Muscle Structure + Adaptation Flashcards

1
Q

What are the origins of skeletal muscle?

Where does muscle form from?

A

Muscle forms from somites (paraxial mesoderm)

Paracrine signalling from notochord and neural tube triggers mesenchymal epithelial transition

The somite forms resulting in a hollow ball of epithelial cells, further paracrine signalling allows formation of four different groups of cells

  • 1) Sclerotome (bone, ribs and cartilage)
  • 2) Myotome (muscle precursors)
  • 3) Dermomyotome (myotome and dorsal dermis)
  • 4) Syndetome (tendons)
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2
Q

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

A

Myf5 and MyoD

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3
Q

Briefly summarise myogenesis

A
  • Muscle cells start as mesodermal cells
  • Paracrine factors induce Myf5 and MyoD
  • Expression of paracrine factors cause them to become commited to a myogenic fate = MYOBLAST
  • MYOBLAST differentiate, increase in number and exit cell cycle
  • Structural proteins expressed and myotubes form
  • Myotubes align + fuse to form a muscle fibre
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4
Q

What is biphasic muscle development?

A

initial primary round of muscle differentiation which then allows other secondary muscle fibres to form from that

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5
Q

Satellite cells

A

Muscle stem cells

  • Sit dormant on muscle fibres until they are activated allowing regeneration and postnatal growth
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6
Q

What is the embryonic fibre number?

A

Fibre number generally set at birth

  • genetically determined
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7
Q

How can the embryonic fibre number be affected?

A
  • Temperature
  • Hormones
  • Nutrition
  • Innervation

These have an effect on myogenic regulatory factors (MRF) in expression duration

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8
Q

What is hypertrophy?

A

Increase in fibre size

  • Muscle stem cells (MuSCs) called satellite cells. Undifferentiated muscle precursors, self-renewing
  • MuSCs proliferate and incorporated into muscle fibres. Return to quiescence when not needed
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9
Q

Why is it important to maintain the cytoplasm to nuclei ratio?

A

Muscle fibres are multinucleated

Nuclei along cell are required to produce proteins required for the muscle to function, (the muscle fibre requires many mitochondria and structural proteins along the length of the muscle cell)

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10
Q

What is hyperplasia?

A

Increase in cell/fibre number after birth

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11
Q

In what way is muscle mass increase during exercise?

Hyperplasia or hypertrophy?

A

Muscle mass is increased through hypertrophy and not hyperplasia - however instances where muscle fibre number is increased through hyperplasia

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12
Q

What supports the theory for hyperplasia?

A

AVIAN STRETCH MODEL

  • Weight on wings
  • Development of muscle on their backs
  • Count number of muscle fibres in quail
  • Increase in fibre number

CAT WEIGHT LIFTING MODEL

  • Cat wrist flexion
  • Increase in fibre number in paw required to lift weight
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13
Q

What are the proposed mechanisms for hyperplasia occuring?

A

Fibre splitting = muscle itself splits and hypertrophy occurs to increase muscle mass

Proliferation of Satellite Cells = form their own muscle fibres

Evidence for this is lacking as difficult to remove muscle from humans and count fibres = ethically doesnt seem accurate

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14
Q

What is the diversity in the muscle fibre type?

A
  • Vertebrate sarcomere structure the same
    • But molecular variabillity depending on function e.g heart, smooth and cardiac muscle
      • This can be due to:
        • Multiple isoforms of myofibrillar proteins
        • Titin isoforms
        • Troponin and Tropomyosin isoforms
        • Myosin isoforms
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15
Q

What is the purpose of the different isoforms?

A
  • Titin = elastic properties
  • Troponin and tropomyosin Isoforms = determine sensitivity to Ca2+
  • Myosin isoforms = different chemo mechanical transduction, ATP hydrolysis, shortening velocity leading to resistance to fatigue
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16
Q

What are the two different types of muscle fibres?

A
  1. Slow twitch muscle fibre
  2. Fast twitch muscle fibre
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17
Q

What are the properties of slow twitch muscle fibres?

A
  • Virtually inexhaustible
    • High number of mitochondria - aerobic respiration
  • Extensive blood supply and abundant myoglobin (dark in colour)
    • MYOGLOBIN = acts as an oxygen storage unit providing oxygen to the working muscles
18
Q

What are the properties of fast twitch muscle fibres?

A
  • Fatigue easily
  • Fewer mitochondria - mainly undergo anearobic metabolism
  • Glycolytic in nature (follows from anearobic resp)
  • Poor vascularisation + lack of myoglobin (hence white colour due to lack of myoglobin)
19
Q

What parts of the chicken have slow and fast twitch muscle?

A
  • Dark meat (contains myoglobin) e.g chicken legs contains slow twitch fibres
    • Used for walking and standing which they do most of the time + doesnt use much energy
  • White meat (poor vascularization + lack of myoglobin) e.g wings and breast
    • Doesnt use much energy, brief bursts of flight, requires lots of energy and muscle tires fast
20
Q

Describe the split in fibre type due to 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%
21
Q

What type of muscles does a marathon runner have?

A

Adapted to her environment

  1. Muscles small but fatigue resistant
  2. Muscle dense and strong for their size High oxidative capacity of muscles
  3. Work over very long periods of time
  4. Not explosive strength (difficult for marathon runners to have the energy to perform the last high explosive strength at the end)
22
Q

What type of muscle does a sprinter have?

A

Muscles adapted for explosive release of force:

  1. Rapid powerful contractions
  2. Easily fatigued at maximum effort
  3. Low oxidative capacity via mitochondria
  4. High force per cross-sectional area of muscle (more hypertrophic)
23
Q

What type of muscles does a powerlifter have?

A

Muscle adapted for immense strength:

  1. Muscles are hypertrophied even more than sprinter
  2. Higher glycolytic content
  3. Fatigue easily
  4. High muscle to total body mass ratio
  5. Muscle size beginning to interfere with locomotion
24
Q

Describe the myosin gene cluster

A

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

25
Q

What are the three main types of myosin?

A

2B, 2A and 2X.

26
Q

What is the significance of each MHC isoform?

A

They are able to split ATP at different rates

Fastest 2B > 2A > 2X > 1 > emb slowest

27
Q

What are the gender differences in muscle?

A
  • Difference in myosin isoforms
    • Type 1 - more in females than males
    • Type IIA - more in males than females
  • Females have more slow twitch muscle fibres whereas males have more fast twitch muscle fibres
  • Males have a large fibre cross sectional area (more hypertrophied and easily hypertrophied)
    • This is due to males having TESTOSTERONE
28
Q

What is the function of testosterone?

A

Primary male sex hormone : required for the development of the male reproductive system

But also Promotes secondary sexual characteristics: muscle + bone mass, body hair, deep voice

29
Q

What is the effect of testosterone in muscle formation?

A
  • Promotes the commitment of mesenchymal pluripotent cells into the myogenic lineage and inhibit adipogenesis
    • Promotes muscle differentiation at the expense of fat cells
      • In adults taking testosterone will stimulate satellitle cell replication, muscle protein synthesis, fibre hypertrophy
30
Q

What type of molcule is testosterone?

A

Natural anabolic androgenic steroid (AAS)

31
Q

What exactly does testosterone stimulate?

A

Stimulate satellite cell replication, muscle protein synthesis, fibre hypertrophy

32
Q

What are the effects of taking anabolic steroids?

A
  • High blood pressure
  • Cardiac and respiratory problems
  • Liver disease
33
Q

How is a muscle repaired?

A
  • When muscle is damaged, it has a regenerative property if its not too severe it will be fibrosis and scar tissue
  • In a normal tear of muscle fibre you will get necrosis, blood and haematoma
  • Satellite cells divide using the haematoma to build on and fuse together
  • Increased expression of MYF5 and MYOD
  • Differentiation by MYOGENIN and formation of structural proteins and sarcomere
  • Muscle fibre will self renew
    • Process of synaptic innervation and vascularisation
34
Q

What are the phases of regeneration?

A
  1. Degeneration/inflammation phase
  2. Regeneration phase
  3. Remodelling phase
35
Q

What happens through the degeneration/inflammation phase?

A

A) Degeneration/inflammation phase: (first few days) Myofibrerupture and necrosis, formation of hematoma, inflammatory response (e.g neutrophils will remove debris)

36
Q

What is the regeneration phase?

A

4-5 days pi. Phagocytosis of damaged tissue, Satellite cell activation and proliferation, forming a pool of myoblasts

37
Q

What is the remodelling phase?

A

2/3 wks maturation of regenerated myofibers, restoration of blood supply and innervation, recovery of muscle functional capacity and also fibrosis and scar tissue formation.

38
Q

What is sarcopenia?

A

Age related loss of muscle mass

Impact of muscle loss is falls, injury, disabillity

39
Q

What is the loss of muscle mass associated with?

A

Gain in fat mass decreased number in satellite cells and recruitment

40
Q

What biochemical and metabolic changes occur as a result of sarcopenia?

A

Biochemical and metabolic changes: mitochondrial mutations, reduced oxidative and glycolytic enzyme activity

Reduced endocrine function, reduced physical activity