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Physiology 2410 > Lecture 18- Skeletal muscle > Flashcards

Lecture 18- Skeletal muscle Flashcards

1
Q

what are the 4 steps to tight binding in the rigor state?

A
  1. ATP binds to myosin, myosin releases actin
  2. myosin hydrolyzes ATP into ADP+P and myosin binds weakly to actin
  3. power stroke begins when tropomyosin moves off the binding site, head swivels and myosin releases P
  4. myosin releases ADP at the end of the power stroke
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2
Q

what is excitation contraction coupling?

A

generation of tension depends on electrical activity

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3
Q

what is the sarcoplasmic reticulum?

A

modified endoplasmic reticulum

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4
Q

what does the sarcoplasmic reticulum consist of?

A

high Ca++ concentration
powerful ATPase transporter
Ca++ binding protein called calsequestrin

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5
Q

what does the powerful ATPase transporter of the sarcoplasmic reticulum do?

A

uses ATP to pump Ca++ from cytoplasm into sarcoplasmic reticulum

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6
Q

where are t- tubules located?

A

run perpendicular from surface of muscle cell membrane into central portions of the muscle fiber, they are aligned on the edges of the A band
continuous with surface membrane

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7
Q

what does the spread of an action potential down a t- tubule release?

A

Ca++ from sarcoplasmic reticulum into cytosol through voltage gated Ca++ channel (dihydropyridine receptor)

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8
Q

what happens after Ca++ leaves the T- tubule and enters the cytosol?

A

ryanodine receptor Ca++ release channel opens and some Ca++ leave

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9
Q

what is the process of excitation contraction coupling? (8)

A
  1. AP invades the presynaptic terminal (Ca++ enters) and causes release of ACh
  2. ACh binds to the receptor, allows entry of Na+, causes EPSP large enough to trigger an AP
  3. AP invades the T-tubule system
  4. AP causes the dihydropyridine receptor to open which causes the ryanodine channel to open, this causes a massive release of Ca++ thus an increase in intracellular Ca++ concentration
  5. Ca++ binds troponin. troponin pulls tropomyosin away from the myosin binding site on the actin protein thus myosin binds tightly
  6. power stroke
  7. actin filaments slide towards centre of the sarcomere
  8. free Ca++ pumped back into sarcoplasmic reticulum
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10
Q

when does rigor mortis occur?

A

2-4 hours after death and peaks at around 12 hours

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11
Q

what happens to Ca++ after death?

A

intracellular Ca++ rises because it leaks out of SR
Ca++ allows troponin tropomyosin complex to move aside and allow myosin cross bridges to bind to actin

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12
Q

what happens to cross bridges with rigor mortis?

A

they cant detach because theres no ATP to separate actin and myosin. once bound cross bridges cant detach

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12
Q

when does rigor mortis subside?

A

when enzymes start to break down myosin heads

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13
Q

what occurs after rigor mortis?

A

relaxation of muscle

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14
Q

what happens with relaxation of muscle after rigor mortis?

A

-AP stop arriving
-ACh dissociates from AChR and receptor gets degraded
-Ca++ ATPase pumps free Ca++ back into SR
-Ca++ dissociates from troponin and is pumped back into SR
-Tropomyosin moves back into position blocking cross bridge binding site
-muscle ceases to maintain tension

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15
Q

how do you get a muscle back to its original length?

A

pulled by titin
pulled by antagonistic muscle (best way)

16
Q

what are 3 processes in contraction-relaxation process that require ATP?

A
  1. splitting of ATP by myosin ATPase for power stroke
  2. active transport of Ca++ back into sarcoplasmic reticulum
  3. Na/ K+ ATPase
17
Q

what are the 4 main energy sources used for muscle contraction?

A

stored ATP
creatine phosphate
oxidative phosphorylation
glycolysis

18
Q

how long does the energy from creatine phosphate give you?

A

4-5x the energy of stored ATP but that is only around 4-5 minutes worth of energy, thus is in limited supply

19
Q

how does creatine phosphate work?

A

creatine kinase has a forward or backward reaction.
backward reaction is when ATP-P-P-P attach one of their phosphates onto creatine creating ADP-P-P and creating phosphate-P
the forward reaction would be opposite the ADP-P-P gets phosphorylated into ATP-P-P-P

20
Q

when is oxidative phosphorylation used?

A

during light to moderate exercise

21
Q

how does oxidative phosphorylation work?

A

uses stores of glycogen in muscle
aerobic exercise
adequate supply of oxygen

22
Q

oxidative phosphorylation has a good yield of ATP, what is it?

A

30- 32 ATP per glucose molecule

23
Q

when is anaerobic glycolysis used?

A

when you’re at the end of a marathon and you go into oxygen debt

24
Q

anaerobic glycolysis has a very low ATP yield, what is it?

A

2 ATP per glucose molecule
this builds up lactic acid, acidifies muscle and contribute to fatigue

25
Q

what causes muscle fatigue?

A

central fatigue
peripheral fatigue

26
Q

what is central fatigue?

A

psychological

27
Q

what is peripheral fatigue?

A
  • decrease in release of ACh
  • nicotinic receptor gets desensitized (may not get EPSP)
  • Changes in of muscle RMP
    -impaired Ca++ release by SR
    -intracellular pH of muscle can change and produce lactic acid (causes damage to muscle cells)
28
Q

what is the big difference between neuron membrane potential and muscle fiber membrane potential

A

muscle fiber membrane potential has a 2 millisecond synaptic delay which in turn takes more time for ACh to diffuse

29
Q

what are the 3 phases of tension during one muscle twitch?

A

latent period
contraction phase
relaxation phase

30
Q

what are single twitches?

A

tension generated, then relaxed state
slow and will eventually decay

31
Q

what is summation?

A

combination of twitches, can generate tension before first twitch reaches relaxation

32
Q

what is summation leading to unfused tetanus?

A

tension that builds up over time but has points of relaxation called tetanus, they arent full relaxation (slide 60)
reaches maximum tension and is high frequency

33
Q

what is summation leading to complete tetanus?

A

the most force a motor unit can generate

Physiology 2410 (21 decks)

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