muscle contraction Flashcards

1
Q

motor unit

A

motor neuron + it’s muscle fibers

large fibers - large movement

small - fine movement (eye)

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2
Q

NMJ

A

presyn = axon terminal

postsyn = muscle endplate

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3
Q

steps at the NMJ

A
  1. Ap conducted into pre-syn terminal
  2. depolarize pre-syn terminal
  3. Opening of VG-Ca2+ channels and entry
  4. fusion of vesicles w membrane - Ach into cleft
  5. Ach binds receptor on post-syn membrane
  6. opening of channels on post-syn membrane - Na and K travel down gradient
  7. generation of EPP
  8. Ach broken down into coline and acetate - choline back to pre-syn

10.

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4
Q

EEP characteristics

A

latency - delay from AP –> muscle

graded - size dep on how many vesicles of Ach released

quantal - goes up step by step (each vesicle) - adds up to full potential

decremental conduction - gets smaller further away from end plate

high safety factory (skel muscle) - as long as EPP what it’s supposed to be you will get AP!

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5
Q

decremental conduction

A

if EEP but NOT AP

at nmj you can still see the EEP but it goes away (still see same strong AP far away)

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6
Q

muscle structure

A

muscle - fascile - muscle cell (fiber) - myofibrils (in muscle cell covered by SR) - myofibrils - sarcomere (with actin and myosin)

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7
Q

T tubules

A

formed from invaginations of plasma membrane

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8
Q

triad

A

sarcoplasmic reticulum cisterna on either side of transverse tubule

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9
Q

skeletal muscle excitation

A
  1. AP into T tubules
  2. VG L-type Ca channel conformational change
  3. Ca release channel open (mechanically cated, Ca gated)
  4. mytoplasmic [Ca] increases

Ca DOES NOT MOVE through L-type channels in the T tubules

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10
Q

how do skeletal and cardiac muscle excitation differ

A
  1. Ca enters through L type channels
  2. no mechanical link between L type and SR ca release (80% from SR, 20% from membrane)
  3. can be modulated
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11
Q

tropomyosin

A

binds to actin and troponin

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12
Q

TnT

A

troponin T

binds to tropomyosin

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13
Q

TnC

A

tropinon

binds to Calcium

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14
Q

TnI

A

interferes

troponin

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15
Q

how does troponin work

A

increased Ca –> binds to TnC –> actomyosin complex formed –> tension increases

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16
Q

E-C coupling in skeletal muscle

A

muscle action potential

increase in Ca - myoplasm

Ca-troponin

increase muscle tension

decrease muscle tension

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17
Q

SERCA

A

Ca-ATPase - pumps Ca back into SR

primary active transport

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18
Q

calsequestrian

A

bound to ca in SR

19
Q

relaxation in skeletal musche

A
  1. l type Ca channels close
  2. Ca-gated channel inactivated
  3. SERCA pump back in
  4. Ca binding proteins in cytoplasm
20
Q

differences betwen cardiac and skeletal uscle relaxation

A

sarcolemma:

Ca-Na pump

Ca pump

SR:

PLN –> increases SERCA

all can be regulated

21
Q

Ca release channels in skeletal muscles

A

mechanically and ionically

22
Q

crossbridge system

23
Q

isometric tension

A

length - no change

tension - increasing

head rotates developing isometric contraction

acheives 45% by stretching neck of myosin (not enough tension to shorten sarcomere)

recruits more and more muscle fibers until enough muscle tension

24
Q

isotonic tension

A

length - shortening

tension - no change

muscles can’t change length and tension at same time

25
26
muscle resting length-tensison
more stretched - increased resting tension
27
Titan
mechanism of passive and restoring force generation when tighten muscle - titan stretches molecular basis for resting tension
28
fused tetanus
summation of tetanic stimulus until it fuses
29
how to increase active tension
increase stimulus frequency recruit motor units
30
active tension
total tension when contract (measured) - resting tension hihest at resting length
31
sliding filament model
1. F due to interaction of thick and thin filaments 2. muscle filament length is constant 3. filaments can slide past each other 4. isometric F is proportional to thick and tin filament overlap
32
isometric force and length
due to interaction of thick and thin filaments 0 tension when 0 overlap or full over lap most tension when meet - no overlap middle when slight overlap same in cardiac and skeletal muc
33
length-tension plot
shows changesin isometric tension with sarcomere (muscle) length
34
isometric
for more tension - add crossbridges and muscle fibers same length - recruit more don't shorten until have enough tension
35
isotonic
when muscle begins to shorten - no more crossbridges or muscle fibers are added
36
what if lifting more than you can hold up isometrically?
first need titan to lift for a second but then will drop it
37
preload
determines initial muscle length determined by amt of blood in the heart (resting tension)
38
afterload
determines force required to shorten and end muscle length pressure in orta (what pushing against but doesn't know it's there)
39
shortening velocity
depends on myosin isoform (ATPase) and force against which muscle contracts (afterload) at heaviest load - muscle can't contract - V = 0 AND preload (at heavy - few xb available for fast cycling, at light - many xb available for fast cycling) high BP- can't contract as fast bc so much afterload 1. afterload 2. preload 3. myosin isoform(ATPase)
40
velocity and afterload
bigger F pumping against - lower Velocity
41
shortening velocity and myosin ATPase
Myosin ATPase (EC 3.6.4.1) is an enzyme with system name ATP phosphohydrolase (actin-translocating). [1] This enzyme catalyses the following chemical reaction ATP + H2O ADP + phosphate. ATP hydrolysis provides energy for actomyosin contraction.
42
shortening velocity and preload
resting length - number of crossbridges ready to be formed for fast cycling
43
power
afterload x velocity of showertening max power = 1/3 max load rate of doing work dep on: 1. myosin ATPase 2. load (afterload) 3. resting load (preload)
44