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Limbs and Back > Skeletal Muscle - Contraction and Training > Flashcards

Skeletal Muscle - Contraction and Training Flashcards

1
Q

What stimulates contraction in skeletal muscle?

A

Somatic motor neuron.

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2
Q

What is a motor unit?

A

One nerve fibre and the muscle fibres it innervates.

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3
Q

What is the connection between the muscle and the nerve called?

A

A neuro-muscular junction (NMJ); the gap in-between is the synaptic cleft.

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4
Q

What is contained within the axon terminal of the motor neuron and why?

A

There are many vesicles of acetyl choline (ACh) neurotransmitters to allow the action potential to pass on to the sarcolemma.
*Electrical impulses cannot cross the synaptic cleft hence the need for chemical signals in the form of neurotransmitters.

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5
Q

Where are T-tubules found and what surrounding structures are there? What is it’s function?

A

T-tubules run around myofibrils and are themselves surrounded by sarcoplasmic reticulum (SR). It connects with the outer membrane and contains calcium ion channels (gated).

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6
Q

Where are Ca ions stored before contraction?

A

In the terminal cisternae which are part of the sarcoplasmic reticulum.

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7
Q

What is required by thin filaments to initiate contraction?

A

Calcium ions.

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8
Q

Describe contraction (general)?

A

The movement of thick and thin filaments of the sarcomere relative to each other, to cause active shortening of a muscle fibre.

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9
Q

Describe the sequence of events at the pre-synaptic neuro-muscular junction.

A
  1. Action potential is propagated along the somatic motor neuron to the presynaptic axon terminal.
  2. This causes the opening of voltage-gated calcium channels - causing in influx of Ca from the extracellular fluid.
  3. Increased concentration of Ca causes vesicles containing ACh to fuse with the presynaptic membrane, releasing ACh into the synaptic cleft (exocytosis).
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10
Q

Describe the sequence of events at the post-synaptic neuro-muscular junction.

A
  1. ACh binds to receptors on the post-synaptic membrane (sarcolemma), opening ligand-gated channels on the membrane surface.
  2. Na ions (abundant in extracellular fluid) then flow through these channels into the sarcolemma (where there are high concentrations of K ions), causing the membrane to become more positive.
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11
Q

Describe the sequence of events after the neuro-muscular junction.

A
  1. Sodium ions flow through the ligand-gated channels on the sarcolemma, causing the membrane to become more positive; eliciting a muscular action potential.
  2. The action potential travels along the sarcolemma and propagates down the T-tubules causing calcium channels to open. *Mediated by ryanodine receptors on SR surface.
  3. These channels open due to a change in voltage.
  4. Calcium then moves from the terminal cisternae into the T-tubules and to the thin filaments.
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12
Q

What is the thick filament of the sarcomere?

A

Myosin (which has two heads);

  • One to bind to ATP
  • One to bind to actin sub-units on the thin filament.
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13
Q

What is the thin filament of the sarcomere?

A

Actin with two regulatory proteins;
Troponin - binds to Calcium
Tropomyosin - blocks myosin binding sites on actin.

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14
Q

Describe the Sliding Filament Theory.

A
  • Calcium binds to Ca binding sites on the TnC sun-unit on troponin.
  • This causes a conformational change in shape of troponin and as it is attached to tropomyosin, pulls the tropomyosin with it; uncovering the myosin binding sites.
  • ATP simultaneously binds to tropomyosin causing hydrolysis of ATP and thus a conformational change in shape of myosin, moving it closer to the actin sub-unit. ADP remains attached.
  • Myosin now binds to actin forming cross bridges enabling it to pull the thin filaments closer to the midline (centre of the sarcomere). This causes the release of ADP.
  • This move towards the midline allows actin to generate tension and contraction in muscle.
  • Actin towards M-line and myosin towards Z-line.
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15
Q

What happens when no more stimuli is received by muscle fibres?

A
  • Calcium release channels close
  • Intracellular Ca levels return to normal
  • Contraction stops
    Calcium restored to reservoirs in the SR by active transport pumps moving Calcium back into the terminal cisternae for storage.
  • New ATP binds to myosin when ADP is released, causing myosin to detach to the actin and is ready for ATP hydrolysis again.
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16
Q

How much ATP is stored in muscles before contraction?

A

Not much - only enough to sustain a few twitches.

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17
Q

How is contractile activity sustained?

A

Metabolism must produce ATP molecules as quickly as they are broken down during contractile activity.

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18
Q

What are the ways to regenerate ATP for contraction?

A

There are 3 ways:

  1. Phosphorylation of ATP by creatine phosphate
  2. Phosphorylation of ATP by oxidative phosphorylation in mitochondria
  3. Phosphorylation of ATP by glycolytic pathways in the cytosol
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19
Q

Describe Creatine Phosphate.

A
  • High energy molecule in high concentrations in sarcoplasm.
  • Used when muscle demand for energy > available ATO supply
  • Creatine phosphate and ADP couple up in the presence of creatine kinase producing ATP (reversible reaction)
    ADP + CT > C + ATP
  • The energy released when the chemical bond is broken between creatine and phosphate is similar to that of ATP breakdown.
    Yield - 1 ATP per CT molecule
  • Used for short bursts of vigorous exercise (15 seconds of muscle contraction)
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20
Q

What are the benefits and limitations to ATP regeneration by creatine phosphate?

A
  • Rapid formation however limited to the amount of creatine phosphate available
  • Use of CP at the start of contraction provides time for the slower processes to increase their rates of ATP formation to match the rate ATP breakdown.
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21
Q

Describe Oxidative Phosphorylation.

A
  • Moderate levels of activity will mostly have ATP regenerated using this method.
  • First 5-10mins; breakdown of muscle glycogen into glucose to provide ATP
  • Next 30mins; blood-bone glycogen and fatty acids breakdown is more dominant
  • After this; mostly fatty acid breakdown.
  • Conversion of glucose into ATP is slower but more complete.
  • Aerobic
    Yield - 36 ATP / glucose
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22
Q

Describe glycolysis.

A
  • Produces small ATP quantities but produces them rapidly when enough enzymes and substrates are available.
  • Anaerobic
    Glucose obtained from;
    1. Blood
    2. Stores of glycogen with contracting muscle fibres
  • Side production of pyruvate acid which converts into lactic acid.
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23
Q

What is a major determinant for the fibre Type composition of an individual?

A

Genetics.

This will determine was type of training/activity is best for you.

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24
Q

What Type of fibres are associated with a high force output?

A

Type II.

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25
Q

Loss of fat - strength or endurance training?

A

Both.

26
Q

What happens with training?

A

Proliferation (hypertrophy) of a particular fibre type instead of an actual change in fibre type.

27
Q

How is strength training carried out?

A
  • Small number of repetitions using large force contractions
  • 10-20 contractions repeated 2/3 times, twice a week so short total time
  • Risk of injury is high so essential to warm-up/stretch
28
Q

What fibres are used for strength training?

A

Type IIB

  • High loads // quick fatigue
  • Type IIA & IIB will enlarge
29
Q

Name and describe the early stages of strength training.

A

Neural Response

  • Rapid muscle gain
  • First 4-6 weeks
  • Improved activation of motor units and improves tolerance to muscle pain
  • Higher maximal firing rates
30
Q

Name and describe the intermediate stages of strength training.

A

Hypertrophy

  • Larger motor units grow
  • Significant hormonal changes; more growth factors secreted e.g. Insulin-like Growth Factors (IGFs), testosterone, insulin levels all elevated
  • Improvement of connective tissue
31
Q

Is hypertrophy in strength training a fast or slow process and why?

A

Slow
- Starts with development of new contractile filaments added laterally to existing myofibrils.
- Then fibril splits; enlarged fibrils divide longitudinally so fibrils become more numerous
NOT hyperplasia

32
Q

What happens after hypertrophy in strength training? What might be an inclination for athletes?

A

After 5-6 months; plateau in progress.

  • Steroids can increase muscle mass (E.g. testosterone) but could thin out connective tissue (different growth factors needed to strength tendons)
  • Thus the individual is at risk of muscle and tendon tears
  • If athlete gets a tear; sign they could be on steroids
33
Q

How is endurance training carried out?

A

Large number of low force contractions e.g. 3km run is 3000 low force contractions
- Aerobic respiration

34
Q

What happens to muscle mass in endurance training?

A

It is reduced.

35
Q

What Type of fibres are developed in endurance training?

A

Type 1 (Slow Twitch).

36
Q

What are the benefits of endurance training?

A
  • Improved cardiovascular performance (more 02)
  • Better cardiac output
  • Better regional blood flow
  • Expansion in blood flow
  • More oxygen improves metabolic performance so enzyme concentrations increase; improving mitochondrial density and existing mitochondria get bigger
37
Q

How are motor units controlled? (Precise/Fine and more general)

A

Fine control motor units consists of one motor neuron innervating only a few muscle fibres.
Less fine control is when a motor neuron innervates many muscle fibres.

38
Q

What is motor unit recruitment?

A

The number of motor units activated during a contraction.

39
Q

In terms of motor unit recruitment, what is the type of overall movement dependant on?

A

The overall movement is dependant on the recruitment of;
- different sizes of motor units
- different strengths of motor units
- number of motor units activated
Bigger motor unit recruitment; stronger contraction
Heavy object being lifted; more units required

40
Q

How are motor units used efficiently within muscle?

A

Motor units are used by active muscle to;

  • Conserve energy
  • Prevent muscle fatigue and
  • Ensure tension is sustained for as long as possible
41
Q

Definition of fatigue.

A

Inability to maintain power output, reversal by rest.

* Fatigue is not an injury.

42
Q

What are reduced as an effect of fatigue?

A
  • Power, force and most sensitive; velocity.
    Power = Force x Velocity
  • Shortening velocity and relaxation rate also reduced.
  • Recovery time dependant on nature of fatigue
43
Q

What happens to the tension of muscle fibres after continual stimulation?

A
  • When muscle fibres are continually stimulated, tension developed eventually decreases even though the stimulus remains.
  • Decline in tension due to previous contractile activity.
44
Q

What is recovery time of muscle fatigue dependant on?

A
  • Amount of rest after exercise

- Duration and intensity of training

45
Q

What is central fatigue?

A
  • Within the nervous system
  • Loss of excitability of the motor cortex (fails to send excitatory signals to motor neurons)
  • Stops someone exercising even if muscles themselves are fatigued
    I.e. the mental ability to initiate central commands to muscle during a period of increasingly distressful sensations
  • Also includes failure of transmission in peripheral nerve and NMJ
46
Q

In what type of people does central fatigue occur?

A
  • Occupational workers

- Boredom

47
Q

Give an overview of peripheral fatigue?

A
  • Muscle fatigue
  • Failure of E-C coupling, failure of T-tuuke AP, failure of SR activation causing less Ca ions to be released (reducing force)
  • Failure of force generation at cross-bridges
  • Failure of ATP generation due to energy stores depleting
48
Q

E-C coupling failure usually occurs in what type of training?

A

Short, high intensity exercises.

49
Q

Explain what occurs in the failure of Excitation-Contraction Coupling leading to fatigue.

A
  • High AP firing rates (for big contractions) triggers release of K+ leading to an extracellular accumulation of K+ in muscle
  • This accumulation in T-tubules makes them unexcitable as AP cannot pass through them to the terminal cisternae for triggering calcium release
  • As T-tubule population fails, less sarcomeres are involved in contraction
  • Rapid recovery
50
Q

What ions cause muscle fatigue?

A

Muscle fatigue is NOT due to reduced levels of ATP.
- If so; the muscle would be rigid, not fatigued
Actually due to increased concentrations of;
ADP, Pi (inorganic phosphate) and H+ (incomplete Krebs cycle will leak out lactic acid)
These impair calcium fluxes and force delivery at cross bridges.

51
Q

How do these ions cause muscle fatigue?

A

Metabolic increases of ADP, Pi and H+ cause:

  • Any accumulation will inhibit/slow down ATPase function (to break down ATP into ADP and a free phosphate)
  • Calcium handling will be inefficient: decreases rate of uptake, release and storage in the SR
  • Decreases sensitivity of thin filament proteins to activation by Calcium

Thus directly or indirectly inhibiting binding and power stroke of actin-myosin cross bridges.

52
Q

Describe muscle physiology in short duration, high power activity.

A
  • Contractions last a few seconds
  • Muscles don’t run out of glucose as ATP generated via creatine phosphate breakdown
  • Creatine phosphate supplements can e used to generate more ATP
  • Contstriction of blood vessels
53
Q

Describe muscle physiology in low intensity, long duration activities.

A
  • Changes in regulation of ryanodine receptor channels
  • Channels become leaky: Ca levels elevated activating proteases which degrade contractile proteins
    Result: soreness and weakness until new proteins are synthesised to replace damaged proteins.
54
Q

What else contributes to muscle fatigue?

A
  • Low muscle glycogen & blood glucose levels along with dehydration contribute to fatigue.
55
Q

Describe muscle physiology in moderate duration, low power activities.

A

After 1-3 hours; low glycogen levels, reducing mitochondrial function.

56
Q

What can marathon runners be given for energy?

A

4-5hr marathon runners can be given glucose gels while racing as their glycogen levels will be significantly reduced
- 2hr marathon runners don’t need them as glycogen levels won’t have fallen much.

57
Q

Describe muscle physiology in long duration activities.

A
  • Use fats: dense store of ATP
  • Lipids come from adipose and intramuscular stores
  • Humans preferentially metabolise carbohydrates first
  • Very long durations: utilise mostly lipids
58
Q

What is recommended for refuelling energy stores?

A
  • Don’t fully deplete glycogen stores
  • Eat during breaks followed by low intensity (e.g. cycle slower for a bit), allowing gut to absorb nutrients
  • Eat after training for rapid recovery: gut working at maximum
  • After 48hrs: metabolic stores are back to normal
59
Q

What motor units are used during long duration activity?

A
  • Type I (slow fatiguing)
  • Aerobic
  • Good at carbohydrate and lipid metabolism
60
Q

What motor units are used during moderate duration activity?

A
  • Combination of Type I and Type II

- Aerobic

61
Q

What motor units are used during short duration activity?

A
  • All units

- Aerobic and Anaerobic

Limbs and Back (6 decks)

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