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CST - BIOSCI107 > ET : M - Skeletal Muscle > Flashcards

ET : M - Skeletal Muscle Flashcards

1
Q

What is the structure of skeletal muscles?

A
  • Attached to bones via tendons and is responsible for movement
  • Cells “muscle fibres” are long (up to 35cm) and reasonably wide (0.1mm)
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2
Q

What are skeletal muscle cells composed of?

A

Cells are composed of fibrils containing highly organised contractile filaments (myofibrils)

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3
Q

What are myofibrils made up of?

A

Made up of alternating bands of actin and myosin filaments which interdigitate

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4
Q

What is the sarcomere?
what does it consist of
where does it extend from and to

A
  • Basic contractile element
  • Consists of an array of thick filaments (myosin) which interdigitate with thin filaments (actin), attached to Z discs at each end
  • Extends from one Z line to the next Z line
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5
Q

What does a single skeletal muscle cell have many of?

A

peripheral nuclei and myofibrils

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6
Q

Where are the thick (myosin) filaments of a myofibril?

A

They run the entire length of an A band (A band is the dark part)

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7
Q

where are the thin (actin) filaments of a myofibril?

A

They run the length of the I band and partway into the A band (I band is the light part), in the middle of the I band, has a Z disc

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8
Q

What is the Z disc of a myofibril?

A

A coin-shaped sheet of proteins that anchors the thin filaments and connects myofibrils to one another (where thin filaments connect and are held together)

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9
Q

What is the H zone of a myofibril?

A

Lighter mid-region where filaments don’t overlap (has no thin filaments)

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10
Q

What is the M line of a myofibril?

A

Line of protein myomesin that holds adjacent thick filaments together (middle of thick filaments)

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11
Q

What are the T-tubules?

A
  • Deep invaginations continuous with the sarcolemma (the surface membrane of the muscle cell) at each junctions of the A and I bands
  • Goes around every myofibril
  • Allows action potentials to be carried deep within the muscle cell
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12
Q

What is the Sarcoplasma Reticulum (SR)?

A
  • An extensive network of a subcellular membrane-bound compartment surrounding the fibril
  • Calcium storage site which releases calcium that activates contraction
  • Sacromeres are surrounded by the SR whose terminal cisterns lie close to the T-tubules
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13
Q

What are the thick filaments composed of?

A

Composed of myosin, where each myosin has 2 high molecular weight sub-units each with a globular head and a tail

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14
Q

In thick filaments, what are the globular heads capable of?

A

They are an enzyme capable of hydrolyzing ATP

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15
Q

In thick filaments, how are the heads and tails structured/arranged?

A

The 2 tails intertwine to form a helix. Tails come in and are joined at the middle and the heads are poking out at the ends (away from the M line), arranged in a polarized fashion

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16
Q

In thick filaments, what are the low molecular weight proteins called and where may they be bound?

A

‘Light chains’ and they may be bound near the myosin globular region

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17
Q

In thick filaments, what do the ‘light chains’ regulate?

A

They regulate the catalytic ability of myosin to hydrolyse ATP

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18
Q

In thick filaments, what can the myosin molecules also form?

A

Filaments with the myosin molecules polarised along the filament

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19
Q

What anchors the thick filament to the Z line?

A

Titin

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20
Q

What are the thin filaments composed of?

A

Composed of primarily globular actin proteins

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21
Q

How are the thin filaments composed?

A

They are composed of a double stranded helical actin chain (polymers)

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22
Q

What are the regulatory proteins associated with actin and what do they regulate?

A

Troponin and tropomyosin, they regulate whether myosin can bind onto the actin

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23
Q

What is the dip in the actin?

A

Myosin binding site

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24
Q

At rest, what are tropomyosin and troponin doing?

A
  • Tropomyosin is lying on top of the actin binding sites to stop the myosin from binding to the actin
  • Troponin is what Ca2+ binds onto
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25
Q

What happens when Ca2+ binds onto the troponin?

A

It changes shape and pulls the tropomyosin off the binding sites

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26
Q

The M line in the sacromere is best described as an area rich in?

A

Myosin tails

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27
Q

What is the sliding filament theory of muscle contraction?`

A

As the sacromere contracts/shortens, the thin filaments are pulled over the thick filaments, where the Z line is pulled towards the M line and the I band and H zone become narrower and the A bands don’t change length

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28
Q

What are the major 4 steps of the cross-bridge cycle?

A
  1. Cross-bridge formation
  2. Power stroke
  3. Detachment
  4. Energization of the myosin head
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29
Q

What occurs during cross-bridge formation?

A

Myosin starts in its high-energy state, where ATP has been hydrolyzed to ADP and a phosphate. Myosin binds to the actin binding site to form a cross-bridge (cross-bridge can only occur in the presence of Ca2+ when the myosin binding site on actin is exposed)

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30
Q

What occurs during the power stroke? where is the energy for this from?

A

ADP is released. The myosin head rotates to its low-energy state (about 45 degrees to the actin), pulling the thin filament with it, towards the centre of the sarcomere (while it remains attached to the actin). Energy for power stroke is ultimately provided by ATP that binds to the myosin head

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31
Q

What is the result of the power stroke?

A

Shortening of the sarcomere (Z lines slightly shorten)

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32
Q

What occurs during detachment?

A

A new ATP molecule binds to the empty ATP-binding site on the myosin head. The ink between the myosin head and actin (actin-myosin bind) is weakened and the myosin detaches. The detached myosin head remains in its low-energy state

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33
Q

What happens if there’s no ATP?

A

No detachment (myosin remains attached to actin), muscle is stiff

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34
Q

What occurs during the energization of the myosin head?

A

Myosin heads is stretched out. Myosin head hydrolyzes ATP to ADP and a phosphate. The myosin head moves back to its high-energy state (about 90 degrees to the actin)

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35
Q

What is the only naturally occurring ion that can initiate muscle activation?

A

Ca2+

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36
Q

How does Ca2+ contribute to the cross-bridge cycle?

A

Ca2+ ions provide the “on switch” for cross-bridge cycle to begin. It binds to troponin and the tropomyosin moves to expose the myosin binding sites on actin

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37
Q

What is the critical threshold that Ca2+ must remain above for the cross-bridge cycle to continue?

A

0.001 - 0.01mM

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38
Q

What are the sources for changes in Ca2+ levels?

A

From outside the cell and/or release from internal Ca2+ stores (SR)

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39
Q

What allows the movement of Ca2+ ions into the cytosol?

A

Opening of Ca2+ channels in the SR

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40
Q

How will the Ca2+ levels change inside the cytosol?

A

Ca2+ levels will increase as the Ca2+ levels outside the cell and in the stores are usually higher than inside the cytosol (Ca2+ ions will passively move down its conc. gradient)

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41
Q

What are the active transport pumps (Ca2+ ATPase) doing?

A

Constantly moving Ca2+ from the cytoplasm back into the SR

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42
Q

How is Ca2+ removed from the cytoplasm?

A

It is an active process which is ultimately linked to ATP hydrolysis by ion pumps in the surface membrane

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43
Q

How does Ca2+ contribute to muscle relaxation?

A

Relaxation is brought about by the Ca2+ influx channels closing and the pumps returning the Ca2+ to the stores and/or extracellular space

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44
Q

What is isotonic contraction?

A

The tension developed by the muscle remains almost constant, while the muscle length changes. It’s velocity variable

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45
Q

What is isometric contraction?

A

The tension developed doesn’t exceed the resistance of the object (tension variable) and there is no change in muscle length (length constant)

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46
Q

When the muscle doesn’t shorten but develops isometric force, what is the determinant of the no. of attached cross-bridges?

A

The amount of overlap between thick and thin filaments

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47
Q

Under normal conditions, what is the optimal resting sarcomere length?

A

2.0 - 2.2μm, this is where the greatest tension produced/maximal force developed due to max. no of cross-bridges formed

48
Q

At optimal resting length, what is the normal range of sarcomere lengths in the body?

A

75 - 130% of the optimal length

49
Q

What normally limits the range of sarcomere lengths to the range where max. isometric force is developed?

A

The range of motion of the joints (between bones)

50
Q

How can the range of sarcomere lengths increase?

A

During injuries

51
Q

In terms of the length-tension relationship, what happens at lengths <2.0μm?

A

Active force development is reduced as the ends of filaments collide and start to interfere with each other (extensive overlap)

52
Q

What happens when the sarcomere length is at about 1.2μm?

A

There is no tension as thick filaments meet the Z lines and sarcomeres can’t shorten

53
Q

In terms of the length-tension relationship, what happens to the passive force at lengths >2.2μm?

A

Passive force increases as elastic connective tissue around the muscle cells is stretched

54
Q

In terms of the length-tension relationship, what happens to the active force at lengths >2.2μm?

A

The active force declines (reduced tension) as it reduces the extent of overlap between the filaments and thus, the no. of possible cross-bridegs interactions along the sarcomere (less myosin can grab onto actin)

55
Q

What is total tension?

A

Total Tension = Active + Passive Force

The sum of active tension dependent on sarcomere length and passive tension

56
Q

What is a motor unit?

A

Consists of a motor neuron and all the muscle fibres it innervates

57
Q

What causes neurotransmitter, ACh to release at the neuromusclar junction?

A

An action potential in the motor nerve axon

58
Q

What does the ACh activates?

A

Its receptors (Ca2+ ion channels)

59
Q

What does the ACh receptors do?

A

Depolarises the muscle membrane and lead to an action potential

60
Q

What does the action potential from the ACh receptors lead to?

A

At the axon terminal, voltage-gated Ca2+ channels open and Ca2+ enters as conc. is lower inside the cell (Ca2+ is released from the Ca2+ stores in the muscle (SR))

61
Q

What does Ca2+ entering the axon terminal trigger?

A

The vesicles containing ACh to fuse with the terminal membrane, releasing ACh (via exocytosis) into the neuromuscular junction (synaptic cleft)

62
Q

What does the binding of ACh to the receptors on the muscle end plate cause?

A

Opening of ligand (ACh) gated ion channels

63
Q

What does the opening of ligand (ACh) gated ion channels allow?

A

The movement of predominantly Na+ into the muscle cell making it less -ve (end plate potential) as when Na+ comes in, the membrane depolarizes

64
Q

Why are the effects of ACh short lasting?

A

The enzyme (acetylcholinestarase) rapidly breaks down ACh

65
Q

What occurs if sufficient ligand-gated channels are opened?

A

The end plate potential reaches threshold, voltage-gated Na+ channels open and a muscle action potential is triggered

66
Q

Where is the muscle action potential propagated?

A

Along the sarcolemma, into the T-tubule system

67
Q

At rest, the muscle cell is highly ______

A

polarised

68
Q

During an action potential, when the cell is stimulated at the neuromuscular junction, why does it rapid depolarises?

A

Due to the voltage-gated Na+ channels opening for Na+ ions to rush in, increasing Na+ permeability

69
Q

During an action potential, when does the cell begin to repolarise?

A

When voltage-gated Na+ channels close and voltage-gated K+ channels open, increasing K+ permeability while decreasing Na+ permeability

70
Q

During an action potential, the membrane potential starts to decrease when?

A

Voltage-gated K+ channels begin closing

71
Q

What happens when the membrane potential stabilizes at resting level?

A

Conc. of Na+ and K+ across plasma membranes are restored

72
Q

What does the action potential that is coming down the T-tubules come in close contact to and what does it result in?

A

SR, it results in voltage-gated Ca2+ channels in the SR opening

73
Q

What happens when the voltage-gated Ca2+ channels in the SR open?

A

Ca2+ is released into the cytosol

74
Q

When the Ca2+ is released, what does it bind to and what does it result in?

A

Troponin, when the Ca2+ conc reach a critical threshold, the myosin binding sites on the actin filament are exposed, allowing cross-bridge cycle to occur

75
Q

What happens when Ca2+ levels fall?

A

Contraction ends as Ca2+ is actively pumped back into the SR via Ca2+-ATPase pumps and troponin moves back, covering the myosin binding sites. The muscle “twitch” is complete

76
Q

What is creatine phosphate?

A

For brief periods (<15 secs), it can as an “ATP” store

77
Q

What does the enzyme, creatine phosphokinase do?

A

Transfers phosphate from creatine phosphate to ADP to give ATP (Creatine Phosphate + ADP = Creatine + ATP)

78
Q

Is the creatine phosphate muscle metabolism anaerobic or aerobic?

A

Anaerobic (doesn’t require oxygen but will run out fast)

79
Q

What is the purpose of anaerobic glycolysis?

A

Good for short intense exercise (fast but inefficient) as dominant system from about 10 - 30 secs of maximal effort

80
Q

What does anaerobic glycosis accumulate which ultimately stops the anaerobic mechanism?

A

Accumulation of metabolic products (lactate and H+) limits duration to max. 120 secs, as it inhibits cell reactions

81
Q

How is ATP supplied in anaerobic glycolysis?

A

ATP is supplied by the continuing metabolism of pyruvate to lactate

82
Q

What is the purpose of aerobic glycolysis?

A

Important for postural muscles and endurance exercise so it’s efficient but, comparatively slow (max. 300W)

83
Q

What does aerobic glycolysis require?

A

Oxygen, so good blood supply

84
Q

What is a muscle twitch?

A

The brief contraction in all the muscle fibres in a motor unit in response to a single action potential

85
Q

What is type 1 muscle fibre?

A

Slow oxidative (“slow twitch”)

86
Q

What is type 2B muscle fibre?

A

Fast glycolytic (“fast twitch)

87
Q

What is the max. ATPase rate for both type 1 and type 2B?

A

Type 1 - Slow

Type 2B - Fast

88
Q

What is the SR pumping capacity for both type 1 and type 2B?

A

Type 1 - Moderate

Type 2B - High

89
Q

What is the diameter for both type 1 and type 2B?

A

Type 1 - Small

Type 2B - Large

90
Q

What is the mitochondria/myoglobin/blood supply for both type 1 and type 2B?

A

Type 1 - High

Type 2B - Low

91
Q

What is the glycolytic capacity for both type 1 and type 2B?

A

Type 1 - Moderate

Type 2B - High

92
Q

What is the primary ATP pathway for both type 1 and type 2B?

A

Type 1 - Aerobic

Type 2B - Anaerobic glycolysis

93
Q

What is the type 1 (“slow twitch”) motor unit?

A

Units with neurons innervating the slow efficient aerobic cells (maintaining posture and walking)

94
Q

What is the type 2 (“fast twitch”) motor unit?

A

Units with the neurons innervating the large fibres that fatigue rapidly but develop large forces (jumping and weight lifting)

95
Q

How is force regulated?

A
  1. Rate of stimulation of individual motor units (the no. of action potentials in one motor neuron)
  2. The no. of motor units recruited
96
Q

Is a twitch longer or shorter than an action potential and when does it just starts?

A

Longer, just starts when an action potential has finished

97
Q

In terms of rate of stimulation, what does a single stimulus produce?

A

A single twitch (the muscle contracts and relaxes)

98
Q

In terms of rate of stimulation, what does a low stimulation frequency result in and why?

A

Temporal/wave summation and results in unfused/incomplete tetanus, as another stimulus is applied before the muscle relaxes completely (partial relaxation) so more tension

99
Q

In terms of rate of stimulation, what does a high stimulation frequency result in and why?

A

Fused (complete) tetanus, as there is no relaxation at all between stimuli since there’s lots of action potentials, so barely see a twitch (individual twitches can’t be seen at all, have been fused together to make one big contraction)

100
Q

In terms of rate of stimulation, what does increased frequency result in?

A

Temporal summation

101
Q

In terms of recruitment, what happens as more motor units are recruited?

A

The amount of force developed and tension increases

102
Q

In terms of recruitment, generally, what motor unit is recruited first?

A

Small oxidative motor units (aerobic - type 1) as they are the most fatigue resistant

103
Q

In terms of recruitment, generally, what motor unit is recruited last?

A

Large glycolytic motor units (anaerobic - type 2)

104
Q

In terms of skeletal muscle fibre recruitment, what can be graded by recruitment of different motor units

A

Contractile function

105
Q

In terms of skeletal muscle fibre recruitment, what ensures that small oxidative motor units are recruited first and large glycolytic motor units last?

A

Operation of the size principle

106
Q

How can fibre types change?

A

Depending on the nature of neuronal stimulation so physical training can alter the composition of a muscle to match the demands place upon it, by changing both innervation patterns and production of new muscle fibres (by division of existing fibres)

107
Q

In terms of altering the composition of a muscle, what does sustained use and reduction in activity lead to?

A

Sustained use leads to muscle hypertrophy, while a reduction in activity (due to loss of innervation or lack of exercise) leads to muscle atrophy

108
Q

What is the cell length?

A

Up to 35cm

109
Q

What is the cell shape?

A

Cylindrical

110
Q

How is contraction initiated?

A

Neurogenic (voluntary)

111
Q

What is the conductivity of skeletal muscles?

A

Electrically isolated

112
Q

How long is an action potential?

A

~1ms

113
Q

How are the contractile filaments organised?

A

Into sarcomeres

114
Q

What is the shape of the SR?

A

Extensive

115
Q

Are skeletal muscles striated?

A

Yes (‘banded’ appearance)

CST - BIOSCI107 (13 decks)

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