on actin) 7. ATP molecule attached to myosin head is hydrolysed, changing its conformation 8. Myosin head binds actin and forms cross bridge and ‘power stroke’ occurs 9. Calcium is transported back to SR by (SERCA ATPase) and the muscle relaxes due to active site on actin being blocked by tropomyosin once again

Body logistics (39 decks)

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