Muscle Physiology Flashcards

1
Q

Function of Nebulin?

A

stabilizes thin filament in certain types of muscle

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2
Q

Filament polarity?

A
  • polarity of proteins (actin/myosin) switches when you cross from one side of the sarcomere to the other side
  • produces force in a certain direction
  • length of filaments is fixed to slide past each other during contraction
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3
Q

What helps pull muscle sarcomere back to original length?

A

agonist/antagonist pairs pull muscle back

-biceps/triceps

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4
Q

Sarcomere length tension relationship, passive?

A
  • if muscle is relaxed and it is passively stretched out to increase sarcomere length, the sarcomere increases its force to resist stretch (like rubber band)
  • not interaction between actin/myosin
  • greater length= greater force
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5
Q

Sarcomere length tension relationship, active?

A
  • does useful work
  • subtract passive work from total
  • due to actin/myosin interaction
  • there is an optimal length where actin/myosin interaction is greatest and force is greatest
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6
Q

Sarcomere length is too long, tension relationship?

A
  • actin and myosin are stretched beyond overlap
  • no interaction
  • force goes to 0, no contraction
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7
Q

Force of contraction is proportional to what?

A

number of myosin heads interacting with actin

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8
Q

Plateau region, length-tension relationship?

A
  • bare zone
  • any change in length has little effect on the number of myosin heads that can interact with actin (.2 microns)
  • amount of overlap changes but the number of heads remains constant
  • result of the change of polarity at halfway point of sarcomere
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9
Q

Sarcomere length is too short, tension relationship?

A
  • opposing sides start to interfere and overlap each other
  • tension decreases with decreasing sarcomere length until they crash into Z disk
  • thick and thin filaments are compressed, cannot function properly
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10
Q

What is the bare zone?

A
  • center without myosin heads

- area where polarity flips

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11
Q

Frank Starling law of heart?

A
  • greater the volume of blood entering heart during diastole, the greater the volume of blood ejected during systole and greater the force
  • there is a balance between venous return and systolic delivery
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12
Q

Passive tension, skeletal vs heart muscle?

A
  • skeletal- passive starts where active tension peaks
  • cardiac- passive starts before active muscle peaks
  • results in resting state of cardiac muscle shorter than skeletal muscle
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13
Q

Length tension relationship, Cardiac vs skeletal muscle?

A
  1. Cardiac
    - trades mechanical efficiency for self regulation
    - shorter optimal sarcomere length, stretched as blood fills heart
    - the stretching moves cardiac sarcomeres to a more optimal length for greater interactions and contraction
    - if heart is stretched too much, loses its ability to pump (CHF)
    - resting tension starts to rise earlier
  2. skeletal
    - operates at maximal mechanical efficiency
    - generates most force at resting length
    - dip in total tension
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14
Q

How does Myosin detach from actin?

A
  • need ATP

- stays attached if no ATP, Rigor Mortis

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15
Q

T/F

Each myosin head cycles independent of the others.

A

True

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16
Q

Steps of sarcomere filament sliding?

A
  1. Calcium influx, cross bridge binds to actin
  2. cross bridge moves
  3. ATP binds myosin, causing cross bridge to detach
  4. Hydrolysis of ATP, energizes cross bridge
17
Q

Force velocity relationship?

A
  • the heavier the load, the slower the velocity of muscle contraction
  • if the load is less than isometric force, you can contract
  • the lower the load, the faster the contraction
  • as load increases, velocity of concentric contraction decreases, once the load reaches max force that can be supported, the velocity of eccentric contraction increases
18
Q

Slow oxidative (type 1) muscle fibers characteristics?

A
  • slow contraction velocity
  • oxidative phosphorylation primary source of ATP
  • many mitochondria
  • high Myoglobin content (red fibers)
  • slow rate of fatigue
  • low glycogen and glycolytic enzymes
  • made for endurance
19
Q

Fast Oxidative Glycolytic (type 2a) muscle fibers?

A

combination of slow and fast twitch fibers

20
Q

Fast Glycolytic (type 2b, 2x) muscle fibers?

A
  • fast contraction velocity
  • Glycolysis primary source of ATP
  • few mitochondria
  • high glycogen and glycolytic enzymes
  • fast rate of fatigue
  • low Myoglobin content (white muscle)
  • made for short burst exercise
21
Q

Muscle triad?

A
  1. junctional SR
  2. T tubule
  3. junctional SR
    - skeletal muscle has a lot of triads, cardiac muscle has few
22
Q

Excitation-contraction coupling in skeletal muscle?

A
  • mechanical coupling
  • depolarization of T-tubule membrane causes conformational change to voltage sensitive protein
  • releases calcium from SR
23
Q

Excitation-contraction coupling in cardiac muscle?

A
  1. depolarization of T-tubule membrane causes conformational change of voltage sensitive protein to release calcium from extracellular space
  2. Calcium binds to receptor on SR membrane
  3. Channel opens in SR to release more calcium
  4. After a certain amount of time, the channel closes
    - positive feedback
    - difficult to tetanize cardiac muscle
24
Q

How does calcium get sequestered back into SR?

A

-ATPase pump brings calcium against its electrochemical gradient back into the SR

25
Q

Control of contraction in skeletal muscle?

A
  • Troponin C- binds calcium
  • Troponin I- turns off the switch, when calcium is no longer bound (inhibitory peptide)
  • Troponin T- glues complex to Tropomyosin
  • when calcium binds, Tropomyosin is removed, exposing the myosin binding site on Actin (regulation step)
26
Q

Neural control of contraction, one twitch?

A
  • action potential at motor end plate (1 msec)
  • calcium in cytoplasm peaks (5 msec)
  • tension of muscle peaks (25 msec)
  • sarcomere active for 60 msec
27
Q

Fused tetanus?

A
  • multiple twitches close in time together
  • calcium levels remain high in cell
  • sustained contraction
28
Q

Excitation contraction coupling in smooth muscle?

A

calcium phosphorylates the myosin regulatory light chain to activate it

29
Q

Effect of epinephrine on smooth muscle?

A
  • relaxation (depends on particular smooth muscle)
  • relaxes bronchioles
  • activates arterioles
30
Q

Latch bridge in smooth muscle?

A
  • only in smooth muscle
  • ATP turns system on as a regulatory mechanism
  • Myosin is dephosphorylated and dissociates from Actin very slowly, forming a latch bridge
  • smooth muscle can hold contraction without using more ATP, and very little ATP is needed to create another movement
  • efficient system