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24 Cards in this Set

  • Front
  • Back
-acetylcholine binds to nicotinic acetylcholine receptor
- Ligand gated non-selective cation channel
- Na and K flow across membrane to depolarize motor end plate membrane --> end plate potential
end plate potential
- can initiate an AP
- AP initiates an elevation in cytoplasmic Ca and activation of contractile apparatus
motor unit
- motor nerve fiber and muscle cells it innervates
- small where fine control needed
motor unit recruitment
- increase muscle force by activating more motor units
tetanic contraction
- muscle contraction lasts much longer than AP
- individual twitches summate
- high stimulation leads to tetany
Regulation of skeletal muscle force
1) motor end plate recruitment
2) frequency of stimulation
Excitation- contraction coupling
- in T tubules L type Ca channels (DHP R) activate Ca release channels (ryanodine R)
L-type Ca channels
- open Ca channels
1) direct physical interaction
- DHP and ryanodine R mechanically coupled
- depolarization induces conformational changes in DHP (L type) which changes ryanodine R
- primary mechanism for SR ca release in skeletal muscle
2) CICR extracellular Ca opens ryanodine R
- active uptake of Ca into SR by Ca-ATPase pump
-calsequestrin in SR, acts as a Ca reservoir
Activation of contractile apparatus
- Ca binds troponin C, rotates tropomyosin, uncovering myosin-binding sites on actin
- myosin activates and cross bridge cycling occurs
actin myosin interaction
- weak binding of myosin to actin
- one head docks into actin site at a time
- actin docking --> P release --> lever arm swings to power stroke moves actin by 100 mA
- ADP dissociates, ATP binds to active site --> catalytic core to weak binding site
thick filaments
- cross bridges at opposite ends of filament rotate towards middle of filament, pulling thin filaments from opposite Z bands towards each other
ATP in contractile process
1) dissociates actin and myosin
- via conformational change, cocking myosin head in prep to interact with actin
- P from ATP dissociates to form ADP-Pi complex bound to myosin (without enough Ca, stays this way)
2) energy for cross-bridge cycling
- Ca moves tropomyosin, myosin binds weakly to actin, structural change occurs to make it bind strongly --> P release --> power stroke --> myosin head rotates on actin filament, ADP released
3) fuels Ca-pumps needed for relaxation
Passive tension
- tension from stretching a muscle (from connective tissue)
- intrinsic of muscle (even dead muscle)
active tension
- contracted muscle
- only in living muscle (actin myosin interaction)
total tension
sum of passive and active tension
Frank - Starling Law
- amount of active tension at each length increases to a maximum and then decreases
- based on physical overlap of thin and thick filaments
- ↑ in stretched length, extent of filament overlap ↓
- after ideal point where filaments overlap with the least distance, they start to move away from each other with more stretch, so active tension ↓
- short muscle length --> SR can't relase as well, and troponin/tropomyosin don't activate myosin well
Where is Starling's law most applicable?
- cardiac muscle, since skeletal muscle exists at peak length
isometric contraction
force generated by contractile apparatus is insuffcient to enable muscle to shorten
isotonic contraction
- focre generated shortens a muscle
- enzyme that hydorlyzes ATP for energy to cross-bridge cycle
slow twitch
- oxidative
- sustained contractions
- fatigue resistant
- red
- type 1
- low glycogen
- postural muscles
fast twitch-
- quick bursts of activity
- type 2a
- standing, walking
- fatigue resistant
- red
- oxidative
- high mitochondria
- type 2b
- high glycogen
- jumping
- fatigable
- white
- high glycogen
- few mitochondria
- shift from 2b to 2a occurs with endurance and weight training