Mod 3 Physiology

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  1. What are the basic functions of muscle?
    • 1) movement
    • 2) posturing
    • 3) internal motility and storage
    • 4) heat
  2. What is the basic organization of skeletal muscle?
    Muscle->muscle fasicle->muscle cell (fibre)->myofibril
  3. List some of the key structures in the muscle fibre
    • 1) sarcolemma (cell membrane)
    • 2) sarcoplasm (cytoplasm)
    • 3) T-tubules (invaginations in the sarcolemma)
    • 4) Sarcolasmic reticulum (Ca++ storage)
  4. Describe the organization and components of a sarcomere
    Image Upload 1
  5. Explain the function of the following in a sarcomere: tropomyosin; tropinin, actin, myosin
    • Tropomyosin: covers the myosin binding sites on actin
    • tropononin: Ca++ causes a conformational change in this and causes the tropomyosin to move.
    • actin: thin helical filaments attached to Z-line (move)
    • myosin: two heads each with an actin binding site and an ATP binding site
  6. What is a motor unit?
    One motor nueron and all of the muscle fibres that it innervates.
  7. Describe how signalling happens at the NMJ
    • 1) AP comes down motor neuron
    • 2) Causes influx of Ca++ in neuron
    • 3) Causes ACh vesicles to fuse with the cell membrane and release ACh into the neurosynaptic cleft
    • 4) ACh binds to ligand-gated Na+ channels (2/channel) on the muscle cell
    • 5) Causes depolarization and eventually action potential
    • 6) ACh is eventually taken back up by neuron or degraded by AChE
  8. Describe Excitation Contration Coupling (what happens when an AP is running along sarcolemma)
    • 1) AP runs down the T-Tubules into the cell
    • 2) AP causes a conformational change in DHPR membrane protein on T-Tubule surface
    • 3) DHPR mechanically causes conformational shape change in ryanodine receptors on the sarcoplasmic reticulum
    • 4) ryanodine receptors allow Ca++ to rapidly leave the SR into the sarcoplasm
    • 5) Ca++ is taken up by the SERCA pump (away from T-tubule - SR interface)
  9. Describe the cross-bridge cycle
    • 1) The Ca++ binds to the troponin, which causes the tropomyosin to be moved off the binding sites
    • 2) The (cocked) myosin head binds to one of these sites
    • 3) The ADP and P detach and the head flexes (power stroke)
    • 4) New ATP binds to the head, causing to to detach from the actin
    • 5) ATP dephosphorylates, causes the myosin head to "cock" (now ready to bind to a new actin site) and on and on...
  10. How do: botox, succinylcholine, and myasthenia gravis affect the NMJ?
    botox: prevents the ACh vesicle from fusing with the presynaptic membrane, thus preventing its release.

    succinylcholine: ACh receptor agonist (i.e. it binds to the same receptors, causing them to open and in this case STAY OPEN), prevent any further action potentials

    myasthenia gravis: autoimmune condition where antibodies bind to the ACh receptors. This prevents the ACh from binding, and also causes the destruction of the ACh receptors.
  11. How does the cross-bridge cycle generate force?
    Force is generated during the power stroke.
  12. What are the 5 factors that influence force generation
    • 1) Motor Unit size: how many muscle fibres are innervated by one neuron?
    • 2) Motor Unit Recruitment: smaller motor units recruited first, larger motor units added as more strength is needed. Smooth movements
    • 3) Muscle Length/Stretch: There is a "peak" contractile force at resting length
    • 4) Muscle fibre diameter: more sarcomeres added in parallel will generate a larger force
    • 5) Frequency of stimulation: contraction can sum on top of previous contractions (stronger force)
  13. Name and describe the three energy sources for muscles
    • 1) Creatine Phosphate: In all muscle types; used up quickly and replenished quickly; 
    • 2) Glycolysis: predominantly in IIb fibres; small capacity; fairly rapid
    • 3) Oxidative Phosphorylation: Predominantly in I and IIa; slow supply, but can make lots of ATP
  14. What causes muscle fatigue?
    • ATP depletion
    • impaired Ca++ release from SR
    • depletion of O2
    • central fatigue
    • impaired AP conduction
  15. Contrast AP generation in smooth and skeletal muscles
    • Smooth muscle doesnt NEED a nerve to depolarize
    •   -CAN use NMJ transmission
    •   -Graded response (due to local factors or mechanical stim)
    •   -Spontaneous depolarization (fluctuation of ions over membrane)

    • Smooth muscle doesnt need depolarization to contract
    •   -ligand gated receptors that release second messenger that cause Ca++ release in SR
  16. Difference in cell components between smooth and skeletal muscle
    • Smooth:
    •   -calmodulin and myosin light chain kinase (MLCK)
    •   -actin and myosin not organized like in skeletal (no striations)
    •   -it is the interaction of calmodulin and MLCK that allow the myosin-actin cross bridging to occur (activate myosin and make it ready to bind) 
  17. difference in activation of contraction between skeletal and smooth muscle
    • 1) how Ca++ increases:
    •   i)VG Ca++ channels on membrane open because of AP
    •   ii)Excell Ca++ enters and stimulates Ca++ release from SR
    •   iii) second messenger signal to SR
    •   iv) auxillary Ca++ channels can open if SR Ca++ is depleted

    • 2) effect of Ca++ influx
    •   Ca++ binds calmodulin -> activated calmodulin activates MLCK -> MLCK hydrolyses ATP -> loose Pi binds and activates myosin -> myosin is now ready to go
  18. Difference in cross bridge cycling between skeletal and smooth muscles
    smooth: much slower because there is much lower ATPase activity on the myosin molecule
  19. Difference in termination of contraction between smooth and skeletal muscle.
    • Requires two events:
    • 1) Removal of Ca++ from sarcoplasm
    • 2) Dephosphorolization of myosin
    •   -deactivate MLCK
    •   -dephosphorylate myosin
    •   -myosin returns to inactivated state
Card Set:
Mod 3 Physiology
2012-12-04 22:36:24

Mod 3 Muscle Phsiology
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