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Flashcards in Skeletal Muscles Deck (58):
1

Basic structure of skeletal muscles

Skeletal muscle
>Fascicles
>>Muscle Fibres
>>> Myofibrils

2

Skeletal muscle and its components lined with...?

Skeletal muscle - Epimysium
Fascicles - Perimysium
Muscle fibres - Endomysium

3

Location of nuclei of myofibrils?

On edges due to packing of myofibrils
Multinucleated

4

Which structure do nerves innervate in muscle

Muscle fibres

5

How many muscle fibres innervated by one nerve in strong but not precise muscles (glut. max.)?

>2000

6

How many muscle fibres innervated by one nerve in precise but not strong muscles (orbit)?

+/- 10

7

Microcirculation supporting muscles - architecture?

Arcades of arterioles in the PERIMYSIUM which give rise to transverse terminal arterioles which penetrate the endomysium giving rise to the capillary network.

8

Terminal arteriole and its venule in muscle are called?

Microvascular unit (MVU)

9

Nebulin

Controls length of actin, template for regulation of filament length.

Extends from Z line

10

Tropomyosin

Responsible for covering or exposing actin areas for myosin head binding

11

Tropomodulin

Covers active area to which myosin heads attach to

12

Titin

Maintains integrity of sarcomere when the myosin heads are moving -

connects myosin to M and Z line

When muscle is stretched titin unwinds - most muscle injury occurs in overextension -> titin becomes separated from Z line

13

Contraction cycle

1. ATP breaks link between mysoin and actin - RELEASE
2. Bending of myosin head (ATP=>ADP) - BENDING
i. Head binds to new site of actin
ii. Phosphate released
3. Head bends forcing shortening of sarcomere - FORCE GENERATION
i. ADP released
ADP release leads to REATTACHMENT to mysoin (RIGOUR)

14

T tubule excitation

○ Ach released from motor neuron axon terminal
○ Action potential generation in sarcolemma
○ T tubule is a pouch of sarcolemma reaching the SR
○ AP reaches T tubule and SR > triggers Ca2+ release from SR
○ Ca2+ binds to troponin - exposure of actin sites for myosin
○ Crossbridge contraction cycle starts
○ Ca2+ actively reuptaken to SR following AP
○ Tropomyosin blacks myosin-binding sites

15

Embyrological origin of muscles

Paraxial mesoderm - muscle fibres and trunk

16

Somites formed from?

Trunk limb (tongue and larynx) muscles derived from paraxial mesoderm

17

Myogenesis

involves a proliferative stage and the migration of cells from the dermomyotome to form the myotome

18

Initial cells that determine destination of mature cells

Founder cells

19

When are satellite cells activated?

After muscle damage

20

Roles of satellite cells?

Post natal growth of muscle.
Proliferation and fusing to make myofibrils - muscle regeneration (terminally differentiated multinucleated myofibres)

21

Proportion of satellite cells in foetal muscle?

30%

22

Proportion of satellite cells in adult?

3.8%

23

Location of satellite cells

In development - centrally
Mature muscle - migrate to edges

Outside sarcolemma but within basal lamina

24

Satellite cells nuclei size?

Large nucleus to cytoplasmic ratio

25

6 processes in muscle development:

1. Change of direction from cranio-caudal (few retain it: rectus abdominis, erector spinae)
2. Fusion (rectus abdominis)
3. Splitting of myotomes into layers (intercostal muscles)
4. Splitting into 2 or more parts (trapezius, SCM)
5. Degeneration (aponeurosis)
6. Migration (diaphragm, lat dorsi - nerve supply maintained)

26

Type 1 muscle fibres

- T1 fibres have many mitochondria (black dots on electron micrograph).
- Endurance muscles - don’t generate a lot of force but can work for long times
--> Back, posture muscles

27

Type 2 muscle fibres

- Work for shorter amounts of time
- Generate greater force
Few mitochondria -> base metabolism on anaerobic respiration

28

Muscle maturation

- Occurs in childhood
- Initially muscle slow to relax
○ Reaches adult values at 10yo
- In males due to testosterone maturation occurs more quickly (after 12yo)
- Muscle makes up 25% of body bulk at birth
○ Increases by adulthood
3.5x in females
5x in males

29

Strength muscle training

increase the number of sarcomeres -> larger cross sectional area
Improvement by recruitment of more muscle fibres

30

Endurance muscle training

Trained by increasing delivery of O2
○ Increases VO2 max
○ CO
○ Neuromuscular excitability
- Decreases - HR, Overloads muscle

31

Muscle fatigue effectes

- 'an exercise induced reduction in the ability of the muscle to produce force or power'
- Increased extracellular K+ = failure of excitation
- Decrease in calcium sensitivity
- Creatinine supplements can increase ATP amounts - increase performance
- Accumulation of lactic acid - small impact
○ Blood lactic acid give indication on anaerobic metabolism
- Reduction of ATP which in turn reduces Ca2+ release (binding sites available) - decreases rate of ATP usage - therefore reduction in power output
- Lack of energy - glycogen can deplete, its unevenly distributed

32

Strength training effects - 6-8 weeks

Motor learning - no increase in strength, but better performance
- Increase strength but no change in muscle size - synchronization of motor unit firing and increased ability to recruit all available motor units
Packing density of contractile element increases

33

Strength training effects - 10-12 weeks

Hypertrophy can be seen
○ Significant and prolonged activity is required
Slow growing will not cause stretch marks on skin

34

Rest in strength training

Allows for turnover in contractile proteins by multiple satellite cells' nuclei

35

Resistance training effect 24-48h

Muscle protein synthesis enhancement - increased amount of satellite cells

36

How are new muscle fibres created?

Satellite cells - divide and incorporate into muscle fibres (quicker response to training)
Muscle cells cannot divide

37

Movement associated with greater satellite activation

Eccentric rather than concentric muscle contraction

38

Muscle hypertrophy achieved by

- Increase in RNA and protein synthesis
- Increase in number of nuclei from satellite cells

○ Resistance training is very effective in producing new satellite cells

○ Increase in satellite cell number precedes muscle hypertrophy
Minimal fibre damage is a possible trigger

39

Optimal power in endurance training for best response

60%
less damage - rested fibres take over once working ones get tired

40

Endurance training premise

- You want to go for much longer
○ Rate of delivery of oxygen and ability of cells to utilise it
○ Delivery of nutrients - blood vessels around muscle

- Decrease with age -> age-related O2 uptake changes

- Endurance training -> slightly breathless, but not distressed or exhausted

41

Effects of endurance training

○ Increase in satellite cell number!
○ Cardio and resp improvement
§ better delivery and use of O2
○ Capillary density improvement
§ Smaller O2 diffusion distance
○ Mitochondria change and increase in size and number
§ Better O2 metabolism
○ Enhanced glucose uptake and insulin sensitivity
§ Counteracts insulin resistance in T2DM
○ Increases fatty metabolism
§ Better preserved glucose store
§ Increased endurance
○ Cardiac muscle hypertrophy
§ Increased CO
§ Decreased HR
-> Prolongs the time for which exercise can occur

42

What is increased by training to produce more force?

Ca2+ release (as more glycogen is available from lower glycogenesis)

43

Overtraining

- Overtraining may lead to chronic fatigue and loss of muscle strength

- early indication - decrease in neuromuscular excitability (usually the result of endurance training e.g. swimming, cycling and running.)

- Due to successive alterations in metabolism -> main energetic stores shift from carbohydrate Inand lipids to protein.

44

Muscle regeneration stages

1. Muscle injury
2. Degeneration
3. Inflammation
4. Regeneration
5. Remodelling/ repair

45

Degeneration of muscle

Necrosis of myofibres

46

Inflammation

Neutrophils and macrophages (debris removal, cytokines production)

47

Regeneration

Satellite cell activation
Stem cell recruitment
Regenerating fibres

48

Remodelling/ repair

ECM remodelling
Angiogenesis
Functional recovery

49

What cell can activate satellite cells?

Macrophages

50

Detailed regeneration phase of muscle injury

○ Myotrauma to muscle fibre
○ Satellite cell activation and proliferation
§ Satellite cells fuse to damaged myofibre
§ Satellite cells also can fuse together to create new myofibres
○ Myofibre regenerates and has central nuclei
○ Nuclei peripheralise - regenerated myofibre
- Maturation and re-innervation of fibre

51

Peak of muscle bone and strength and consecutive decrease in muscle mass per decade?

25-30 years old
- Then 6% decrease in skeletal muscle mass per decade

- Impacts basal energy requirements and maximal aerobic capacity

52

Gender differences in muscle loss

Greater in women - can be diminished by HRT

53

Lifelong endurance training

Can increase aerobic powers but doesnt change muscle strength

54

Max VO2

Mid-twenties, half that at 70

55

Changes to muscle fibres with ageing

- Type 2 fibres (strength) are lost much more than Type 1 fibres (endurance)

56

Changes in ageing

○ Decline of myosin synthesis
○ Decreased ability of muscle remodelling after injury
§ Decreased muscle mass and reduction in strength and endurance
○ Reduced ability of myosin head to locate receptors on actin filament
§ Decreased force of contraction
○ Reduced calcium release due to receptor loss
§ Inhibition of depolarisaton
○ Loss of satellite cells
§ Failure to maintain muscle cell fibre size
§ More muscle injuries
§ Longer recovery
○ In all reduced number and size (cross sectional and length) of muscle fibres
§ Loss of muscle mass
§ Decreased power
□ Type II fibres preferentially lost
§ Decreased range of movement
□ Due to loss of muscle fibre length

57

How to counteract T2 fibre loss

Endurance exercise -> better insulin sensitivity, prevents decline in mitochondrial respiratory capacity

58

Decline in muscle function slope

Linear
accompanied in increase in connective tissue proportion
Isometric strength also reduces with age
(contractility also affected)