Lab 3 - Skeletal muscle contraction Flashcards

1
Q

Describe how an action potential initiated at the NMJ can cause an increase in incracellular calcium. How is the intracellular calcium concentration returned to normal?

A

When the action potential invades the presynaptic terminal it depolarises it, there are voltage gated sodium channels on the axon that are responsible for the propagation of the action potential and the depolarisation of the action potential spreads into the nerve terminal and opens voltage gated calcium channels that are located throughout the terminal and many are at the same location as the vesicles to allow for tight coupling

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2
Q

Tropomyosin

A

Tropomyosin covers myosin binding sites on actin

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3
Q

Troponin

A

troponin binds calcium

calcium binding sites blocked, calcium binds to troponin complex which then moves tropomyosin out of the way, exposing myosin binding sites

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4
Q

Tetanus

A

When the frequency of muscle contraction is such that the macimal force is generated without any relaxation of the muscle

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5
Q

Twitch

A

The period of contraction and relaxation of a muscle after a single stimulation

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6
Q

The force transducer …

A

produces a voltage output in proportion to the force applied to it

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7
Q

EDL (extensor digitorum longus)

A

fast twitch fibres

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8
Q

Soleus

A

slow twitch fibres

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9
Q

In this experiment of EDL and soleus what is recorded

A

In this experiment the two channels are recorded. One shows the stimuli delivered, and the othe rshows the muscle response. These two channels are useful to show the time delay of the muscle response after the stimulus

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10
Q

Minimum contraction tension

A

Find the stimulus voltage when the contraction first occurs, and measure the tension developed

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11
Q

Maximum contraction tension

A

Find the stimulus voltage where the contraction is at its maximum, and measure the tension developed

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12
Q

Describe how the twitch amplitude changed when you increased the stimulus voltage.

A

Twitch amplitude increases with increasing stimulus voltage until maximum is reached where increase in the stimulus voltage will not increase the twitch amplitude anymore

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13
Q

Why did the twitch amplitude change when you increased the stimulus voltage? (and Q3 part 1 what is the mechanism for the increase).

A

Recruited more muscle fibers with increasing voltage

• Larger fibres recruited first (due to lower resistance with artificial stimulus)

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14
Q

In this experimental set up, explain the process for the observed twitch amplitude change. How would this be different in the body?

A

Recruit more motor units
(motor unit: alpha motor neuron + all fibres it innervates)
• Smaller motor units recruited first

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15
Q

Time to peak

A

from start of the response until maximum tension occurs

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16
Q

Latency

A

from the onset of the stimulus to the start of the response (time delay)

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17
Q

Fusion frequency

A

is the frequency where individual twitches can no longer be seen in response to stimuli (referred to as tetanus or a tetanic contraction). Individual twitches become fused at this particular frequency

at fusion frequency the response will be a jagged line and not a smooth one like textbooks

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18
Q

EDL has a _____ time to peak than soleus

A

faster

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19
Q

Explain why the latency and duration of the contraction differ for EDL and soleus.

A

• • •
Soleus has a higher proportion of slow twitch fibres
EDL has a higher proportion of fast twitch fibres
Compare the cellular characteristics of slow vs fast twitch fibres

20
Q

Ryanodine receptors - slow twitch

A

low density = slower calcium release

21
Q

Ryanodine receptors - fast-twich

A

high density = faster calcium release

22
Q

Myosin type - slow twitch

A

slow ATP hydrolysis = slow cross bridge cycling

23
Q

Myosin type - fast twitch

A

fast ATP hydrolysis = fast cross bridge cycling

24
Q

SERCA pump - slow twitch

A

SERCA2a pumps Ca2+ back into SR slowly = slower drop in tension

25
Q

SERCA pump - fast twitch

A

SERCA1a pumps Ca2+ back into SR rapidly = faster drop in tension

26
Q

Energy production - slow twitch

A

oxidative = lots of ATP generated by requires oxygen and is slower

32-36 ATP

27
Q

Energy production - fast twitch

A

glycolytic = fewer ATP generated quickly but creates lactic acid

2 ATP

28
Q

Mitochondria - slow twitch fibres

A

many

29
Q

Mitochondria - fast twitch fibres

A

few

30
Q

Oxidative enzymes - slow twitch

A

many

31
Q

Oxidative enzymes - fast twitch

A

few

32
Q

Myoglobin - slow twitch

A

abundant

33
Q

Myoglobin - fast twitch

A

sparse

34
Q

Type I =

A

slow twitch

oxidative

35
Q

Type IIA

A

fast twitch

oxidative-glycolytic

36
Q

Type IIB

A

fast twitch

glycolytic

37
Q

Slow twitch fibres

A

Fatigue resistant
Abundant in postural muscles
Utilised most during endurance activities

38
Q

Fast twitch fibres

A

Fatigues easily
Abundant in muscles of power or fine movement
Utilised most during power and sprint activities

39
Q

Fused tetanus soleus vs edl

A

Fused tetanus happens at a lower frequency for Soleus than for EDL.
There is a difference in how smooth the fused tetanus trace is, Soleus is smoother, EDL fluctuates.
EDL does not hold peak tension for long
(it fatigues quickly).

40
Q

If you applied continuous stimulation for a period of 30 minutes to EDL and soleus muscle, what would you expect to occur to the tension recorded in each muscle?

A

EDL - fast twitch therefore quick fatigue

Soleus - slow twitch therefore slow fatigue

41
Q

Why is the tetanic force greater than the twitch?

A
  1. Each AP causes Ca2+ release, many AP’s cause a lot of Ca2+to be released
  2. Ca2+ reuptake lower than release
  3. Sustained Ca2+ available in cytoplasm
  4. Because tissue does not relax, elastic recoil does not need to be overcome with each twitch
42
Q

Active tension =

A

total tension - passive tension

43
Q

Describe what occurred to the muscle twitch as you increased the length of
the muscle and explain why.

A

Increased then decreased

More cross-bridges = more tension

44
Q

Results of active tension experiment support which theory of skeletal muscle contraction?

A

Sliding Filament Theory: Actin and myosin slide over one another

45
Q

Myasthenia gravis

A
Autoimmune disease
• Antibodies to nicotinic ACh receptors
• AChR receptors blocked/destroyed
• Decreased efficiency at NMJ
• Muscle weakness (especially of
frequently used muscles)
46
Q

During clinical tests, Mrs CHB was given a repetitive closely timed stimulus (Repetitive Nerve Stimulation Test) on the ulnar nerve and the muscle action potential was recorded on flexor carpi ulnaris. Would the test show any abnormalities? If yes, how does it differ to normal conditions?

A

Yes - EMG decreased in amplitude with successive stimulation

47
Q

What would be the effect of administering edrophonium chloride (acetylcholinesterase blocker) to Mrs CHB on her arm weakness and ptosis?

A
  • Increase availability of ACh by blocking AChE
  • Relieve symptoms of muscle weakness and ptosis
  • Temporary
  • Diagnostic