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NSF > skeletal + smooth muscle > Flashcards

skeletal + smooth muscle Flashcards

1
Q

brief ultrastructure sarcomere + how shortens

A

actin filaments attached z lines but don’t reach completely 1 to next
* gap bridged myosin filaments

  1. myosin heads form cross bridges w actin fibres - requires 1ATP
  2. both ends myosin filaments move simultaneously = z lines pulled together + sarcomere shortened
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2
Q

structure sarcoplasmic reticulum (SR)

A
  • tubules wrapped around each myofibril like lace
  • enlarged end regions = terminal cisternae
  • stores Ca2+ as SR Ca ATPase pumps it out cytosol
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3
Q

relative Ca2+ conc inside + outside cell, and in SR

A

higher outside cell (but low for both)
high in SR

applies all body cells

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4
Q

t tubules structure

sk musc

A

sarcolemma invaginated to form narrow tubes filled extracellular fluid

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5
Q

myosin prot mol structure

A

2 polypeptide chains wrapped around each other, each ending hinged globular head
* each head has binding site for actin, and one for ATP

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6
Q

sliding filament model

A

thick + thin myosin + actin filaments slide relative to each other to shorten sarcomere, and so myofibril, myocyte, and whole muscle

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7
Q

contraction

A

creation tension in muscle
* tension directly proportional to no. cross bridges bet actin + myosin

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8
Q

types contraction

A
  1. isotonic = muscle contracts, shortens, enough force created to move load
  2. isometric = muscle contracts, no shorten, not enough force move load
    * possible due elastic components that stretch so muscle same length despite shortening sarcomeres
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9
Q

steps to control + cause contraction

w/in musc cell

A
  1. initiation - events at NMJ
  2. excitation-contraction coupling
  3. Ca2+ signalling
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10
Q

what happens at NMJ

neuromuscular junction

A
  1. somatic motor neuron releases Acetyl choline (Ach)
  2. Ach binds nicotinic cholinergic receptor on motor end plate
  3. activates ligand-gated Na+ channs = influx Na+ into muscle = depolarisation
  4. end plate pot (EPP) created, always leading muscle a pot (at NMJ)

sk musc only contracts if stimmed motor neuron

acetylcholinesterase already in cleft, immediately breaking down Ach but enough to trigger response 1st
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11
Q

excitation-contraction coupling defn

A

series events from excitation by motor neuron to contraction

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12
Q

excitation-contraction coupling steps

A
  1. muscle depol (a pot) travels across sarcolemma by sequential opening Na+ channs + into cytosol by t-tubules
  2. depol = Ca2+ released adjacent SR down conc grad
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13
Q

Ca2+ signalling to cause contraction

A
  1. Ca2+ released SR binds troponin
  2. conformational troponin = tropomyosin released binding site on actin
  3. myosin binds AS on actin + cross bridge cycles occur (15ms)
  4. then relaxation phase (25ms) as Ca2+ levels decrease so less cross bridge cycles
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14
Q

cross bridge cycle, w role ATP

A

myosin head binding actin AS, hinging + pulling actin filament along by sliding filament model to contract + apply force, and unbinding
* ATP has to bind myosin head for it to detach - it is hydrolysed so E available repeat power stroke, after which ADP + Pi detach

ON REPEAT

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15
Q

causing muscle relaxation

A

decrease cytosolic Ca2+ levels = unbinds = AS covered + elastic els pull filaments back resting position
1. SR Ca2+ ATPase - pump Ca2+ back into SR
2. p mem Ca2+ ATPase - pump Ca2+ out cell
3. Na+ Ca2+ exchanger - Ca2+ out, Na+ in across sarcolemma

all against conc grad Ca2+

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16
Q

effect no ATP on Ca2+ signalling in muscle

A

pumps to maintain normal conc grads stop working = mems become leaky = ions diff down conc grads = Ca2+ in sarcoplasm increases = crossbridge formation but no ATP release myosin head = muscles stiffen (rigor mortis)

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17
Q

muscle twitch

A

single contraction relaxation cycle in muscle fibre

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18
Q

latent period

A

delay bet start muscle a pot + start twitch (from after crossbridge formed) due biochem steps b4 crossbridge formation

relaxation phase longer than contraction phase as more has to happen

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19
Q

myasthenia gravis

A

immune destruction postsyn Ach receptors = less recptors = lots Ach broken down b4 time to bind = not enough binds = muscle not activated = can’t contract
* causes muscle weakness
* Edophonium (Tensilon) = reversible acetylcholinesterase inhibitor so more time Ach bind - only works couple mins + poisonous large doses

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20
Q

factors affecting force sk musc contraction

A

no. crossbridges, therefore
* composition motor unit
* frequency a pots
* length-tension relationship

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21
Q

how to achieve graded responses in sk musc and why want

A

each cell all or nothing response but can change no/type motor units activated
* some motor units have 2000 muscle fibres (postural), some 3 (ocural)
to determine force of throw etc

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22
Q

motor unit

A

motor neuron + all sk muscle fibres it innervates

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23
Q

tetanus

as word def

A

sustained contraction w no relaxation bet twitches = max crossbridges + max force

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24
Q

twitch summation

A

faster + closer together a pots arrive, more wuickly crossbridges form as can’t get rid Ca2+ in relaxation period

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25
Q

how does length-tension relationship affect force in sk muscle

A

length = amount overlap
tension = no cross bridges
start too long or short = can’t form crossbridges as overlap prevents or filaments too far apart = no contraction

imagine arms way back either side - harder pull weight than if start further forward

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26
Q

pathways for synth ATP in sk musc

A
  1. creatine phosphate (only sk)
  2. glycolysis
  3. oxidative phosphorylation

anaerobic, anaerobic, aerobic

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27
Q

how is ATP synthed from creatine phosphate

sk musc only

A

resting musc conts creatine phosphate, storing E in phosphate bond

replenished at rest, used up in exercise

28
Q

nos important mols made glycolysis, citric acid cycle + oxidative phosphorylation

diagram

A
29
Q

myoglobin

A

only found musc w greater affinity O2 than Hb so facilitates aerobic metabolism
* more saturated w O2 at any given partial press
* when low partial press + Hb unloads, myo takes up

gives meat red colour due oxymyoglobin Fe2+

30
Q

glycolysis synth ATP waste products

A

for each ATP 1 waste H+ = gradual acidosis of blood

31
Q

reversible formation/breakdown NADH

A
32
Q

comparison rate formation ATP + release E in muscle by diff pathways

A

creatine phosphate fastest, then glycolysis; oxidative phosphorylation slowest
* also less ATP?E from glycolysis

33
Q

sources glucose in sk musc

A
  1. blood - insulin-dependent entry
  2. glycogen broken down glycogenolysis
34
Q

3 types sk muscle fibre

A
  1. red slow oxidative (1/2 size)
  2. white fast glycolytic
  3. intermediate = glycolytic but more oxidative w endurance training - for standing, walking

born w set no types

35
Q

red slow oxidative sk musc structure + function

A
  • lots myoglobin, lots mitochond, lots caps around, little glycogen
  • for aerobic synth ATP w oxidative phosphorylation
  • slow crossbridge cycling = slow continuous contraction
  • fatigue resistance
36
Q

slow white glycolytic sk musc

A
  • large + white (little myoglobin), few mitochond, few caps around, lots glycogen
  • synth ATP anaerobically in glycolysis = quick
  • fast crossbridge cycling = fast contraction
  • lots myofilaments = powerful
  • fatigue fast due depletion glycogen + build up lactate
37
Q

how is sk musc activity important for maintaining body temp

A

70-80% E used by muscles lost as heat

38
Q

how long before rigor mortis sets in after death

A

depends glycogen metabolism + so how long glycolysis can cont producing ATP
1. how much glycogen available at start
2. speed metabolism = temp (ambient temp + size/obesity animal for how fast heat lost)

typically 8-15 hrs

39
Q

why is meat hung

A

allow proteolytic enzs break down actin-myosin bonds so meat more tender

40
Q

pH musc post death

and effect on meat

A

anaerobic metabolism = decreasing pH as waste H+ glycolysis not removed in blood
* more glycogen = more metabolic waste = lower pH

low pH good as inhibits bacterial growth + meat less likely spoil (high pH meat dry, firm + dark asw)

41
Q

why might glycogen in animal at slaughter be decreased

A
  1. poor body condition - emaciated
  2. exhausted/stressed animals - used up in transport + handling before slaughter
42
Q

factors affecting quality of meat

A
  • amount glycogen in muscle at death
  • if hung after slaughter
43
Q

prot markers that might indicate skeletal muscle damage

A
  • creatine kinase
  • myoglobin

both only found sk musc

44
Q

myopathy

A

any disease causing damage sk musc

45
Q

types smooth (visceral) musc

A
  • GI
  • reproductive - in uterus
  • urinary - bladder
  • ocular - eye (iris)
  • vascular - bvs
46
Q

purpose vascular sm musc

A
  • constrict/relax for vasoconstriction/dilation
  • change resistance to flow
  • change blood press
  • change perfusion
47
Q

structure actin/myosin sm musc

A
  • contractile unit = myosin mol centre 12-15 actin
  • actin filaments attach anchoring pts on cell mem (dense plates) + w/in cell (dense bodies)
  • actin filaments interconnected by myosin filaments
  • crossbridge formation = actin filaments pulled together (still sliding)

no troponin or sarcomeres

actin + myosin not lined up rigidly enough for striations
48
Q

why are myosin filaments longer in sm musc than sk

A

longer w more myosin heads so sm musc can stretch whilst maintaining enough overlap w actin for optimal - tension - can contract even when super stretched or super squished

49
Q

how does sm musc contract

A

sliding filament similar sk musc where myosin head binds actin followed powerstroke

ATP still required release myosin head

50
Q

why is it useful that sk + sm musc have diff excitation-contraction coupling

A

drugs can target one w/o affecting other

51
Q

2 types contraction sm musc

A
  1. phasic = alternates contract + relax, e.g. uterus
  2. tonic = slow, sustained, continual contraction, e.g. bvs
52
Q

why does sm musc contract/relax slower than sk or cardiac

A
  • myosin hydrolyses ATP lower rate
  • cross bridge cycles slower
53
Q

excitation-contraction coupling sm musc

A
  1. Ca2+ sarcoplasm binds calmodulin, activating myosin light chain kinase (MLCK)
  2. MLCK catalyses phosphorylation myosin
  3. phosphorylation myosin enhances myosin ATPase, so drives contraction

myosin light chain phosphatase (MLCP) dephosphorylates myosin = decrease myosin ATPase activity = drives relaxation

54
Q

structural diffs sm musc in comp sk

A
  • no NMJ
  • no t-tubules
  • no troponin
  • less well-developed SR
  • no sarcomeres
55
Q

how is cytosolic Ca2+ increased sm musc

A

EXTERNAL ENTRY
1. elec signal: through v-gated Ca2+ channs p mem when depoled - spread by a pot thru gap junctions neighbouring cells down conc grad
2. chem signal: ligand-gated/receptor-operated channs - excitatory or inhibitory, e.g. hormones, NTs from ANS

INTERNAL
3. Ca2+ released SR - much less extensive + important than sk

Ca2+ 2 messenger >1 can act on sm musc at same time

56
Q

myogenic sm musc meaning + types

A

contraction originates from property musc itself
1. unstable mem pots, e.g. uterus - channs spontaneously open + close + if depol reaches threshold then a pot
2. stretch, e.g. bvs - press/force distorting sarcolemma opens channs = depol = Ca2+ v channs…

57
Q

spontaneous changes mem pot types

A
  1. pacemaker pots = oscillating mem pots regularly reaching threshold for Ca2+ entry, myometrium
  2. Slow waves = cyclic depol/repol regularly reaching threshold Ca2+ entry, gut

no external stim needed

58
Q

myometrium

A

sm musc layer uterus that gens contractions for menstruation, childbirth etc

59
Q

release NT by ANS to stim sm musc

A

over wide area allow diffusion + spread
* individual nerve fibres can stim lots sm musc cells
* followed by spread excitation even further across gap junctions

v few sm musc cells directly connected nerve fibres

60
Q

single unit muscles

A

cells connected gap junctions + contract as single unit for communication w neighbouring cells - when all cells need contract same time, e.g. uterus

most common

61
Q

multiunit muscles

A

individual activation/inhibition cells for fine control as cells not linked electrically + functions independently, e.g. iris + ciliary body (extention iris)

62
Q

how gap junctions work

A

allow direct communication bet cells so contract as single unit

cytoplasm continuous bet cells = small ions so elec activity spreads cell -> cell

63
Q

how is sm musc resistant fatigue

A
  • use less E than sk to gen + maintain force long time
  • ATP largely derived oxidative phosphorylation
  • creatine phosphate present relatively low concs
64
Q

why is sm musc contraction so much slower

A

physically longer get Ca2+ in (lack t-tubules + generalised receiving signal

note all have same force
65
Q

parturient paresis (milk fever)

cause, symptoms, treatment

A

much less Ca2+ in blood so:
* constipation + bloat (from gas) due GI stasis
* uterine inertia = difficulty w birth as uterus can’t contract enough force
* recumbancy - tuck head into flank
* retain urine
* tremors, staggering, then on floor (sk musc)
* hypothermia as no heat from movement/shivering
* pupils dilated + don’t respond well

give Ca2+ but slowly or heart beat crazy

66
Q

asthma

cau

A

caused bronchoconstriction
* can’t cause low Ca2+ as would affect every musc in bod
* salbutamol agonist symp ANS as mimics mol that causes sm musc airways dilate

salbutamol for humans, equivalent used in horses

NSF (22 decks)

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