Muscle Flashcards

1
Q

Repeating contractile unit that when chained together make a myofibrils

A

Sacromere

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2
Q

Ends of sacromere

A

Z disk

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3
Q

Middle of a sarcomere

A

M line

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4
Q

Thin filaments only

A

I band

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5
Q

Entire length of thick filaments

A

A band

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6
Q

Middle of A band, with thick filaments only

A

H Zone

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7
Q

describes how sarcomeres allow muscles to contract.

A

Sliding Filaments Theory

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8
Q

Muscles are arranged around _____to allow for movement.

A

joints

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9
Q

Muscles that close joints

A

Flexors

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10
Q

Muscles that open joints

A

Extensors

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11
Q

Muscles are _____in opposing patterns, to allow for all directions of movement.

A

arranged

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12
Q

Muscles that have opposite effects on the same joint

A

Antagonists

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13
Q

Muscles that have cooperative effects on the same effect

A

Synergists

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14
Q

Biceps and triceps muscles are arranged around the ____joint

A

elbow

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15
Q

A collection of muscle fibers

A

Muscle Fascicle

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16
Q

A collection of myofibrils (Individual chains of sarcomeres)

A

Muscle fiber

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17
Q

Skeletal muscle contraction is _____—a muscle fiber must be “activated” by a motor neuron via an NMJ.

A

neurogenic

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18
Q

) How does AP in a motor neuron become a Ca2+ signal in the muscle fiber?

A

Excitation-contracting coupling

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19
Q

How does a Ca2+ signal cause sarcomeres to start shortening?→

A

Sliding filaments theory and Power strokes

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20
Q

Wraps around actin to block binding sites on actin

A

Tropomyosin

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21
Q
  • AKA: Ca+2- sensing protein

- Binds to Ca+2= causing unbounding of tropomyosin from action- allowing Actin to bind to Myosin

A

Troponin

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22
Q
  1. Motor neuron AP reaches axon terminal→Ach in synaptic cleft.
  2. Ach binds to nicotinic AchRs. These mixed-cation channels open→Na+ enters cell→depolarization.
    -Graded potential called an endplate potential (EPP).
  3. Endo-plate Potential depolarizes Vm to Vthresh, activates VGNaCs and VGKCs→skeletal muscle AP.
  4. AP invades t-tubules (indentations in membrane).
  5. AP activates dihydropyradine receptors (DHPRs) in t-tubule membrane.
  6. DHPRs are physically connected to ryanodine receptors (RyRs) in
    sarcoplasmic reticulum membrane.
    -Activation of DHPR→Activation of RyR.
  7. RyRs are Ca2+ channels. Activation of RyR→Ca2+ flow from SR into
    cytosol. Ca2+ signal!
A

Skeletal Muscle Excitation-Contraction Coupling:

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23
Q

is a long filamentous protein with myosin binding sites spaced along it.

A

Actin

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24
Q

is a helical protein wrapped around actin, covering the myosin binding sites (at rest).

A

Tropomyosin

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25
Q

______ is a Ca2+ binding/sensing protein that also interacts with tropomyosin (more soon)

A

troponin

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26
Q

Myosin has “heads” projecting off the filamentous part.

A

myosin atpase (part of head with ability to bind to and hydrolyze/use ATP

27
Q

Heads can bind to the myosin binding sites on actin, forming a _____ (if binding site is uncovered).

A

cross-bridge

28
Q

At “rest,” myosin heads have hydrolyzed ______ and are swiveled back into high-energy conformation.

A

ATP: (holding ADP+Pi)

29
Q

● When ↑[Ca2+], Ca2+ binds to _____.

A

Troponin

30
Q

________ cycle to actually shorten sarcomere:

A

Power Stroke

31
Q

Power stroke cycle steps

A
  1. Myosin head binds to actin.
  2. Myosin head releases Pi, causes swivel from high-energy to
    low-energy conformation.
    -Drags actin—therefore Z-disk—toward M line.
  3. Myosin head releases ADP, binds new ATP.
  4. ATP binding breaks cross-bridge.
  5. Myosin hydrolyzes new ATP, swivels back to high-energy
    conformation.
  6. If Ca2+ still around→go again.
32
Q

To allow relaxation, Ca2+ must get ___from troponin so tropomyosin can cover the myosin binding site again.

A

away

33
Q

How is Ca+2 cleared from cytosol

A

Cleared from the cytosol back into the SR by the SR/ER Ca+2 ATPase

34
Q

is used to measure the contraction of a muscle.

A

Tension

35
Q

2 types of tension:

A
  • Passive and Active Tension
36
Q

Result of stretch in the muscle

A

Passive tension

37
Q

Actin/Myosin Cross Bridges

A

Active tension

38
Q

show the tension a muscle can generate at a given, set length.

A

Length-Tension Curve

39
Q

The length-Tension Curve for passive tension increases as ___ increases

A

length

40
Q

The active tension a muscle can generate relies entirely on the_____.

A

number of myosin heads that can bind to actin

41
Q

What kind of overlap length is required for optimal myosin/actin overlap. generate

A

Medium lengths→optimal myosin/actin overlap→maximum possible

active tension.

42
Q

As length increases, active tension ___, then plateaus at optimal lengths,
then ___.

A

Increases/ decreases

43
Q

is the tension you’d actually measure in a muscle while it’s contracting

A

Total tension

44
Q

How to calculate total tension

A

Total Tension= Active Tension + Passive tension

45
Q

—multiple APs→multiple twitches that happen “on top” of each other→a
stronger contraction.

A

Summation

46
Q

A steady, sustained, maximal contraction in a skeletal muscle resulting from many high-frequency APs

A

Tetanus

47
Q

The “point” of a muscle contraction is to move a _____.

A

load

48
Q

are those where the muscle’s tension is constant, but its length changes

A

Isotonic contraction

49
Q

are those when the muscle builds up tension, but its length never changes

A

Isometric contraction

50
Q

Three different types of skeletal muscle fiber in humans:

A

types I, IIA, and IIX.

51
Q

CHECK FIGURE AND GRAPH PG.20 and 17

A

CHECK FIGURE AND GRAPH PG.20 and 17

52
Q

Every muscle has three fiber types-only the __ changes

A

Ratio

53
Q

How does Myosin ATPase activity and rate of ATP use explain rate of fatigue

A

↑ATPase activity→↑ATP use→↓Time to ATP depletion→↑Fatigability.

54
Q

Why are smooth muscles ‘‘SMOOTH?’’

A

No real myofibrils or organized sarcomeres-just in actin and myosin scattered around.

55
Q

differences between smooth and skeletal muscle—smooth muscle:

A
  • Doesn’t really fatigue (myosin ATPase is really slow).
  • Has small, single-nucleated cells
  • □ Contraction is entirely involuntary—controlled by autonomic nervous system.
56
Q

2 types of smooth muscle?

A
  • Multi unit: Each smooth muscle cell contracts independently
  • Single Unit: Smooth muscle cells connected to each other by gap junctions (Waves of depolarization = Waves of contraction)
57
Q

smooth muscle excitation-contraction coupling

A
  1. AP activates voltage-gated Ca2+ channels.
  2. Ca2+ binds to the Ca2+-sensing protein Calmodulin (CaM)
  3. The Ca2+:CaM complex activates an enzyme called Myosin Light Chain Kinase (MLCK)
  4. The function of MLCK is to phosphorylate myosin heads (aka the myosin “light chain”).
  5. Phosphorylation of myosin heads→↑Myosin ATPase activity→↑Power Strokes and ↑Contraction
  6. To relax, must clear Ca2+ from cytosol back into ECF. Done by Na+/Ca2+ Exchanger and Ca2+ ATPase.
  7. Myosin Light Chain Phosphatase (MLCP) dephosphorylates myosin heads
58
Q

How is AP generated in the smooth muscle?

A
  • Single-unit smooth muscle: generate APs on their own

- Multi-unit smooth muscle get depolarized via Ca+2 channel activation= increasing Ca+2 cytosol

59
Q

Examples of multi-unit smooth muscle

A

Eye Iris ( gets AP from autonomic Neurons )

60
Q

How can

smooth muscles generate their own APs

A

slow-wave depolarization and pacemaker potential

61
Q

Examples of unstable memebrane potential

A

Slow-wave Depolarization and Pacemaker potential

62
Q

Vm drifts around, sometimes reaching threshold and causing an AP, other times not.

A

Slow-wave Depolarization

63
Q
  • Vm is driven upward consistently, causing APs at consistent intervals
A

Pacemaker Potentials

64
Q

Factors that effect smooth muscle

A
  • Hormones that activate Gq-coupled receptors—e.g. oxytocin on oxytocin receptors in uterus—cause contraction.
  • Hormones that activate Gs-coupled receptors—ie. epinephrine on β2 receptors—cause relaxation.
  • Can happen totally independent of membrane potential changes—just need to activate Ca2+ channels.