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24 Cards in this Set
- Front
- Back
ACh
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-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 |
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end plate potential
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- can initiate an AP
- AP initiates an elevation in cytoplasmic Ca and activation of contractile apparatus |
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motor unit
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- motor nerve fiber and muscle cells it innervates
- small where fine control needed |
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motor unit recruitment
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- increase muscle force by activating more motor units
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tetanic contraction
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- muscle contraction lasts much longer than AP
- individual twitches summate - high stimulation leads to tetany |
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Regulation of skeletal muscle force
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1) motor end plate recruitment
2) frequency of stimulation |
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Excitation- contraction coupling
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- in T tubules L type Ca channels (DHP R) activate Ca release channels (ryanodine R)
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L-type Ca channels
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- 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 |
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relaxation
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- active uptake of Ca into SR by Ca-ATPase pump
-calsequestrin in SR, acts as a Ca reservoir |
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Activation of contractile apparatus
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- Ca binds troponin C, rotates tropomyosin, uncovering myosin-binding sites on actin
- myosin activates and cross bridge cycling occurs |
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actin myosin interaction
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- 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 |
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thick filaments
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- cross bridges at opposite ends of filament rotate towards middle of filament, pulling thin filaments from opposite Z bands towards each other
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ATP in contractile process
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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 |
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Passive tension
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- tension from stretching a muscle (from connective tissue)
- intrinsic of muscle (even dead muscle) |
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active tension
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- contracted muscle
- only in living muscle (actin myosin interaction) |
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total tension
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sum of passive and active tension
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Frank - Starling Law
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- 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 |
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Where is Starling's law most applicable?
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- cardiac muscle, since skeletal muscle exists at peak length
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isometric contraction
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force generated by contractile apparatus is insuffcient to enable muscle to shorten
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isotonic contraction
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- focre generated shortens a muscle
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Myosin
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- enzyme that hydorlyzes ATP for energy to cross-bridge cycle
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slow twitch
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- oxidative
- sustained contractions - fatigue resistant - red - type 1 - low glycogen - postural muscles |
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fast twitch-
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- 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 |
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exercise
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- shift from 2b to 2a occurs with endurance and weight training
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