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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
how does length-tension relationship affect force in sk muscle
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 ## Footnote imagine arms way back either side - harder pull weight than if start further forward
26
pathways for synth ATP in sk musc
1. creatine phosphate (only sk) 2. glycolysis 3. oxidative phosphorylation | anaerobic, anaerobic, aerobic
27
how is ATP synthed from creatine phosphate | sk musc only
resting musc conts creatine phosphate, storing E in phosphate bond | replenished at rest, used up in exercise
28
nos important mols made glycolysis, citric acid cycle + oxidative phosphorylation | diagram
29
myoglobin
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
glycolysis synth ATP waste products
for each ATP 1 waste H+ = gradual acidosis of blood
31
reversible formation/breakdown NADH
32
comparison rate formation ATP + release E in muscle by diff pathways
creatine phosphate fastest, then glycolysis; oxidative phosphorylation slowest * also less ATP?E from glycolysis
33
sources glucose in sk musc
1. blood - insulin-dependent entry 2. glycogen broken down glycogenolysis
34
3 types sk muscle fibre
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
red slow oxidative sk musc structure + function
* 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
slow white glycolytic sk musc
* 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
how is sk musc activity important for maintaining body temp
70-80% E used by muscles lost as heat
38
how long before rigor mortis sets in after death
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
why is meat hung
allow proteolytic enzs break down actin-myosin bonds so meat more tender
40
pH musc post death | and effect on meat
anaerobic metabolism = decreasing pH as waste H+ glycolysis not removed in blood * more glycogen = more metabolic waste = lower pH ## Footnote low pH good as inhibits bacterial growth + meat less likely spoil (high pH meat dry, firm + dark asw)
41
why might glycogen in animal at slaughter be decreased
1. poor body condition - emaciated 2. exhausted/stressed animals - used up in transport + handling before slaughter
42
factors affecting quality of meat
* amount glycogen in muscle at death * if hung after slaughter
43
prot markers that might indicate skeletal muscle damage
* creatine kinase * myoglobin | both only found sk musc
44
myopathy
any disease causing damage sk musc
45
types smooth (visceral) musc
* GI * reproductive - in uterus * urinary - bladder * ocular - eye (iris) * vascular - bvs
46
purpose vascular sm musc
* constrict/relax for vasoconstriction/dilation * change resistance to flow * change blood press * change perfusion
47
structure actin/myosin sm musc
* 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
48
why are myosin filaments longer in sm musc than sk
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
how does sm musc contract
sliding filament similar sk musc where myosin head binds actin followed powerstroke | ATP still required release myosin head
50
why is it useful that sk + sm musc have diff excitation-contraction coupling
drugs can target one w/o affecting other
51
2 types contraction sm musc
1. phasic = alternates contract + relax, e.g. uterus 2. tonic = slow, sustained, continual contraction, e.g. bvs
52
why does sm musc contract/relax slower than sk or cardiac
* myosin hydrolyses ATP lower rate * cross bridge cycles slower
53
excitation-contraction coupling sm musc
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
structural diffs sm musc in comp sk
* no NMJ * no t-tubules * no troponin * less well-developed SR * no sarcomeres
55
how is cytosolic Ca2+ increased sm musc
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
myogenic sm musc meaning + types
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
spontaneous changes mem pot types
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
myometrium
sm musc layer uterus that gens contractions for menstruation, childbirth etc
59
release NT by ANS to stim sm musc
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
single unit muscles
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
multiunit muscles
individual activation/inhibition cells for fine control as cells not linked electrically + functions independently, e.g. iris + ciliary body (extention iris)
62
how gap junctions work
allow direct communication bet cells so contract as single unit cytoplasm continuous bet cells = small ions so elec activity spreads cell -> cell
63
how is sm musc resistant fatigue
* use less E than sk to gen + maintain force long time * ATP largely derived oxidative phosphorylation * creatine phosphate present relatively low concs
64
why is sm musc contraction so much slower
physically longer get Ca2+ in (lack t-tubules + generalised receiving signal
65
parturient paresis (milk fever) | cause, symptoms, treatment
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
asthma | cau
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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