MSS12 Skeletal Muscle Contraction Flashcards Preview

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Flashcards in MSS12 Skeletal Muscle Contraction Deck (20)
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1
Q

Muscle fibre structure

A
  1. ***Myofibril
    - thin filament
    - thick filament
  2. ***Sarcoplasmic reticulum
  3. ***T tubules (invagination of sarcolemma)
  4. Sarcolemma
  5. Sarcoplasm
  6. Nuclei
  7. Mitochondria
2
Q

Myofibril: Thin filament + Thick filament

A

Thin filament (attach at Z line (formed by Actinin)):

  1. Troponin (C + I + T) (豆)
  2. Tropomyosin (strand)
    - -> F-actin strand (Troponin + Tropomyosin)
  3. G-actin molecules (with Active site) (珠)
  4. ***Nebulin (中軸)

Thick filament (attach at Z line by ***Titin (彈弓)):

  1. Myosin head
  2. Hinge
  3. Myosin tail
  4. M line

Sarcomere: ***Z line to Z line

3
Q

Titin and Nebulin

A

Both: Giant Accessory Protein

Titin:

  • ***from Z disk to M line
  • provides elasticity
  • stabilizes myosin
  • aids in ***restoring resting sarcomere length after contraction (i.e. during relaxation)

Nebulin:

  • lying along thin filament
  • attach to Z disk (formed by Actinin)
  • ***do not extend to M line
  • ***align actin (作為中軸)
4
Q

Sliding filament theory

A

During contraction:

  • ***Z lines move closer
  • A band stays same width (whole length of thick filament)
  • I band + H band smaller (unoverlapped area of **thin and **thick filament respectively)

—> Sarcomere (Z line to Z line) shorten simultaneously
—> ends of myofibrils pulled towards its centre (M line)
—> thick filament 將 thin filament 拉向自己中心

5
Q

Optimal resting length

A

normal range of sarcomere length: 75-130% of the optimal length

6
Q

Length of overlap

A

Maximum tension produced when:
Zone of overlap is large but thin filament do not extend across sarcomere’s centre (M line) (i.e. thin filament唔好撞到M line)

Short resting lengths:
thin filament extend across centre of sarcomere (thin filament撞到M line)
–> **interfere with the normal orientation of thick and thin filament
–> ↓ tension production
–> further shorten
–> thick filament contact Z line (thick filament撞埋Z line)
–> sarcomere cannot shorten
–> **
myosin heads cannot pivot
–> tension cannot be produced

Long resting lengths:
sarcomere stretched too far
–> zone of overlap ↓
–> **cross-bridge interaction ↓
–> further ↓ in zone of overlap
–> thick and thin filament cannot interact
–> cannot produce active tension (cannot contract)
–> normally prevented by **
titin filaments (connect myosin to Z disk) + connective tissue

7
Q

Skeletal muscle contraction

A

3 stages:

  1. Neural control:
    - NMJ
    - Graded / Action potential
    - Neurotransmitter release
  2. Excitation-contraction coupling
    - Propagation of action potential
    - ***Ca release
    - Actin-myosin interaction
  3. Tension production
    - Threshold / Maximal stimulation
    - Twitch / Summation / Tetanus
8
Q

***Exicitation-contraction coupling

A
  1. Motor neurone release ACh at NMJ
  2. Net entry of Na through ACh receptor-channel initiates muscle action potential along ***sarcolemma
  3. Action potential reaches **T-tubule alters **Dihydropyridine receptor (DHP) conformation
  4. DHP receptor open ***Ryanodine (RyR) receptor Ca release channel on SR
  5. Ca release into cytoplasm
  6. Ca bind to ***Troponin C (thin filament)
  7. Troponin-Ca complex pulls Tropomyosin away from Actin’s Myosin-binding site (exposing binding site on Actin)
  8. Actin-Myosin binding
  9. Myosin heads power stroke
  10. Actin filament slide towards centre of sarcomere (M line)

Myosin head uncoupled from Actin **after binding to ATP
—> **
Hydrolysis of ATP advances Myosin head by short distances (recock head)
—> Cross-bridge formation: myosin head tightly bound to actin by **releasing Pi
—> Force generation: power stroke after **
releasing ADP, Myosin head move towards M-line
—> Reattachment: Myosin bind tightly to new actin

9
Q

Sources of ATP at different muscular activities

A

Resting muscle:
Breakdown **Fatty acids —> ATP —> used to build **energy reserves:
- Creatine phosphate (Creatine + phosphate from ATP)
- Glycogen

Moderate activity:
Breakdown Glucose (from glycogen) / **Fatty acids —> ATP
—> supply to myofibrils (
*Oxidative phosphorylation, require adequate supply of oxygen)
—> used for Power contraction

Peak activity:
Breakdown **Glucose (from glycogen) / **Creatine phosphate —> ATP
—> **Glycolysis (pyruvate —> lactate)
—> **
Lactate as by-product
—> Mitochondrial activity (Oxidative phosphorylation) produce about 1/3 of ATP consumed

CP produce **less energy and **shorter duration than Glycogen

10
Q

Delayed-onset muscle soreness (DOMS)

A
  • several hours after exercise
  • may last 3-4 days
  • highest when activity involves ***eccentric contractions
  • **CK + **myoglobin blood levels elevated –> indicating muscle plasma membrane damage

3 Mechanisms:

  1. small tears in muscle tissue
    - -> loss of enzymes, myoglobin, other chemicals that stimulate pain receptors
    - -> however amount of pain is not directly correlated to amount of biochemical changes
  2. muscle spasms
  3. tears in CT framework / tendons
11
Q

Summation of contractions

A
  1. Single twitch:
    muscle relaxes completely between stimuli
  2. Summation:
    stimuli close together do not allow muscle to relax fully
  3. Unfused tetanus:
    summation but stimuli are still far enough apart to allow muscle to relax slightly between stimuli
  4. Complete tetanus:
    close stimuli summation leading to ***steady tension / maximum tension
    –> after a period tension ↓ despite continuing stimuli due to fatigue
12
Q

Development of tension in a twitch

A

Fast muscle (short time to reach maximum tension after stimulus): Eye muscle
Intermediate: Gastrocnemius muscle
Slow muscle: Soleus muscle

Presence of latent period:
from stimulus開始計: time needed for **conduction of action potential (very quick) and **subsequent release of Ca by SR (less quick but still quicker than development of twitch force)

13
Q

Isotonic vs Isometric contractions

A

Isotonic contraction:

  • muscle contracts
  • ***shortens
  • creates enough force to move the load
  • ***peak tension = amount of load (< peak tension capabilities)
2 types:
1. Concentric:
muscle length shorten on stimulation
2. Eccentric:
muscle elongates as it generates tension
--> when ends, unopposed load stretches muscle until either:
- muscle tears
- tendon breaks
- elastic recoil of skeletal muscle sufficient oppose the load

Isometric contraction:

  • muscle contracts
  • but ***NOT shorten
  • force CANNOT move the load
14
Q

Muscle performance vs Endurance

A

Muscle performance:
***maximum amount of tension / force produced by a particular muscle group

Endurance:
amount of ***time during which the individual can perform a particular activity

Factors determining performance capabilities:

  1. ***Type of muscle fibres
  2. ***Distribution of muscle fibres
  3. ***Size of muscle fibres
  4. Physical ***conditioning / training
15
Q

Fast vs Slow muscle fibres

A

Slow (Red muscle):

  • **Slow oxidative, slow-twitch oxidative / Type I S
  • ***smaller diameter
  • darker colour due to ***myoglobin
  • ***fatigue resistant
  • surrounded by more ***extensive capillary network
  • many mitochondria (for ***oxidative phosphorylation)
  • ***low glycolytic enzyme conc in sarcoplasm
  • main substrate for ATP generation: Lipids, Carbs, a.a. (***aerobic)

Intermediate:
***Fast resistant, fast-twitch oxidative / Type II-A

Fast (White muscle):

  • **Fast fatigue, fast-twitch glycolytic / Type II-B
  • ***larger diameter
  • paler colour
  • ***easily fatigue
  • -> reach peak twitch tension in 0.01s after stimulation
  • ***few mitochondria
  • ***high glycolytic enzyme conc in sarcoplasm
  • main substrate for ATP generation: Carbs (***anaerobic)
16
Q

Proportion of fast, intermediate, slow fibres in skeletal muscle

A
  • Variable
  • Can change with physical conditioning
  • -> athletic training: ↑ ratio intermediate:fast fibres (more fatigue resistant)
17
Q

Muscle Hypertrophy + Atrophy

A

Muscle satellite cell: interposed between muscle fibre and external lamina

  • ***multipotent
  • myogenic precursor

Hypertrophy:

  • enlargement of stimulated muscle
  • ↑ fusion of satellite cells –> ***↑ myonuclei no.
  • ***↑ protein synthesis, ↓ proteolysis
  • -> ↑ fibre size
  • repeatedly stimulated to produce near-maximal tension (e.g. bodybuilder muscle)

Atrophy:

  • ↓ muscle size, tone, power
  • not regularly stimulated
  • e.g. spinal cord injuries paralysis / neuromuscular disease
  • -> physical therapy / direct electrical stimulation as substitute for nerve stimulation
18
Q

Protein synthesis

A

No. of myonuclei x Protein synthesis per myonucleus

19
Q

Detraining

A

↓ in muscle fibre size but NO ↓ in myonuclei

20
Q

Exercise-associated muscle cramps

A

Sudden, involuntary contraction of skeletal muscle

Possible causes:

  • ***inadequate blood supply
  • ***mineral depletion
  • ***nerve compression

Prevention:

  • electrolyte supplement, hydration
  • stretch muscles

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