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  1. What are sarcoplasmic reticulum (SR)? where can you find them?
    - Modified version of endoplasmic reticulum that wraps around myofibrils.

    - It consist of Ca2+ which are released from longitudinal tubules
  2. Why is Ca2+ important in muscle?
    - They aid in the contraction of muscles
  3. What are the contractile proteins in myofibril?
    - Myosin – ability to create movement

    - Actin – makes up the thin filaments of muscle fiber
  4. Where would you find myosin and what is its shape/ form?
    - Long tail and round head connected by hinge (allows for a swivel mov’t)

    - When 250 myosin come together they form a swiveling staircase
  5. What are sarcomeres and where would you find it?
    - Sarcomeres are pattern segment in myofibril.

    - Starts and ends with z disk (thin filiments/ I band ) --> A band (mainly thick filaments but over laps with thin filiments (actin) H zone --> z disk
  6. What are t-tubules and where are they located?
    - T-tubules are lumen in the muscle fiber (myofibrils) that allow for action potential to reach the center at a faster rate
  7. What would happen if we didn’t have t-tubules?
    - Action potential would run at a slower rate b/c it would rely on diffusion of + ions from cytosol --> delaying myofibrils response
  8. What are the regulatory proteins of myofibrils?
    - Tropomyosin – protein polymer that wraps actin to prevent binding of myosin to actin (* cock blocker) (when muscle isn’t contracting)

    - Troponin – turn on/off contraction à b/c its a Ca binding complex of 3 proteins, which positions tropomyosin
  9. What are the giant accessory proteins in myofibrils?
    - Titin – huge elastic protein (largest, 25,000 AA)

    *helps stabilize*

    *returns muscle to rest place*

    - Nebulin – inelastic huge protient hat attaches to z disk from thin filaments (helps align actin)

  10. What is muscle tension?
    - The force created by contracting muscles
  11. What is the weight or force that opposes contraction of muscle?
    - Load
  12. What does cross-bridging movement of actin and myosin result in?
    - Overlapping of actin and myosin slide pass each other (energy dependent) during contraction resulting in the sliding filament theory of contraction
  13. How can you stop muscle from contraction?
    - Decrease the level of Ca in cytosol

    - Ca2+ ATPase pumps Ca2+ back in to the sarcoplasmic reticulumà stops Ca2+ from binding to troponin
  14. What happens when sarcomere contracts during contractions?
    - The sarcomere gets shorter b/c myosin binds to actin forming a power strike (overlapping in H zone)
  15. What is the power strike?
    • - Occurs during contraction, in which Ca binds to troponin -->
    • allows tropomyosin to shift -->
    • creates myosin binding site to open-->
    • myosin hydrolyses ATP (releases Pi ) -->
    • crossbridge tilting of 45 degrees from 90
  16. What happens when ATP is hydrolyzed in the myosin?
    - ATP releases Pi leaving ADP

    - The myosin head moves from 90 degrees to 45 (cock blocker is removed)

    - Head swivels and swings toward M line
  17. What is excited-contraction coupling?
    - Process in which muscle Ψ initiates ca signals at neuromuscular junction

    - --> turns on contraction – Relaxation cycle (muscle twitched)
  18. The 4 major components of excited contraction coupling?
    - Release of Ach by a somatic motor neuron

    - Ψ of myofibrils

    - Increase in Ca2+ from sarcoplasmic reticulum

    - Ca binds to troponin
  19. What is a muscle twitched?
    - Single muscle contraction-relaxation cycle
  20. What is the neurotransmitter of neuromuscular junction?
    - Acetylcholine
  21. What are the two unique things about skeletal muscle?
    - Cant initiate there own contraction

    - Are not control directly by hormones
  22. What does acetylcholine bind to in neuromuscular junction?
    - Motor end plate (receptors)

    - These receptors allows influx of Na --> Ψ b/c more Na in cell due to ∆ membrane
  23. What is the calcium channels involved in the t-tubules?
    - Dihydropyridine channels (DHP) (voltaged gated)

    - DHP is mechanically linked to ryanodine recptors channels on SR
  24. What are the main proteins involved in restoring the system back to normal (contraction)?
    - Myosin ATPase – crossbridge mov’t and relase

    - Ca ATPase – collect excess ca in cytosol and pumps back to SR

    - Na – K ATPase – restores the amount of Na in cytosol to initial state (in order for another contraction to occur)
  25. What are the factors that causes muscle fatigue?
    - Physical – muscle cant generate power input

    • - Psychological – (central fatigue) long day at work
    • --> tired --> party --> you rally
  26. What are the proposed mechanisms of fatique that occur in neuromuscular junction and Ec - coupling?
    - Decrease in Neurotransmitter release (dosnt occur w/normal excesice)

    *Ach not synthesized fast enough in axon to keep up with firing rate

    *threshold at motor end plate not reachedà no Ψ in t-tubule (due to in activity of Na – K ATPase)
  27. What are the proposed mechanisms of fatique that occur in Ca2+?


    - depletion of glycogen stored in muscle --> leak of Ca2+ from SR

    - increase in Pi from phosphocreatine in muscle fiber b/c Ca2+ binds to it to form Ca2+ phosphate (major in fatigue)

  28. What are the difference between red muscle (oxidative fibers) differ from white muscles (glycotic
    fibrers)?
    - White muscles have less myoglobin, O2 larger diameter few BV --> run out of O2 --> rely on aerobic glycolysis --> faster fatigue

    - Red muscle have more myoglobin --> red color --> 02 binding pigment à more oxygen diffusion due to smaller diameter --> rely on glucose

    *Better oxidative phosporylation for ATP production*
  29. What happens when the sarcomere length is shorter the optimal resting length?
    - The actin and myosin will overlap before the initial contraction begins

    - Preventing crossbridge formation (mov’t of actin by myosin ATPase)
  30. what is the difference between summation of incomplete (unfused) and complete tetanus?
    - Incomplete has action potential that are close together w/ a slight point and reaches maximum tension

    - Complete tetanus also reaches maximum tension, but the Ψ does not relax between stimulus --> steady tension

    ( fatigue causes lost of tension even when continuous stimulus)
  31. How can we increase the tension that developed?
    - We can change the rate of the Ψ in muscle fiber
  32. How can muscles create graded contraction of varying forced and duration?
    - Muscles are composed of multiple MU of different type (diversity)


    § Changing the type of MU that are active

    § Changing the number of MU that are responding
  33. What happens during isotonic contraction?
    - Creates force and moves load (bicep curls)

    § Primary muscles shortens
  34. What happens during eccentric contraction?
    - Resisting the weight from pulling down completely

    § Muscles have a delayed muscle sorness
  35. What are isometric contraction?
    • - Contraction that
    • create force w/o moving load (front/lateral raises)

    § Muscles doesn’t shortens b/c load is not being moved

    § Not enough force is created to move load
  36. Why does the muscle shorten during isotonic contraction?
    - b/c the sarcomere shortens more after the elastic components are stretched
Author
mingojimen
ID
69295
Card Set
312
Description
medical lab
Updated