skeletal + smooth muscle Flashcards
brief ultrastructure sarcomere + how shortens
actin filaments attached z lines but don’t reach completely 1 to next
* gap bridged myosin filaments
- myosin heads form cross bridges w actin fibres - requires 1ATP
- both ends myosin filaments move simultaneously = z lines pulled together + sarcomere shortened
structure sarcoplasmic reticulum (SR)
- tubules wrapped around each myofibril like lace
- enlarged end regions = terminal cisternae
- stores Ca2+ as SR Ca ATPase pumps it out cytosol
relative Ca2+ conc inside + outside cell, and in SR
higher outside cell (but low for both)
high in SR
applies all body cells
t tubules structure
sk musc
sarcolemma invaginated to form narrow tubes filled extracellular fluid
myosin prot mol structure
2 polypeptide chains wrapped around each other, each ending hinged globular head
* each head has binding site for actin, and one for ATP
sliding filament model
thick + thin myosin + actin filaments slide relative to each other to shorten sarcomere, and so myofibril, myocyte, and whole muscle
contraction
creation tension in muscle
* tension directly proportional to no. cross bridges bet actin + myosin
types contraction
- isotonic = muscle contracts, shortens, enough force created to move load
- isometric = muscle contracts, no shorten, not enough force move load
* possible due elastic components that stretch so muscle same length despite shortening sarcomeres
steps to control + cause contraction
w/in musc cell
- initiation - events at NMJ
- excitation-contraction coupling
- Ca2+ signalling
what happens at NMJ
neuromuscular junction
- somatic motor neuron releases Acetyl choline (Ach)
- Ach binds nicotinic cholinergic receptor on motor end plate
- activates ligand-gated Na+ channs = influx Na+ into muscle = depolarisation
- end plate pot (EPP) created, always leading muscle a pot (at NMJ)
sk musc only contracts if stimmed motor neuron
excitation-contraction coupling defn
series events from excitation by motor neuron to contraction
excitation-contraction coupling steps
- muscle depol (a pot) travels across sarcolemma by sequential opening Na+ channs + into cytosol by t-tubules
- depol = Ca2+ released adjacent SR down conc grad
Ca2+ signalling to cause contraction
- Ca2+ released SR binds troponin
- conformational troponin = tropomyosin released binding site on actin
- myosin binds AS on actin + cross bridge cycles occur (15ms)
- then relaxation phase (25ms) as Ca2+ levels decrease so less cross bridge cycles
cross bridge cycle, w role ATP
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
causing muscle relaxation
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+
effect no ATP on Ca2+ signalling in muscle
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)
muscle twitch
single contraction relaxation cycle in muscle fibre
latent period
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
myasthenia gravis
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
factors affecting force sk musc contraction
no. crossbridges, therefore
* composition motor unit
* frequency a pots
* length-tension relationship
how to achieve graded responses in sk musc and why want
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
motor unit
motor neuron + all sk muscle fibres it innervates
tetanus
as word def
sustained contraction w no relaxation bet twitches = max crossbridges + max force
twitch summation
faster + closer together a pots arrive, more wuickly crossbridges form as can’t get rid Ca2+ in relaxation period
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
imagine arms way back either side - harder pull weight than if start further forward
pathways for synth ATP in sk musc
- creatine phosphate (only sk)
- glycolysis
- oxidative phosphorylation
anaerobic, anaerobic, aerobic
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
nos important mols made glycolysis, citric acid cycle + oxidative phosphorylation
diagram
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+
glycolysis synth ATP waste products
for each ATP 1 waste H+ = gradual acidosis of blood
reversible formation/breakdown NADH
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
sources glucose in sk musc
- blood - insulin-dependent entry
- glycogen broken down glycogenolysis
3 types sk muscle fibre
- red slow oxidative (1/2 size)
- white fast glycolytic
- intermediate = glycolytic but more oxidative w endurance training - for standing, walking
born w set no types
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
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
how is sk musc activity important for maintaining body temp
70-80% E used by muscles lost as heat
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
why is meat hung
allow proteolytic enzs break down actin-myosin bonds so meat more tender
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
low pH good as inhibits bacterial growth + meat less likely spoil (high pH meat dry, firm + dark asw)
why might glycogen in animal at slaughter be decreased
- poor body condition - emaciated
- exhausted/stressed animals - used up in transport + handling before slaughter
factors affecting quality of meat
- amount glycogen in muscle at death
- if hung after slaughter
prot markers that might indicate skeletal muscle damage
- creatine kinase
- myoglobin
both only found sk musc
myopathy
any disease causing damage sk musc
types smooth (visceral) musc
- GI
- reproductive - in uterus
- urinary - bladder
- ocular - eye (iris)
- vascular - bvs
purpose vascular sm musc
- constrict/relax for vasoconstriction/dilation
- change resistance to flow
- change blood press
- change perfusion
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
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
how does sm musc contract
sliding filament similar sk musc where myosin head binds actin followed powerstroke
ATP still required release myosin head
why is it useful that sk + sm musc have diff excitation-contraction coupling
drugs can target one w/o affecting other
2 types contraction sm musc
- phasic = alternates contract + relax, e.g. uterus
- tonic = slow, sustained, continual contraction, e.g. bvs
why does sm musc contract/relax slower than sk or cardiac
- myosin hydrolyses ATP lower rate
- cross bridge cycles slower
excitation-contraction coupling sm musc
- Ca2+ sarcoplasm binds calmodulin, activating myosin light chain kinase (MLCK)
- MLCK catalyses phosphorylation myosin
- phosphorylation myosin enhances myosin ATPase, so drives contraction
myosin light chain phosphatase (MLCP) dephosphorylates myosin = decrease myosin ATPase activity = drives relaxation
structural diffs sm musc in comp sk
- no NMJ
- no t-tubules
- no troponin
- less well-developed SR
- no sarcomeres
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
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…
spontaneous changes mem pot types
- pacemaker pots = oscillating mem pots regularly reaching threshold for Ca2+ entry, myometrium
- Slow waves = cyclic depol/repol regularly reaching threshold Ca2+ entry, gut
no external stim needed
myometrium
sm musc layer uterus that gens contractions for menstruation, childbirth etc
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
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
multiunit muscles
individual activation/inhibition cells for fine control as cells not linked electrically + functions independently, e.g. iris + ciliary body (extention iris)
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
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
why is sm musc contraction so much slower
physically longer get Ca2+ in (lack t-tubules + generalised receiving signal
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
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
