Muscle Flashcards

1
Q

What is the structure of skeletal muscle?

A

Flexor/extensor antagonistic pairs attached to bone

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2
Q

Differentiate between the different types of contraction?

A

Isotonic contraction: shortening relates to flexor

Eccentric: lengthening relates to extensor
- Both able to contract through both forms

Isometric Contraction: tension changes but the length remains the same
- Change in muscle tone e.g carrying shopping back

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3
Q

What is the structure of myofibers?

A
  • Large and cylindrical
  • Multinucleate
  • Packed with myofibrils extending around the length of the structure
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4
Q

What are t-tubules?

A

T tubules: membrane invaginations that contact ECF

- CM of myofiber in more contact with myofibrils

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5
Q

What is the sacroplasmic recticulum?

A

Sarcoplasmic reticulum: intracellular Ca stores surrounding each myofibril
- In close contact with membrane and t tubules

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6
Q

How does excitation contraction coupling occur in skeletal muscle?

A
  • Z lines come closer together
    • Increased Calcium concentration
    • Myosin heads pivot
  1. AP propagates along myofiber T tubules
  2. Depolarisation activates dihydropiridine receptors (DPHR) so conformational change
    - DPHR is on T tubules on sacrolemma (membrane of myofibre)
  3. Change in shape allows DHPR to make contact with ryadine receptors (RyR) on SR
  4. Opening of RyR so Ca2+ released from intracellular stores in scarolemma
    - Depolarisation causes increase in intracellular Ca

AP–>conformational change on DPHR–>touch RyR–>release intraceulluar Ca

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7
Q

What is the structure of a sarcomere?

A

Z line: defines SM lateral boundaries
Actin: polymer of thin filament of two twisted alpha helices, displays polarity
Myosin: thick filament–> “motor proteins”

- Contains "globular heads" that interact with actin  Titin: very large "spring like" filament anchoring myosin to Z line, keeps myosin in bplace Nebulin: large filament associated with actin, doesn't really do anything Cap Z and tropomodulin: associated with positive and negative ends of actin respectively 

Tropomysoin: forms a chain along each actin filament and associated with the tropomyosin is another protein, troponin.

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8
Q

Explain the sliding filament theory?

A
  1. In calcium presence troponin moves (forms helix around actin) from tropomyosin chain
  2. Movement exposes myosin binding site on actin chain
  3. Charged myosin head binds to exposed site on actin filament (head has ADP bound)
  4. The binding and ADP discharge causes myosin head to pivot –> pulls actin filament towards centre of sarcomere
  5. ATP binds releasing myosin head from actin chain
  6. ATP hydrolysis to ADP provides energy for myosin head to recharge
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9
Q

What is the structure of cardiac muscle?

A
  • Cardiomyocytes are striated
  • Unicellular and uninuclear
  • Intercalated disk: specialised disc connecting individual cardiomyocytes
    ○ Have desmosomes (hold membrane structures together) and gap junction (allows electrical communication between cells)
  • Contraction mechanism is the same as skeletal muscle
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10
Q

How does EC coupling occur in cardiac muscle?

A
  1. AP generated by pacemaker cells in nodes
  2. AP moves down T tubules and opens VGCC so Ca influx
    • no contact between the VGCC and RyR
  3. Ca binds to RyR to cause calcium induced calcium release (CICR)
    • Initiates contraction by binding to troponin
    • Further depolarisation
  4. The rest is the same except there is a different type of troponin

AP–>VGCC–>RyR–>CICR–> further depolarisation

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11
Q

What is the structure of smooth muscle?

A
  • Present in walls of hollow organs e.g blood vessels, GIT
  • Multiplies and gets bigger without gym so doesn’T need as much attention as caridac and skeletal
  • Smooth because no striated actin-myosin pattern, although the filaments are still present
  • Contracts much more slowly than other two
  • do not express voltage-gated Na+ channels
  • irregular actin and mysoin arrangment
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12
Q

How does EC coupling occur in smooth muscle?

A
  1. Depolarisation opens VGCC (slightly different than those in cardiomyocytes) so Calcium influx
  2. Calcium moves into cell and binds to Calmodium (CAM)
  3. Activates Myosin Light chain kinase (MLCK)
  4. MLCK phosphorylates myosin light chains (MLC20) allowing them to form cross-bridges with the actin filaments
  5. Contraction
    • Also causes vasoconstriction

VGCC–>CAM–>MLCK–>change in appearance of MLC20–>contraction

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13
Q

how does muscle maintain low Ca concentration?

A

Ca2+- ATPase that continuously pumps Ca2+ from the cytosol into the sarcoplasmic reticulum (SR).

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