Biological Basis of Muscle Hypertrophy Flashcards

1
Q

Principle of Myoplasticity

What does Myoplasticity refer to

A
  • When gene expression is altered in the cell, it results in an increase or decrease in the amount of specific proteins.
  • This capacity for adaptive change we define as plasticity
  • Myoplasticity therefore refers to the specific ability of the muscle cell to undergo adaptive change
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2
Q

Principle of Myoplasticity

A
  • Approximately 20% of skeletal muscle is composed of proteins (balance being water, salts, other organic molecules)
  • All types of protein can be regulated by alteration in gene expression
    • Within connective tissue
    • Within plasma membranes
    • Within sarcoplasmic reticulum
    • Within myofibrils
  • Myoplasticity is therefore predicated on the ability of genetic machine to change either the quantity (Amount) or variant of protein it expresses for a desired outcome
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3
Q

Principle of Myoplasticity
- Old vs Young
- RT

A

Old vs Young
- In the younger individuals, we can see a larger distribution of the fast twitch muscle fibres than in the old individuals
- When we are older we see a preferential loss in type II muscle fibres

RT
- RT elicits hypertrophy of all fibre types
- Type IIx proportion decreases, IIa increases
- This may be because type IIx requires a lot of energy for less work which may be inefficient

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4
Q

Only size and quality/variant change?
- hyperplasia

A
  • Hyperplasia = increase in number of muscle cells
  • Some evidence of hyperplasia in animal models (cats and birds) , however, little evidence of hyperplasia in humans from training.
  • Principle mechanism for muscular hypertrophy in adult mammals is cellular hypertrophy and not hyperplasia
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5
Q

Principle of Myoplasticity
- Synthesis vs degradation

A

Relates to protein turnover
- Every protein in a cell is transcribed (DNA to mRNA) Translated (mRNA to protein) And degraded (protein to amino acids)

Every protein has a half-life for its existence
The level of any protein in a muscle is proportional to the rate of synthesis relative to the rate of degradation
- Synthesis/degradation ratio

The goal for hypertrophy
- For synthesis to exceed degradation and lead to protein accretion within the muscle over time

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6
Q

Principle of Myoplasticity
HINT: skeletal muscle adaptations are…

A

That skeletal muscle adaptations are characterized by modifications of morphological, biochemical, and molecular variables that alter the attributes of fibres in specific motor units (functionally similar groupings of muscle fibres)

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7
Q

Protein synthesis pathway - important

Possible pathways for increase in protein synthesis

HINT: phosphorylation $ protein kinase

A
  • Phosphorylation, allows coupling and addition of a phosphoryl group (e.g. to a lipid, protein, carbohydrate)
  • Protein Kinase, an enzyme that modifies other proteins via phosphorylation

Possible pathways for increase in protein synthesis
- Resistance training can stimulate the increase in mTOR which leads to increase in protein synthesis
- Dietary Intake also stimulates mTOR which leads to protein synthesis

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8
Q

Protein synthesis pathway - is it valid?
HINT: Data shows a relationship…

A

Data shows a relationship between p70 and resistance training with
With an increase in p70, there is an increase in the % change in 1RM squat strength, % change in whole body FFM, % change I FFM(kg), % change in type IIA fCSA

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9
Q

Acute stimuli facilitating protein synthesis
HINT: myostatin

A
  • Genetic factors
  • Myostatin = is a negative regulator of myoblast proliferation and differentiation e.g. regulates hypertrophy.
  • Myostatin deficiency or knockout can lead to increase muscle mass via not negatively regulating protein synthesis
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10
Q

What stimuli facilitates protein synthesis

A

Muscular tension
- Muscle damage
- Metabolic factors
- Hormones

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11
Q

Muscle Damage
- Exercise induced muscle damage (EIMD)
- Z discs
- EIMD - potential mechanisms of action

A

Very severe z disc streaming related to high levels of muscle damage. Shows broken points within the stream

Potential mechanisms of action
- Signalling via inflammatory cells
* InterLeukin-15
* fibroblast growth factor (FGF)
- Satellite Cell activity
* SC proliferate and adhere to damaged fibres
* Theorised that neurons innervating damaged fibres may also contribute to SC activity as there is a high pop of SC under the myoneural junction
- Insulin-Like Growth Factor - 1 Signalling
- Cell swelling

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12
Q

Muscle Damage
- EIMD
- Sarcoplasmic hypertrophy vs Myofibrillar hypertrophy

A

Sarcoplasmic hypertrophy: during first 4 weeks of training, no actual actin and myosin filaments laid down, it’s just swelling and contains enzymes

Myofibrillar hypertrophy: start to see a perceivable amount of actual myofibrillar hypertrophy at around 8 weeks of training. The edema-induced muscle swelling decreases within the cell.

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13
Q

Muscle Damage
- EIMD
- RT
HINT: the first couple of …

A
  • The first couple of sessions of resistance training, we see the most amount of z disc streaming or muscle damage.
  • We only see a high amount of myofibrillar hypertrophy when the muscle damage is low
  • In the first couple of sessions at the gym, the activity in the muscle including from the satellite cells is actually just repairing the muscle, not trying to make it bigger. Around 2-3 weeks, repair of the muscle decreases and muscle growth increases

In the initial training protocol, the z disc streaming is high while the increase in muscle fibre cross-sectional area is low. It is only when there is no z disc streaming that the muscle cross-sectional area is at its highest.

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14
Q

Metabolic Factors
- Metabolic influence?
- Hypoxic training inclusion…

A

Support:
- Hypoxic training inclusion reduces muscle mass loss post surgery 7 vs 15 % 14 days post
- Improvement in hypotrophy outcomes relative heavy load with intermittent hypoxic
- Therefore, potential metabolites may induce / contribute to hypertrophy pathway

Arguments against:
- Reduce energy clearance or intake capacity invokes fatigue in muscles which consequently requires additional fibers to sustain force output. So the mechanism is still load/tension related
* Can be beneficial for individuals who are injured or are recovering from an injury and want to increase muscle mass quickly without lifting heavy loads

However, recent work found that the addition of blood flow restriction training to a traditional resistance training program preferentially enhanced type 1 fiber cross sectional area in a cohort of elite powerlifters.

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15
Q

Metabolic influence - possible mechanisms

A

Metabolic stress is a vague concept given that 2,700 metabolic enzymes catalyze 900 metabolic reactions (129) and that 4,000 metabolites can be detected in human serum alone (123)
However possible candidates
- Lactate
- α ketoglutarate
- phosphatidic acid
- skeletal muscle protein breakdown

Effects may be acute in nature as chronic energy stress regulators (AMPK) exist in the cell that would likely counteract some of the proposed mechanisms of above named metabolites.

AMPK can block mTOR from phosphorylating. mTor is important for p70

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16
Q

Hormones
- Acute Hormones

A
  • Researcher wanted to know the acute hormonal adaptations to different training volumes and intensities.
  • Increases in cortisol, IGF-1, GH & Testosterone
  • Concluded that acute hormones did not seem to be the driver of hypertrophy.
  • Strongest correlation between hypertrophy and an increase is cortisol. The individuals who had an increase in cortisol showed a correlation to a greater increase in hypertrophy.
17
Q

Hormones
- IGF-1
- AR or Il-6

A

IGF - 1
- MKR - knock out receptor (doesn’t have a receptor for IGF-1)
- The normal mice and the MKR mice showed no difference in phosphorylation

AR or IL-6
- AR (androgen is important for testosterone to make it to the nucleus)
- Moderate correlation between AR protein fold and the muscle fibre cross sectional area
- Interleukin (IL-6: inflammatory maker) smaller correlation to muscle fibre cross sectional area

18
Q

How does the cell infer tension

A

Membrane mechanisms (sarcolemma)
- Phosphatidic acid (PA)
Tensor sensors
- Costameres (connect the Zdisk to the extracellular matrix)
Focal adhesion kinanse (FAK)

Acute hormonal response requires muscle tension. Metabolic factors require muscle movement. Muscle damage is inferred from muscle tension.