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Musculoskeletal > Muscle Structure and Adaptation > Flashcards

Muscle Structure and Adaptation Flashcards

1
Q

What are the origins of skeletal muscle?

A
  • Muscle forms from the somites (paraxial mesoderm)
  • Sclerotome (bone, ribs, cartilage)
  • Myotome (muscle precursors)
  • Dermomyotome (myotome and dorsal dermis)
  • Syndetome (tendons)
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2
Q

Describe the embryogenesis of muscle

A

The muscle is formed from blocks of paraxial mesoderm. It occurs in pairs of these blocks called somites. Paracrine signalling from the notochord triggers the mesenchymal to epithelial transition. The somite forms and there is a hollow form of epithelial cells and due to paracrine signals (hedgehog signalling etc) from the neural tube. The notochord causes the epithelial to mesochymal transition. It forms four groups of cells which form specific tissue types. The sclerotome, the myotome, the dermomyotome and the syndetome. The sclerotome, myotome and syndetome interact with each other to cause movement. The dermomoytome is on the outside.

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3
Q

What are the paracrine factors that induce myogenic commitment to myoblasts?

A

Myf5 and MyoD

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4
Q

What is myogenesis?

A

The muscle cells start off as mesodermal cells, and then the paracrine factors such as hedgehog signalling and FDF signalling tell the cells to start producing regulatory factors such as Myf5 and MyoD. When these are expressed, the cells become committed to a myogenic fate and are known as Myoblasts. The myoblasts differentiate and increase in number and then exit the cell cycle marked by the expression of myogenin. This causes terminal differentiation of the muscle fibres. They start forming tubes and express structural proteins.

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5
Q

What is the biphasic muscle development?

A

Primary and Secondary fibres. Primary round - makes the architecture for other muscle fibres to form.
Secondary round - make up the bulk of the muscle fibres

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6
Q

What are the satellite cells?

A

Cells that cause regeneration and postnatal growth - muscle stem cells.

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7
Q

Where are the muscle stem cells originate?

A

They sit on the muscle fibres (dormat) until they are activated in the case of muscle regeneration and start forming myotubes.

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8
Q

Why is skeletal muscle multi-nucleated?

A

It doesn’t start off as one cell but more as multiple cells which fuse together. This is why they have multiple nuclei.

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9
Q

What is the embryonic fibre number?

A

Fibre number is generally set at birth and is genetically determined.

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10
Q

What can affect fibre number?

A
  • Temperature
  • Hormones
  • Nutrition
  • Innervation
    These can have an effect on myogenic regulatory factors (MRF) in expression duration.
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11
Q

What is the effect of hyperplasia on muscle?

A

It can increase the fibre number.

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12
Q

What is the effect of hypertrophy on muscle?

A

It increases muscle mass

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13
Q

What is postnatal muscle growth?

A

After birth, an increase in muscle mass is due to increase in fibre size (muscle cell size) - hypertrophy.

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14
Q

What are muscle stem cells (MuSCs) called?

A

Satellite cells

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15
Q

What are the properties of satellite cells?

A

These are undifferentiated muscle precursors which are self-renewing.

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16
Q

How is more structural protein produced after birth?

A

The muscle requires more protein and the stem cells start to divide and fuse to the myofibre which produce more structural proteins.

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17
Q

What happens to the satellite cells?

A

They proliferate and incorporated into muscle fibres. These return to quiescence when they are not needed.

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18
Q

Why does the muscle fibre maintain a cytoplasm:nuclei ratio?

A

The reason for this may be because the muscle requires a lot of structural proteins and mitochondria. Nuclei is needed along the cell to produce the proteins required for the muscle fibre to function.

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19
Q

What is hyperplasia after birth?

A

After birth, increase in muscle mass due to increase in cell/fibre number (hyperplasia).

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20
Q

What happens to muscle during exercise?

A

The majority of the time through exercise muscle is increased through hypertrophy not hyperplasia.

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21
Q

What experiments have provided support for hyperplasia?

A
  • Avian stretch model (weight on the wings of the bird, due to constant extra weight, they would increase muscle mass).
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22
Q

What are the proposed mechanisms for hyperplasia occuring?

A

Fibre splitting - the muscle itself splits and then hypertrophy occurs to increase muscle mass.
Proliferation of Satellite Cells - form their own muscle fibres

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23
Q

What are the issues of these mechanisms in humans?

A

Evidence that this occurs in humans is lacking. Removing the muscle from humans to count the muscle fibre however, there may be errors and ethically isn’t seen as accurate.

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24
Q

What are the diversifications of fibre?

A

All vertebrate sarcomere structure is the same. Molecular variability depending on function due to:

  • Multiple isoforms of myofibrillar proteins
  • Titin isoforms
  • Troponin and Tropomyosin isoforms
  • Myosin isoforms
25
Q

What is the purpose of the different isoforms?

A

Titin - elastic properties
Troponin and Tropomyosin Isoforms - determine sensitivity to calcium
Myosin isoforms - different chemo mechanical transduction, ATP hydrolysis, shortening velocity which can lead to the resistance to fatigue

26
Q

What are Type 1 fibres?

A

Slow twitch muscle fibres

  • Virtually inexhaustible
  • This is because they have a high number of mitochondria - aerobic respiration.
  • Oxidation phosphorylation takes place
  • Extensive blood supply and abundant myoglobin
27
Q

What are the two types of Type 2 fibres?

A

Type 2a and 2b

28
Q

What is a type 2a muscle fibre?

A

Fast twitch oxidation fibres

  • Generate more force than slow twitch muscles and are more prone to fatigue.
  • Source of energy and fuel from the Creatine phosphate system and glycogen
  • Recover quicker than type 2b
  • used for long term anaerobic exercise
29
Q

What is a type 2b muscle fibre?

A

Fast twitch glycolytic fibres or white fibres due to colour

  • Do not use oxygen so have a higher fatigue rate and do not recover quickly
  • Use the creatine phosphate system and glycogen but not from sources such as oxygen
  • Contract quickly and generate lots of force
  • Used for short term anaerobic exercises
30
Q

Describe the split between fibre types due to the affect of training

A
  • Untrained individuals 50:50 ratio of fast (IIA and IIX) to slow (I) twitch fibres
  • Long and middle distant runners: 60-70% slow
  • Sprinters: 80% fast twitch
  • Sports requiring greatest aerobic and endurance capacities: slow muscle up to 90-95%
  • Sports with greater anaerobic capacities (strength and power) have fast muscle from 60-80%
31
Q

What determines the fibre types in individuals?

A

It is mainly genetic - for example Olympic athletes will have this tendency depending on the sport they do.

32
Q

Marathon Runner

A
  • Muscles small but fatigue resistant
  • Muscle dense and strong for their size -> high oxidative capacity of muscles
  • Work over very long periods of time
  • Not explosive Strength
33
Q

Strength trainer

A
  • Muscles adapted for explosive release of force
  • Rapid powerful contractions
  • Easily fatigued at maximum effort
  • Low oxidative capacity via mitochondria
  • High force per cross-sectional area of muscle
34
Q

Powerlifter

A
  • Muscles adapted for immense strength
  • Muscles are hypertrophied
  • High glycolytic
  • Fatigue easily
  • High muscle to total body mass ratio
  • Muscle size beginning to interfere with locomotion
35
Q

Describe the myosin gene clusters

A

Myosin sits on the chromosome in a cluster of myosin genes that allows for the different isoforms which gives the different properties to the muscle fibres.

36
Q

What are the three main types of myosin?

A

2a, 2x and 1

37
Q

MHCemb

A

Embryonic myosin

38
Q

MHCIIa

A

MHC2a

39
Q

MHCIIX/d

A

MHC2x/d

40
Q

MHCIIb

A

MHC2B

41
Q

MHCperi

A

Perinatal myosin

42
Q

MHCexoc

A

extracocular

43
Q

What are the different MHC isoform able to do?

A

They are able to split ATP at different rates in the order: fastest 2B > 2A > 2X > 1 > emb slowest

44
Q

What are the gender differences in muscle?

A

There are >3000 genes different between female and male skeletal muscle.
There is differences in myosin isoforms:
- Type 1 - more in females than males
- Type IIA - more in males than females
In males, there is larger fibre cross sectional areas (CSA), this means that there muscle is more easily hypertrophied than in women. This is due to the endocrine differences.

45
Q

Function of testosterone

A

Required for the development of the male reproductive system
Promotes secondary sexual characteristics: muscle and bone mass, body hair, deep voice.

46
Q

What is the affect of testosterone in muscle formation?

A

Promotes the commitment of mesenchymal pluripotent cells into myogenic lineage and inhibits adipogenesis (androgen receptor mediated pathway)

47
Q

What type of molecule is testosterone?

A

It is a natural anabolic-androgenic steroid (AAS)

48
Q

What does testosterone stimulate?

A

It stimulates satellite cell replication, muscle protein synthesis and fibre hypertrophy.

49
Q

What are the affects of synthetic anabolic steroids?

A

It can cause irreversible adverse effects from taking anabolic steroids:

  • High blood pressure
  • Cardiac and respiratory problems
  • Liver disease
50
Q

Explain muscle repair

A
  • When muscle is damaged, it has a regenerative property in the majority of cases if it isn’t too severe - this will be fibrosis and scar tissue. - In a normal tear, necrosis occurs - blood will fill the wound area - haematoma. - The division of the satellite cells which use the haematoma to build upon and fuse together.
  • There is an increase in the expression of Myf5 and MyoD.
  • There is also differentiation of myogenin and the formation of the sarcomeres and the muscle fibres will self-renew.
51
Q

What are the phases of regeneration?

A
  1. Degeneration/inflammation phase
  2. Regeneration Phase
  3. Remodellling phase
52
Q

What happens through the degeneration/inflammation phase?

A

First few days

- Myofibres rupture and necrosis, formation of haematoma, inflammatory response

53
Q

What happens through the regeneration phase?

A

4-5 days post-injury

- Phagocytosis of damaged tissue, SC activation and proliferation

54
Q

What happens through the remodelling phase?

A

2/3 weeks
- Maturation of regenerated myofibres, restoration of blood supply and innervation, recovery of muscle functional capacity and also fibrosis and scar tissue formation

55
Q

What is sarcopenia?

A

Age related loss of muscle mass

56
Q

What is the percentage of muscle mass loss after the age of 30?

A

3-8% decrease per decade and higher after 60

57
Q

What is the impact of muscle loss on the elderly?

A

Falls, injury and disability

58
Q

What is the loss of muscle mass associated with?

A

Gain in fat mass

Associated with decreased satellite cell number and recruitment

59
Q

What are the biochemical and metabolic changes as a result of muscle mass?

A
  • Mitochondrial mutations
  • Reduced oxidative and glycolytic enzyme activity
  • Reduced endocrine function and reduced physical activity

Musculoskeletal (4 decks)

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