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Physiology > 1,3 Phys muscles > Flashcards

1,3 Phys muscles Flashcards

1
Q

SARCOMERE

A

Functional unit of contraction laid down serially (one after another) in the myofibril, extends from Z line to Z line, have thick and thin filaments

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2
Q

Concentric contraction?

A

Shortening; firing enough motor units to cause shortening

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3
Q

Eccentric contraction?

A

Lengthening; less muscle fibers contracting to let gravity lengthen the muscle in a controlled manner

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4
Q

What happens to the I bands, and H zone in a concentric contraction?

A

decreases

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5
Q

What happens in eccentric contraction?

A

A-band does not change, everything else increases

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6
Q

Z-line

A

Distance from; decreases with shortening contraction; is where the actin MEETS in I band

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7
Q

I-band is?

A

Area from end of thick filament to end of thick filament; see ONLY thin filaments, includes z-line

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8
Q

What happens to A-band in contractions?

A

It does NOT change because the length of the thick filament never changes

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9
Q

What is contraction?

A

Is tension generation due to cross bridge cycling, can be a shortening or lengthening of fibers

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10
Q

Thick filaments

A

Myosin, cross bridge heads with ATP binding site and actin binding sites

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11
Q

Thin filaments

A

Actin, tropomyosin, troponin

*globulin actin creates filamentous chains, two filamentous chains wrap together

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12
Q

What does tropomyosin do?

A

Covers the active sites in actin in relaxed muscles, this is where myosin cross-bridge heads bind

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13
Q

What does troponin do?

A

Regulates the movement of tropomyosin molecules on and off the active sites on actin. It binds calcium

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14
Q

What are the 3 binding sites on troponin?

A

Calcium, tropomyosin and actin

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15
Q

What is the calcium binding molecule in skeletal and cardiac muscle?

A

Troponin

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16
Q

What is the calcium binding molecule in smooth muscle?

A

calmodulin

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17
Q

What creates cross-bridges

A

Thick filaments have cross bridge heads and thin filaments have active sites that cross bridge heads bind onto; thus creating a cross-bridge

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18
Q

What is a cross-bridge? How is it involved in contraction?

A

An anchoring point at which the cross bridge heads on the thick filaments ratchet inward on active sites of thin filaments and pull the Z line to the center; this is a shortening contraction

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19
Q

Muscles hierarchy

A

Muscle – muscle fasciculus – muscle fiber or cell – myofibril – sarcomere

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20
Q

What is sarcolemma?

A

Membrane that covers the muscle, has invaginations (that are continuous with sarcolemma) called the transverse tubules

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21
Q

What are the T-tubules?

A

A membrane going down in, action potential race along the sarcolemma are conducted down via t-tubules

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22
Q

Where does the action potential go after sarcolemma?

A

Down t-tubules, signals transduction, sarcoplasmic reticulum

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23
Q

Big function of sarcoplasmic reticulum?

A

Calcium reservoir (especially during periods of relaxation)

24
Q

How does action potential get from t-tubules to sarcolemma?

A

Via signal transduction

25
Q

Where does the sarcoplasmic reticulum release Ca?

A

Into the sarcomere (into cytosol), which then binds troponin, troponin shifts tropomyosin and you can get cross bridge interaction

26
Q

High calcium concentration=

A

Activated muscle

27
Q

Low cytosolic concentration=

A

Relaxed muscle

28
Q

Order of events for cross-bridge binding? MUST KNOW

A

1) Low cytosol, relaxed muscles
2) Calcium dumped into cytosol from sarcoplasmic reticulum, activating muscle
3) Ca binds troponin causing,
4) Tropomyosin to shift
5) This opens up actin active sites
6) Myosin heads will now bind to active sites (due to high affinity)
7) Myosin heads ratchet inward pulling the THIN filament

29
Q

Thin or thick filament moves?

A

thin

30
Q

Events of cross bridge cycling?

A

1) Binding, engagement of actin
2) Release of ADP and inorganic phosphate; This causes power stroke
3) ATP binds to myosin again, head detaches due to lost affinity
4) ATP hydrolysis again, repeat

31
Q

What causes the power stroke?

A

The release of ADP and Pi

32
Q

What causes myosin to lose affinity for actin?

A

Binding of ATP, disengages the active site

33
Q

What are the products of ATP hydrolysis?

A

ADP and Pi

34
Q

Explain rigor mortis

A

Soon after death, muscles become rigid because the ATP machinery stops functioning. You need that ATP to stimulate that disengagement of the actin active site

35
Q

Do muscles after death/rigor mortis ever loosen up?

A

Yes. 24-48 hours after death on temperature bc proteolytic enzymes start breaking up the proteins

36
Q

Motor neuron steps (action potential)

A

1) Motor neuron action potential
2) Ca enters voltage gated channels
3) Acetylcholine release
4) Na entry
5) Local current between depolarized end plates and adjacent muscle plasma membrane
6) Muscle fiber action potential
7) Propagation action potential in muscle plasma membrane acetylcholine degradation

37
Q

Point of action potential?

A

To release the neurotransmitter

38
Q

The neurotransmitter in skeletal muscles?

A

Acetylcholine

39
Q

Nicotinic receptor has the receptor for what to bind?

A

Acetylcholine

40
Q

What is the motor end plate?

A

The area of synapse between the motor neuron and skeletal muscle

41
Q

What is found at the motor end plate? They are part of?

A

Nicotinic receptor that binds acetylcholine, simple translocation channel protein (so when acetylcholine binds, the nicotinic receptor pops open and Na can come in WHICH DEPOLARIZES the area)

42
Q

What is the end plate potential?

A

The depolarization from Na coming in and acetylcholine leaving the end plate

43
Q

So what happens if the end plate depolarizes enough?

A

You get action potential that race along the sarcolemma

44
Q

What does acetylcholinesterase do? Released by?

A

Releases by muscle; Breaks down acetylcholine into an acetate choline so it can no longer stimulate the muscle

45
Q

Signal transduction from t-tubule to sarcoplasmic reticulum?

A

1) Depolarization of t-tubule
2) Activation of dihydropyridine receptor
3) Activation of ryanodine receptor
4) Opening of Ca channel
5) Release of Ca from SR to cytosol

46
Q

Ryanodine receptor is physically a part of? Does what?

A

A Ca+ channel protein on the sarcoplasmic reticulum; therefore, it OPENS Ca channel and there is an efflux/free diffusion of Ca

47
Q

***skeletal muscle contraction requires?

A

Neural stimulation!

48
Q

SIDENOTE: In cardiovascular your must have what SPECIFIC order?

A

1) Membrane depolarization leading to
2) Muscle contraction leading to
3) Pressure generation leading to
4) Blood ejection

49
Q

Nicotinic acetylcholine receptors are _____ gated receptors?

A

ligand

50
Q

Myastenia gravis is?

A

An autoimmune disorder in which the body’s immune system recognizes proteins that make up the acetylcholine-gated receptor complex as foreign, thus initiating an immunological attack on those proteins

51
Q

Myastenia gravis results in loss of?

A

oss of Ach-gated receptors and nerve to muscle signaling ability; leads to muscle weakness

52
Q

Myastenia gravis treatment?

A

Anti-acetylcholinesterase drugs

53
Q

H zone

A

Subdivision of A band where there is ONLY thick myosin

54
Q

I band

A

Thin (actin) only, lighter area

55
Q

A band

A

Actin and myosin area of overlap (BOTH thin and thick filaments). Does not shrink during contraction

56
Q

How do you remember Actin is thin?

A

actIN thIN = I band

Physiology (42 decks)

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