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Exercise Physiology and Pharmacology > Muscle Adaptations to Exercise > Flashcards

Muscle Adaptations to Exercise Flashcards

1
Q

What does muscle contraction depend on?

A

Myofilaments, which include actin and myosin.

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2
Q

How do the connective tissue sheaths of muscle exist?

A

Inner, middle, to outer: endomysium, perimysium, and epimysium.

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3
Q

Endomysium

A

Each muscle cell (fibre) is surrounded by a fine sheet of areolar connective tissue.

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4
Q

Perimysium

A

Muscle cells are bundled together into fascicles which are each surrounded by a layer of dense irregular connective tissue.

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5
Q

Epimysium

A

A layer of dense irregular connective tissue surrounding the whole muscle.

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6
Q

What does endomysium surround?

A

A muscle cell (fibre).

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7
Q

What does perimysium surround?

A

Muscle cells bundled together, known as a fascicle.

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8
Q

What does epimysium surround?

A

The whole muscle.

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9
Q

What are myofibrils?

A

Long rods within sarcoplasm. They are a specialized contractile organelle in the muscle tissue.

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10
Q

What are repeating segments of myofibrils known as?

A

Sacromeres.

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11
Q

What is a sacromere?

A

The basic functional unit of contraction of skeletal muscle.

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12
Q

Z disc

A

The boundary of each sarcomere.

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13
Q

Where are thin filaments located in the sacromere?

A

Thin filaments, also known as actin, extend from the Z disc towards the centre of the sacromere.

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14
Q

Where are thick filaments located in the sacromere?

A

Thick filaments, also known as myosin, are located in the centre of the sarcomere.

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15
Q

How are thick and thin filaments connected?

A

In the sarcomere, the thick filaments (myosin) overlap the inner ends of the thin (actin) filaments.

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16
Q

A bands

A

Full length of the thick filament (including the inner ends of the thin filaments).

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17
Q

H zone

A

Centre part of A band where no thin filaments occur.

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18
Q

M line

A

In the centre of the H zone, containing tiny rods that hold thick filaments together.

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19
Q

I band

A

Region with only thin filaments (lies within two adjacent sarcomeres).

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20
Q

What does the sarcoplasmic reticulum do?

A

It’s a specialized smooth ER that acts as a calcium storage site, allowing for the initiation of muscle contraction.

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21
Q

What happens to the H zone during contraction of muscle?

A

It disappears as actin filaments are pulled inwards, overlapping myosin filaments.

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22
Q

What happens to the Z line during contraction of muscle?

A

Stays the same, but are pulled closer together due to sarcomeres shortening.

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23
Q

What happens to the A band during muscle contraction?

A

The length remains constant.

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24
Q

What happens to the I band during muscle contraction?

A

They shorten greatly.

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25
Q

Explain the sliding filament theory.

A
  1. Phosphorylated myosin head attaches to actin in the thin filaments
  2. Myosin pivots to pull thin filaments inward towards the centre of the sarcomere
  3. Shortening of the sarcomere = muscle contraction
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26
Q

Explain the actions that happen at the neuromuscular junction.

A
  1. Action potential is carried down the presynaptic terminal cell
  2. Voltage gated calcium channels are activated through depolarization and calcium flows into the cell
  3. Allows release of acetylcholine in vesicles into the synaptic cleft
  4. ACh binds to receptor on the post-synaptic cell to allow for depolarization of the motor end plate
  5. Sodium intake is activated in post-synaptic cell and potassium influx activated later on for allowal of action potential
  6. Acetylcholinesterase metabolizes ACh to reduce its efficacy and components are sent back to the presynaptic cell (choline)
  7. Acetate is disregarded in the synaptic cleft
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27
Q

What is excitation-contraction coupling?

A

The link between the generation of an action potential (sarcolemma) and the start of muscle contraction.

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28
Q

How is action potential compare to intracellular calcium?

A

As the response to the action potential increases in muscles, there is an increase in intracellular calcium to allow for greater muscle contractions.

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29
Q

What are T-tubules?

A

Invagination of the sarcolemma that bring ion channels closer to the SR where the calcium stores are. It also allows efficient movement of electrical signals so that whole myofibril contracts.

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30
Q

Explain the process of excitation-contraction coupling.

A
  1. Generation of muscle action potential through acetylcholine release and depolarization of T-tubule
  2. Conformational change in dihydropyridine receptors
  3. The release of calcium from the sarcoplasmic reticulum via ryanodine receptors
  4. The binding of calcium to troponin
  5. Tropomyosin moves and allows interaction of actin and myosin
  6. Cross-bridge cycling and force generation
  7. The re-accumulation of calcium within the SR to stop contraction via the SERCA = relaxation
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31
Q

Where do ryanodine receptors exist?

A

On the sarcoplasmic reticulum.

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32
Q

What is the purpose of ryanodine receptors?

A

They release calcium from the SR into the cytoplasm of the sarcomere to allow for muscle contraction.

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33
Q

What are ryanodine receptors coupled to?

A

Dihydropyridine receptors

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34
Q

What do dihydropyridine receptors do?

A

They are voltage gated channels that sense changes in the membrane potential in the T-tubule during action potentials. They allow for RyR1 receptors to release Ca2+ from the SR.

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35
Q

How do transverse tubules exist?

A

As a triad.

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36
Q

What does tropomyosin do?

A

They block myosin-binding sites on actin molecules, so cross bridges can’t form.

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37
Q

What binds to troponin?

A

Calcium

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38
Q

What happens to tropomyosin when calcium binds to troponin?

A

Their is an induction of a conformational change that allows tropomyosin to move away from the myosin-binding sites on actin, exposing them for a cross bridge to form.

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39
Q

Explain cross-bridge cycling.

A
  1. The active site on actin is exposed due to calcium binding to troponin
  2. The myosin head forms a cross bridge with actin (attached to ADP + Pi)
  3. During the power stroke, the myosin head bends and ADP and phosphate are released (thin filament is dragged towards the center of the sarcomere)
  4. A new molecule of ATP attaches to the myosin head, causing it to detach from actin cross-bridge
  5. ATP hydrolyzes to ADP and phosphate, which returns the myosin to its “cocked” position
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40
Q

What is needed for a contraction to occur (2 requirements)?

A

As long as there is ATP and calcium present.

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41
Q

How is contraction terminated?

A

By the return of calcium to the SR by SERCA.

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42
Q

Explain the mechanism on the fall in intracellular calcium using action potentials.

A
  1. Repolarization to make the membrane potential more negative
  2. Closure of voltage-gated L-type calcium channels
  3. NCX (sodium-calcium exchanger) to remove 1 calcium from the cell for 3 sodium
  4. Uses gradients to function which are maintained and established by Na/K ATPase (3 sodium out and 2 K in)
  5. SERCA pump on the SR uses ATP to pump the remaining calcium back into the SR (against concentration gradient)
  6. Reduction in calcium hides the myosin binding sites = relaxation
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43
Q

What is the SERCA?

A

A sarcoplasmic and endoplasmic reticulum calcium ATPase that allows for calcium to be re-accumulated into the SR.

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44
Q

What regulates the strength of muscle contraction (3 things)?

A
  1. Increase in the rate of AP firing
  2. Increase the number of motor units that you recruit
  3. Increase in the number of cross-bridge cycles
45
Q

What is tetanus?

A

A sustained muscle contraction when the motor nerve that innervates the skeletal muscle fires action potentials at a high rate (50 AP/s).

46
Q

How does the calcium concentration compare in a single twitch and a tetanus force?

A

Same peak in both forces; however, the calcium concentration is sustained much longer in a tetanus force.

47
Q

How does the action potential compare in a single twitch and a tetanus force?

A

Usual, quick action potential in a twitch force and the peak is the same in a tetanus force; however, there is a greater distance between the depolarization and repolarization phase, indicating the greater contraction.

48
Q

What is Henneman’s size principle theory of motor size recruitment?

A

Motor units will be recruited in order from smallest to largest depending upon the intensity (slow > fast IIa > fast IIx). The greater the amount of force required during movement means a greater number/size of motor units are recruited.

49
Q

What is a twitch?

A

A brief, weak contraction produced from a single action potential.

50
Q

What is a motor unit?

A

One motor neuron and the muscle fibers it innervates.

51
Q

What happens when a motor unit is stimulated?

A

All the fibres it’s connected to are stimulated to contract.

52
Q

Does a twitch cause a movement?

A

The stimulation of a single fiber via a single action potential isn’t strong enough to cause movement.

53
Q

When does tetanus occur?

A

If the muscle fiber is stimulated so rapidly that it doesn’t have a chance to relax between stimuli.

54
Q

Why are slow oxidative fibres red?

A

Due to the great number of myoglobin they contain.

55
Q

How much mitochondria do slow fibers contain?

A

A great amount.

56
Q

What do slow oxidative fibre depend on?

A

Oxygen

57
Q

How do slow oxidative fibres contract?

A

They contract slowly and are resistant to fatigue as long as oxygen is present (use ATP at a slow rate).

58
Q

What are slow oxidative fibres used in?

A

They are used in maintaining posture (by providing prolonged contraction) and for aerobic endurance-type activities such as running a marathon.

59
Q

How do fast oxidative fibres (type IIa) contract?

A

They contract quickly and use ATP at a fast rate.

60
Q

What do fast oxidative fibres (type IIa) depend on?

A

Oxygen

61
Q

What are fast oxidative fibres (type IIa) used for?

A

Walking

62
Q

Describe the myoglobin content of fast oxidative fibres (type IIa).

A

A great amount of myoglobin.

63
Q

Describe the myoglobin and mitochondria content of fast glycolytic fibres (type IIx).

A

Very little

64
Q

What do fast glycolytic fibres depend on (type IIx)?

A

Anaerobic pathways to make ATP, thus they don’t depend on oxygen.

65
Q

How do fast glycolytic fibres (type IIx) contract? Why?

A

They contract very rapidly because they contain more myofilaments and they use ATP at a fast rate.

66
Q

Explain the difference in fatigue-resistant between fast oxidative (type IIa) and fast glycolytic fibres (type IIx).

A

Fast oxidative fibres are somewhat fatiguer resistant whereas fast glycolytic fibres tire real easily.

67
Q

Do slow oxidative fibres tire easily?

A

No, they are fatigue-resistant.

68
Q

What are fast glycolytic fibres (type IIx) used in?

A

Intense, short duration movements like weight lifting, throwing a ball, sprinting, etc.

69
Q

How does the twitch relate to the three types of motor units?

A
  1. Slow oxidative = slow twitch
  2. Fast oxidative (type IIa) = fast twitch
  3. Fast glycolytic (type IIx) = fast twitch
70
Q

How does the force relate to the three types of motor units?

A
  1. Slow oxidative = low tension
  2. Fast oxidative (type IIa) = moderate force
  3. Fast glycolytic (type IIx) = high force
71
Q

How does the appearance of fast oxidative fibers differ from fast glycolytic ones?

A

Oxidative ones appear red due to high myoglobin content whereas glycolytic ones are white due to low content.

72
Q

How does the size relate to the three types of motor units?

A
  1. Slow oxidative = small
  2. Fast oxidative (type IIa) = medium
  3. Fast glycolytic (type IIx) = large
73
Q

How does the activation threshold relate to the three types of motor units?

A
  1. Slow oxidative = low
  2. Fast oxidative (type IIa) = moderate
  3. Fast glycolytic (type IIx) = high
74
Q

What do strength gains require?

A

Neural adaptations via plasticity.

75
Q

What are the types of changes that can occur in muscle fibers?

A
  1. Changes in their ATP synthesizing capacity
  2. Change in diameter
    (the two fast twitch muscle fiber types are interconvertible)
76
Q

What increases lead to strength gains?

A

An increase in motor unit recruitment during maximal contraction and an increase in frequency of neural discharge (rate coding).

77
Q

What type of recruitment results in strength gain?

A

Synchronous recruitment of multiple motor units, which leads to more forceful contraction = improves rate of force development = increase in capability to exert steady forces.

78
Q

What do golgi tendon organs do?

A

They monitor changes on muscle tension.

79
Q

What are normal intrinsic inhibitory mechanisms of muscle strength gain?

A
  1. Golgi tendon organs detect muscle tension
  2. Inhibition of muscle contraction if tendon tension is too high
  3. Prevent damage to bones and tendon
80
Q

What does training do to intrinsic inhibitory mechanisms? What does this do?

A

It reduces these inhibitory impulses allowing for the muscle to generate more force.

81
Q

How does the coactivation result in strength gain?

A

Usually, antagonists oppose the agonist force to lower the tension. There is reduced coactivation when training, thus maybe leading to strength gain.

82
Q

Where are golgi tendon organs located?

A

In the tendons of muscle.

83
Q

What does the golgi tendon organ consist of?

A

Endings of afferent fibers entwined within bundles of connective tissues fibers that make up the tendon.

84
Q

How does the golgi tendon work?

A

When extrafusal fibers contract, they pull on the tendon, tightening the connective tissue bundles; this stretches the golgi tendon organs receptor endings. The CNS uses this information to smooth out motor activity.

85
Q

What happens when the sarcomere is active/shortens (in terms of the golgi tendon organ)?

A

The reflex inhibits - in the spinal cord - the motor neurons to the extensor neurons. This activates the golgi tendon organs (inhibits) and stimulates the motor neurons to the flexor muscle.

86
Q

What is hypertrophy?

A

An increase in the mass or girth (diameter) of a muscle without an increase in cell number.

87
Q

Through what exercise does hypertrophy originate from?

A

Resistance exercise.
ex. weightlifting

88
Q

How does resistance exercise lead to hypertrophy?

A

The repetitive and exhaustive stimulation leads to the addition of contractile proteins to myofibrils and muscle enlargement as a whole.

89
Q

How is muscle protein synthesis stimulated?

A

Through exercise and feeding as insulin and branched amino acids like leucine, isoleucine, and valine can directly active protein synthesis.

90
Q

Explain the Akt/mTOR pathway with amino acids.

A
  1. Resistance exercise increases the amount of amino acids made
  2. Leucine is transported across the muscle cell membrane using an amino acid transporter in which glutamine is exchanged for it
  3. Leucine activates mTOR
  4. mTOR undergoes mRNA transcription
  5. Leads to the translation of skeletal muscle protein synthesis
91
Q

Explain the Akt/mTOR pathway with insulin.

A
  1. Insulin binds to a receptor on the muscle cell membrane
  2. It initiates a signaling cascade, beginning with Akt
  3. Akt activates mTOR
  4. mTOR undergoes mRNA transcription
  5. Leads to the translation of skeletal muscle protein synthesis
92
Q

What is the nuclear domain theory?

A

A cell nucleus can only control a limited portion of the cell space. Therefore, for a muscle fibre to grow, it would need to add additional nuclei to maintain the nuclear domain of each nucleus.

93
Q

What are satellite cells?

A

Myogenic stem cells responsible for muscle regeneration throughout lifespan.

94
Q

How does muscle memory relate to the nuclear domain theory?

A
  1. After first training, it results in the acquisition of new nuclei
  2. These nuclei are not lost during detraining (atrophy)
  3. Even though muscle mass is smaller, the nuclei as still there
  4. When re-trained, these nuclei are activated greatly to result in hypertrophy
95
Q

What is hyperplasia?

A

The addition of new muscle fibers that contributes very little to the increase in muscle mass.

96
Q

What can extreme hyperplasia result in?

A

Extreme growth stimuli can increase fibre number.

97
Q

What are muscle fiber properties that change during endurance exercise (running)?

A
  1. Increase in size (hypertrophy) of type I fibers
  2. Changes to percentage of fiber type may occur - but minor
98
Q

What happens to the capillary supply during endurance training?

A

There is an increase in the number of capillaries supplying each fiber (angiogenesis).

99
Q

What happens to the myoglobin content during endurance training?

A

Myoglobin content increases by 75-80% = greater oxidative capacity = better adapted to prolonged activity

100
Q

What happens to mitochondria during endurance training?

A

There is an increase in mitochondrial numbers (biogenesis) and in the mitochondrial oxidative enzyme capacity. There is also an increase in fat oxidation in the mitochondria (breaking fats down to be used for a source of energy = better metabolism).

101
Q

What tissues make up muscle?

A
  1. Muscle tissue (fibers)
  2. Connective tissue (epimysium, perimysium, and endomysium)
  3. Nerve tissue
  4. Vascular tissue
102
Q

How is the recruitment of muscle fibres additive?

A

If you start sprinting, your type IIa fibres are recruited. The slow twitch ones aren’t turned off and are still being used, but not to the rate they were before (not needed for this activity).

103
Q

What in the initial gain in muscle strength due to?

A

Neural adaptations

104
Q

How do neural adaptations relate to unilateral resistance exercise?

A

When just training one leg, it increased in strength; however, the other leg, had a slight increase as well. This showed that even if you don’t train both sides you can still get a neural adaptation in both limbs.

105
Q

Explain exercise in the Akt/mTOR pathway.

A
  1. Resistance exercise increases the level of phosphatidic acid within a muscle cell
  2. This activates the phosphorylation of mTOR
  3. mTOR undergoes mRNA transcription
  4. Leads to the translation of skeletal muscle protein synthesis
106
Q

How can muscle cells repair themselves?

A

By activation of skeletal muscle stem cells, also known as satellite cells.

107
Q

How do satellite cells aid in muscle mass increase?

A

They donate nuclei to maintain the nuclear domain of new muscle fibres.

108
Q

What amino acids help to increase muscle mass?

A

Essential amino acids like leucine and isoleucine.

109
Q
A

Exercise Physiology and Pharmacology (9 decks)

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