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CV Quiz > muscle contraction > Flashcards

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

A
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
Q
A
26
Q

muscle resting length-tensison

A

more stretched - increased resting tension

27
Q

Titan

A

mechanism of passive and restoring force generation

when tighten muscle - titan stretches

molecular basis for resting tension

28
Q

fused tetanus

A

summation of tetanic stimulus until it fuses

29
Q

how to increase active tension

A

increase stimulus frequency

recruit motor units

30
Q

active tension

A

total tension when contract (measured) - resting tension

hihest at resting length

31
Q

sliding filament model

A
  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
Q

isometric force and length

A

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
Q

length-tension plot

A

shows changesin isometric tension with sarcomere (muscle) length

34
Q

isometric

A

for more tension - add crossbridges and muscle fibers

same length - recruit more

don’t shorten until have enough tension

35
Q

isotonic

A

when muscle begins to shorten - no more crossbridges or muscle fibers are added

36
Q

what if lifting more than you can hold up isometrically?

A

first need titan to lift for a second but then will drop it

37
Q

preload

A

determines initial muscle length

determined by amt of blood in the heart

(resting tension)

38
Q

afterload

A

determines force required to shorten and end muscle length

pressure in orta (what pushing against but doesn’t know it’s there)

39
Q

shortening velocity

A

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
Q

velocity and afterload

A

bigger F pumping against - lower Velocity

41
Q

shortening velocity and myosin ATPase

A

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
Q

shortening velocity and preload

A

resting length - number of crossbridges ready to be formed for fast cycling

43
Q

power

A

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
Q
A

CV Quiz (5 decks)

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