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Human physiology > muscles > Flashcards

muscles Flashcards

1
Q

what muscls are voluntary

A

skeletal

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2
Q

which muscles are involuntary

A

smooth and cardiac

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3
Q

features of skeletal muscles

A

elongated cells
multiple nuclei
visible striations

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4
Q

cardiac muscle features

A

branched cels
single or double nuclei
visible triations

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5
Q

smooth muscle features

A

spindle cells
single central nuclei
no striations

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6
Q

how does endothelum-dependent vasular relaxation work?

A 
vessel walls are innervated by nerves
parasympathetic released bradykinin/acetylcholine
Ca flows into endothelial cell
activates nitrix oxide synthase 
diffuses into the cell
causes activation to make GTP and GMP
calcium is taken back up
cell relaxes
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7
Q

briefly describe how smooth muscle relaxes

A 
Ca in
activates bigger store
activates calmodulin
binds to it
phosphryates myosin chain kinase
kinase phosphoryates myosin head 
power stroke
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8
Q

briefly describe smooth mucle relxation

A

calcium removed from cytosol
ATP depenent pump
ATPase decrease
no muscle tension

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9
Q

how domyocardial cells work

A

elecrical impulse sprads through intercollated disks
the pulse triggers electrogenic pups to open allowing Na in
negative potential to positive
influx of Na and Ca
plateau short

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10
Q

what is excitation contraction coupling

A

Ca in through L type channels in T tubules
calcium induced calcium receptors open using RYR
Ca interacts with tropnin revealing binding sites
ca reabsorbed by SERCA and pumups
unbinds from troponin and sarcomere goes back to rest

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11
Q

what is SERCA

A

sarco-endopasmic reticulum Calcium ATPase

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12
Q

define epimysium

A

connective tissue around muscle

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13
Q

define fasciles

A

bundles of muscle fibres within the epimysium

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14
Q

define perimysium

A

connective tissue around fascicles

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15
Q

define endomysium

A

indivual myofibre muscle cells surrounded by connective tissue

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16
Q

define sarcolemma

A

plasam membrane of skeletal muscle

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17
Q

define T-tubule

A

invagination allowing electrical impulses deep into the muscules

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18
Q

define sarcoplsmic reticulum SR

A

surronds each myofibril ear the tubule

key calcium store

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19
Q

define triad

A

where the sarcoplasmic reticulum meets the T tubule

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20
Q

define the A band

A

dark

thick filaments only

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21
Q

define the I band

A

light
thin filaments only
length increases during contraction

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22
Q

define the Z line

A

intersects the I band
filaments attach here
separates adjacent sarcomeres
adheres everything. transmits the force from one sarcomere to another

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23
Q

define the H zone

A

length decreases during contraction

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24
Q

define the M line

A

middle of the A band

thick filaments attach to here

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25
Q

what is a motor unit?

A

a motor neuron and all the myofibrils it innervates

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26
Q

how can motos unit size vary?

A

for fine control there are smaller motor units

larger muscles however use large motor units for more force in movement

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27
Q

what is the presynaptic terminal?

A

the nerve fibre

vesicles containing neurotranmitters are found here to be releseased

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28
Q

how wide is the synpatic celft?

A

20-30nm wide

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29
Q

what neurotransitter is used at the NMJ

A

acetylcholine Ach

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30
Q

what is a voltage gated calcium channels

A

found on the presynaptic membrane of the neurone
when action potentaisl go across the membrane thee channels open allowing calcium into the syanptic space and to the nerve terminal

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31
Q

how do vesicles release theor contents across the cleft?

A

exocytosis

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32
Q

what is an acetylcholine receptor made up of?

A

2 alpha subunits
1 beta
1 gamma
1 delta

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33
Q

what opens Ach gates?

A

2 Ach molecules attaching to the 2 alpha subunits

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34
Q

describe the process of action potentials moving from the nerve to the muscles

A
  1. arrival of action potential at the synapse causes a Ca influx due to opening of voltage gated channels
  2. causes Ach vesicles to move to presynpase membrane and be released via excytosis diffusing across the cleft
  3. they bind Ach receptors on muscle membrane
    depolarization spreads out to other parts of the muscle
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35
Q

what is EPP/ what causes it

A

end plate potential
is made when the muscle depolarises
influx of Na in the muscle leads to the initiation of it

36
Q

what is the end plate potential

A

creates a local positive potential as sodium moves into the muscle fibre
the end plate creates an action potential that can then spread along the muscle membrane causing contraction

37
Q

what breaks down Ach

A

acetylcholinersterase into Acetyl CoA and choline

these are then taken back up by the presynaptic terminal where its synthesised back into the neurotransmitter

38
Q

what is uscle fatigue

A

when the muscle is overstimulated and run out of vesicles

signals are then inhibited

39
Q

define high safety factor

A

each impulse reaching the NMJ is 3 times as much end plate potential needed to stimulate the fibre
therefore teh NMJ is said to have this high safety factor

40
Q

how does muscle fatigue occur?

A

too much stimulation of the uscle too fast leading to a reduced number of vesicles available
impulses fail to be passed onto the muscle

41
Q

what does a drug blocking the release of Ach do?

A

it inactivates the muscles around because there is no releace of the neurotransmitter
muscles cannot contract anymore

42
Q

example of a drug that blocks the release of Ach

A

botulinum

it fuses with the vesicles preventing exocytosis

43
Q

how do drugs stimulate muscle through imitation of ach activity?

A

cause depolarisation of muscle fibres
except they dont get broken back down again so their action can persist for minutes to hours
they cause localised areas of depolarization of fibre at end plate
constant stage of muscle spasm

44
Q

examples of drugs immitating Ach activity

A

methacholine and nicotine

45
Q

how can some drugs inactivate acetlycholinesterase

A

combine with it in the synaptic cleft so it cannot work

therfore with each impulse, additional Ach accumulates and stimulates the fibre repetitively

46
Q

what is the issue with drugs that inactivate acetylcholinesterase

A

causes muscle spasm

if in the larynx it can cause spasm here leading to smothering and death

47
Q

what is an example of a drug inactivating Ach-ase

A

diisopropyl flurophosphte
effective lethal poison with military potential
is effective for weeks
used as a ‘nerve gas poison’

48
Q

examples of drugs that block transmission at junctions

A

curariform drugs

49
Q

what do curariform drugs do

A

prevent the passage of impulses from the nerve ending into the muscles
they compete for receptor sits, when the drug binds Ach cannot

50
Q

theurapeutic uses of drugs which block transmission at jucntions

A

artifical respiration to control convulsions in tetanus

during surgery when compete muscle relaxation is needed

51
Q

describe excitation- contraction coupling

A

Ach released and NMJ
NA enters through Ach receptors initiating an action potential
potential in T tubules alters conformation of DHP receptor
DHP receptor open Ca channels
Ca binds t troponin allowing actin-myosin binding
myosin heads do power stroke
muscle tension

52
Q

what cant myosin be cleaved into?

A

LMM
HMM
light and heavy mereomyosin

53
Q

what allows myosin to reach bindng sites of actin?

A

a hinge on the LMM and HMM parts

it can flex here

54
Q

what are thin filaments made of

A

actin
tropnin
tropmyosin

55
Q

what covers the binding sites on actin for myosin?

A

troponin

56
Q

what is MBS

A

myosin binding sites on actin

57
Q

how is actin made

A

its a chain of gamma actin monomers forming a polymer chain of F actin
this then forms a double helix strand where two strand wrap around each other

58
Q

what causes the cessation of contraction in muscles

A

muscle will keep contracting as long as it has ATP
once the enrgy is depleated the muscle has to stop slowly
contraction is terminated by Ca being removed

59
Q

how is Ca remove?

A

Ca pump called SERCA

60
Q

what si SERCA

A

Ca pump that goes against concentration gradients so required energy/ ATP

61
Q

what happens during rigor motis

A

calcium cannot be taken up from the cytosol space and there is no ATpase actiity
so there are high amounts of it
meaning actin cant dissociate from myosin
contraction cycle stuck
relaxation cannot take place
state of continuous contraction

62
Q

when is ATP used in muscle contraction

A
  • generating high emerg stage from myosin
  • disconecting mysin from actin
  • pumping Ca from cytosol back to SR
63
Q

where can the muscles ge ATp from

A

glycoloysis
ceratin phosphate
krebs cycle

64
Q

what is creatine hosphate

A

a means of storing energy

found in high energy using tissues suchas brain and skeletal muscles

65
Q

how is creatine phosphate used

A

process called substrate phosphylation where ATP is made

66
Q

how is creatine used by athletes

A

could create greater energy reserves but the muscle has limits creatine storage
uses are unknown so far

67
Q

howis glycogen used by musce=les

A

broken down into a form of glucose without any oxygen required

68
Q

how do muscles get oxygen

A

blood

or stored in myoglobin

69
Q

what is mypglobin

A

protein found in muscles for oxygen and iron binding
Myoglobin increases the solubility of oxygen.
Myoglobin facilitates oxygen diffusion

70
Q

what does high pH do to haemoaglobin

A

low H+
promotes tigher binding of oxgen
curve to left

71
Q

whatdt does low pH do to haemoaglobin?

A

higher H+
permites easier release of oxygen
curve to right

72
Q

what happens to lactic acid?

A

absorbed by theliver

converted into pyruvate ad glucose

73
Q

how is oxygen used in revocery afte exercise

A

replenish oxymoyglobin

metabolise fatty acids in the krebs cycle to make energy

74
Q

how is energy used in recover after exercise

A

restore levelss of phospcreatine

syntehsiese glycogen from absorved glucose

75
Q

red muscle

A

oxidative

76
Q

white muscle

A

glycolytic

77
Q

features of oxidative red muscle

A 
small 
high mitochondra
ATP made
slow contractions
red due to high myoglobin
78
Q

what type of contraction do red muscle have

A

ssustained every and can maintain contraction for long times
contractio is slower

79
Q

where are red muscles found?

A

postural muscles

80
Q

features of white glycolytic muscle

A

bigger muscles
low mitochondrai
less dense and light colour
uses glycogen rather than moyglobin

81
Q

how do white glycoloytic muscle contract

A

hugh amount of power

but easily fatigued

82
Q

types of rd muscle

A

fast and slow twitch oxidative muscles

83
Q

what is myosin isoform I

A

slow twitch oxidative red muscle

84
Q

what is moysin isoform type IIA

A

fast twitch oxidative glycolytic red muscle

85
Q

what is myosin isoform IIB

A

fast twitch glycolitic white muscle

86
Q

whats the difference between slow twitch oxidative red muscle and fast twitch oxidative glycolyitic red msucle

A

slow is oxidative and aerobic

fast oxidative glyolytic is glycolytic but becomes more oxidative with endurance training

Human physiology (21 decks)

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