Excitation-Contraction Coupling Flashcards

1
Q

Excitation-Contraction Coupling

A

The process where an electrical stimulus causes Ca2+

to be released from the sarcoplasmic reticulum, causing muscle to contract by sarcomere shortening.

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2
Q

What happens to ACh when it is released into the synaptic cleft.

A
  1. It can diffuse out of the cleft

2. It can be broken down by Acetylcholinesterase into–> [Choline and acetyl-coA] and choline is reuptaked

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3
Q

Excitation-Contraction Coupling

A
  1. AP is conducted down the neuron–> axon terminal.
  2. VGCa2+ will open and cause the influx of Ca2+ into the terminal.
  3. Ca2+ binds to synaptic vesicles.
  4. Synaptic vesicles move to the cell membrane and releases ACh into the NMJ via exocytosis.
  5. ACh will bind to nicotenic cholinergic receptors (Ligand-gated Na+ receptors) in the subneural cleft of the post-synaptic membrane and cause the influx of Na+.
  6. This will cause localized potentials, which will then activate VGNa+ receptors.
  7. Because skeletal muscle is so big, they have [t-tubules] to help reach the depths of the muscles. As the AP travels down the T-tubule, it activates DHP receptors, which are coupled to [ryanodine receptors].
    - Ryanodine receptors are located on the sarcoplasmic reticulum.
  8. Ca2+ is released from the sarcoplasmic reticulum–> sarcolemma.
  9. Ca2+ will then bind to Troponin C, causing tropomyosin to shift away from actin binding sites. This allows the myosin heads to interact with the actin binding sites.
  10. ATP bind to mysoin head (causing it to be active)
  11. ATP–> ADP + Pi which causes the myosin head to cock back and attach.
  12. When Pi, leaves, the powerstroke will occur and actin is pulled to the m-line.
  13. To release, ADP leaves and ATP binds. We are now in the original state
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4
Q

Where are ryanodine receptors located?

A

They are located on the sarcoplasmic reticulum

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5
Q

How many vesicles are stored at each end plate?

How many vesicles are released per AP?

A

300k vesicles are stored at the end plate

125 vesicles are released per AP.

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6
Q

How is Calcium sequestered during repolarization?

A

[ATP-dependent Ca+ pumps] will move Ca2+ back into the sarcoplasmic reticulum

Ca2+ binding to the calsequestrin( located inside the SR) will allow 40x more to

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7
Q

What allows myosin heads to be freely moveable?

A

Myosin heads have 2 hinges.

1st hinge is located where the 2 heads extend from their original connection

2nd hinge is located on each individual head and allows them move independently.

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8
Q

What are the three types of tropinin?

A
  1. Troponin I
  2. Troponin C
  3. Troponin T
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9
Q

Troponin I

A

Strong affinity for actin.

Thus, it covers the actin binding site

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10
Q

Troponin C

A

Strong affinity for calcium

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11
Q

Troponin T

A

Strong affinity for tropomyosin

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12
Q

What causes ATP–> ADP on the myosin head?

A

Myosin head has [ATPase enzymes].

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13
Q

What part of the sarcomere is not overlapped by actin?

A

H-band

Myosin is not overlapped by actin.

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14
Q

Is the force of contraction the same everytime?

A

No

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15
Q

Length tension curve

A

When there is no overlap between actin and myosin, sarcomere length is the greatest and the tension is the lowest. This is not normal.

As overlap occurs, sarcomere shortens and tension increases. [2.25 um and about ~1 relative tension] is normal

As we contract and shorten sarcomere, there is not a lot of tension change because every myosin head is bound to the actin.

  1. All myosin heads are bound to actin sites, the most efficient amount of tension
  2. If we decrease the length of the sarcomere too much, we can overlap: not all myosin heads are bound and tension is decreasing.
  3. Myosin will start bending and crinking because too close. length and tension are really low.
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16
Q

How is force generated?

A

By a motor unit.

Motor unit is a motor neuron and all of the muscles that it innervates.

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17
Q

Which has more nerve fibers: a small or large muscle?

A

Small, more precise muscles (our eye), has more nerve fibers to control it.

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18
Q

Force can also be generated by _____

A

tetany

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19
Q

Summation in tetanus

A

Summation occurs when we add together all individual twitch contractions, allowing us to increase the overall contraction of a muscle.

20
Q

What does summation increase

A
  • the number of motor units that contract at the same time.

- increases frequency of contraction

21
Q

Tetany

A

state of constant contraction

22
Q

Rigor mortis

A

state of constant contracture that lasts 15-25 hours. Similar to tetanus, but method of reaching is different.

-We are stuck in powerstroke: We do not have ATP to release the myosin heads from the binding sites. Thus, they are in a constant state of contracture. This is why bodies are stiff. Evenetually, the sarcolemma will break down and cause the relaxation.

23
Q

Where does the ATP come from?

A

We have stored ATP in muscles, but it only lasts for 2 seconds.

Thus, we have three other mechanisms to get ATP.

  1. Creatine phosphate
  2. Glycolysis
  3. Oxidative mechanisms
24
Q

ATP from creatine phosphate

A

gives us ATP for 8-10s more seconds.

We have a lot of phosphocreatine in our muscles. Phosphate from creatine will be placed on ADP, creating more ATP.

25
Q

Best amount of tension is determined by

A

amount of overlap.

26
Q

ATP from glycolysis

A

provides ATP from 1.3-1.6 minutes.

In anaerobic metablism, pyruvic acid–> lactic acid

27
Q

ATP from oxidative metabolism

A

provides an unlimited amount of ATP as long as we have oxygen and nutrients

28
Q

Different types of muscle fibers

A
  1. Slow twitch

2. Fast twitch (Type 2 A/B)

29
Q

Slow twitch fibers (Type 1)

A

More MT
More Myoglobin
More capillaries.

Utilized oxidative metabolism

30
Q

Fast twitch fibers (Type 2)

A

2x bigger,
Less mT,
2-3x more active phosphocreatine and glycogen systems. Thus, they get ATP from creatine and glycogen.

31
Q

What activities use phosphagen system?

A
  1. 100 meter dash
  2. weight lifting
  3. Basketball
  4. Tennis
  5. Ice-hockey
32
Q

What is the purpose of the t-tubule?

A

To bring the AP into the interior of the muscle fiber.

33
Q

What is the t-tubule?

A

An invagination of the sarcolemma so that we can reach the depths of the muscle fiber

34
Q

During contraction, what part of the sarcomere gets smaller?

A

H band

I band

35
Q

Purpose of subneural clefts

A

Increase SA to allow more ACh receptors and VGNa+ to be present.

36
Q

How many vesicles do we have per end plate

A

300k

37
Q

how many vesicles are released per AP

A

125

38
Q

how many NTs are in one vesicle

A

5-10k

39
Q

when we do have the most efficient amount of tension

A

when all myosin heads are bound to actin

40
Q

what sarcomere length and tension is considered normal

A

2.25 um

and a relative tension of 1

41
Q

where does overlap occur on the sarcomere

A

A band

42
Q

as we begin to contract, and shorten sarcomere, does tension increase or decrease>

A

not a change in tension because every myosin head is now bound to an actin site

43
Q

Perfect amount of overlap occurs when the sarcomere is how long

A

1.8-2 um

44
Q

when overlap occurs what happens

A

Sarcomere length shortens
tension decreases
not all myosin are bound to actin

45
Q

does the A band shorten in contraction

A

no