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Physiology > Muscle Physiology > Flashcards

Muscle Physiology Flashcards

1
Q

Biggest to smallest muscle fibers?

A

(Biggest) Muscle, muscle fascicle, muscle fiber, myofibril, sacrocomere, myofilament aka actin/myosin (smallest)

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2
Q

Actin

A

double stranded **F actin w/ G-actin **where ADP attaches

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3
Q

Tropomyosin

A

Intertwined with actin, lies on top of actin active sites to inhibit contraction

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4
Q

Troponin

A

attached along side of tropomyosin and include subunits I, T, and C.
*itc(y)

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5
Q

Troponin Subunit I

A

ActIn

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6
Q

Troponin Subunit T

A

strong affinity for Tropomyosin

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7
Q

Toponin C subunit

A

strong affinity for Calcium Ca2+ ions

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8
Q

What happens when Ca2+ binds to the troponin complex?

A

Tropomyosin moves and myosin binding sites are exposed.

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9
Q

An action potential travels along/depolarizes a nerve, at the terminal, Ca2+ will go through voltage gated channels stimulating a release of Ach into the synpatic cleft. Ach binds to a receptor on the post synpathic terminal, this causes an influx of …?

A

Sodium, via nicotinic gated channels and then voltage gated channels along membrane.

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10
Q

Sodium influx at the post synaptic cell causes local depolarization that goes where to initiate a muscle contraction?

A

Down the t-tubules and to the sarcoplasmic reticulum.

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11
Q

What is released from the sarcoplasmic reticulum and what does it do next?

A

Ca2+ is released and it binds to troponin to reveal the myosin binding sites. (Scandelous!)

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12
Q

How is Ca2+ pumped back into the sacroplasmic reticulum to stay stored until the next action potential?

A

Ca2+ membrane pump

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13
Q

When the active site is uncovered, what happens?

A

Myosin cross-bridge heads bind and pull actin filament to contract

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14
Q

Fenn Effect

A

In muscle contraction, large amounts of ATP are cleaved to form ADP and Pi.

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15
Q

What is attached to the myosin head when it attaches to the actin (high-energy configuration)?

A

ADP + P

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16
Q

What happens to ADP and P as the power stroke happens?

A

They get released.

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17
Q

How does myosin get released from actin?

A

ATP attaches and it returns to a cocked position
(Low energy configuration)

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18
Q

How does myosin get the ATP –>ADP and Pi

A

ATP Hydrolysis (add water and it releases energy)

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19
Q

Where does the energy from the power stroke come from?

A

Energy stored by the conformational change (myosin binding to actin bond, tilt)

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20
Q

What happens to the tension as the sarcomere shortens?

A

The tension increases. (2.2 micrometers)

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21
Q

At what point does the strength of the contraction (ongoing) rapidly decrease?

A

Further shortening the sarcomere stays at full tension until around 2.0 micrometers, at this point 2 actin filaments begin to overlap as sarcomere lenght continues to decrease to 1.65 micrometers.

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22
Q

Active Tension

A

Increase in tension that occurs during contraction….decreases as muscle is stretched beyond normal length. ATP bound.
*Red

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23
Q

Passive Tension

A

“recoil force”/stretching a rubber band.
Muscle at rest, 2 micrometers, no energy/atp,
*Blue

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24
Q

Total Tension

A

Active + Passive Tension

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25
Q

A stays the same, H/I shorten.
Z-band is a static structure and doesn’t change size.

A
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26
Q

Increasing the load means what for the velocity?
When does the velocity of the contraction becomes zero?

A

Increase load= decrease velocity.
Load equals the max force that the muscle can do.

27
Q

Isometric

A

Muscle remains SAME LENGTH during contraction/relaxation.

28
Q

Isotonic

A

muscle shortens but tension/weight is the same

29
Q

Muscles have both fast and slow twitch fibers, what does a sprinter have?

A

Fast twitch. They are usually bigger people.

30
Q

Marathon runner muscle fiber?

A

Slow fibers

31
Q

Motor Unit

A

All muscle fibers innervated by single nerve fiber

32
Q

Multiple Fiber Summation

A

Increasing # of motor units contracting simultaneously.
Small cuts=big change. OR different motor units are driven asynchronously/alternating by spinal cord.

33
Q

Frequency Summation

A

increasing the frequency of contraction–>tentanization.
As frequency increases, point when each new contraction occurs before the preceding one is over, second is added partially to first= rises progressively, rapid, fused together= TENTANIZATION.

34
Q

An increase in frequence beyond the point of tentanization will have

A

no further effect

35
Q

When the nerve impulse reaches neuromuscular junction, how many vesicles of Ach is released?

A

125 vesicles

36
Q

End plate potential (local)

A

Local.
Caused by sudden influx of sodium ions (bc of ach-gated nicotinic channels)

37
Q

Action Potential

A

Influx of sodium from ach-gated channels, depolarizes across the membrane and then opens the sodium specific voltage gated channels.

38
Q

Where is Ach made?

A

Cytosol of the nerve fiber terminal

39
Q

How is “Ach” reabsorbed?

A

Ach cleave by Acetylcholinesterase into acetate and choline. CHOLINE is reabsorbed actively.

40
Q

Coated pits, made out of what, appear in the terminal nerve membrane? This is when Ach enters the interior of vesicles.

A

Protein Clathrin

41
Q

Sarcoplasmic reticulum has high amounts of what ions? And where does the action potential occur?

A

Calcium , T-tubule

42
Q

What receptor does the action potential encounter first when trying to reach the sarcoplasmic reticulum?

A

DHP
dihydropyridine receptors

43
Q

What are DHP receptors linked to?

A

Ryanodine receptor (RyR) channels, which release Ca2+ out of the SR.

44
Q

How does Ca2+ get back?

A

SERCA
The SarcoEndoplasmic Reticulum Calcium ATPase

45
Q

To store Ca2+ in the sarcoplasmic reticulum, what protein needs to bind to it?

A

Calsequestrin is by far the most abundant Ca(2+)-binding protein in the sarcoplasmic reticulum (SR) of skeletal and cardiac muscle.

It allows the Ca2+ required for contraction to be stored at total concentrations of up to 20mM, while the free Ca2+ concentration remains at approximately 1mM.

46
Q

Multiunit Smooth Muscle

A

Separate smooth muscle fibers, each operating independently. Often innervated by a single nerve ending.

Found in airways to the lungs and large arteries.

47
Q

Unitary Smooth Muscle

A

“Syncytial” smooth muscle/visceral smooth muscle. Mass of connected fibers=single unit. Sheets/bundles.

Found in the walls of hollow organs. Single-unit smooth muscle cells contract synchronously, they are coupled by gap junctions, and they exhibit spontaneous action potential.

48
Q

Describe composition of smooth m. actin filaments?

A

Large number of actin filaments attached to dense bodies, some bonded to each other by intercellular protein bridges. Contraction forces transmitted from one cell to another.

49
Q

In comparison to skeletal/cardiac muscle, how is smooth muscle?

A

Irreguar, prologed tonic contractions, more time, requires less energy, greater maximum force.

50
Q

Upon an influx of Ca+ ions (thru calcium channels or released by SR), what do calcium ions binds REVERSIBLY with?

A

Calmodulin, CaM

51
Q

What does calmodulin-calcium complex join/activates?

A

Myosin Light Chain Kinase (MLCK), a phosphoylating enzyme.

52
Q

What does myosin light chain kinase do?

A

Phosphorylate myosin heads making them** active**. Uses ATP during this conversion too.

53
Q

What is bound to myosin heads making it ready to pull the crap out of actin?

A

ADP and P, which are subsequently released during the power stroke

54
Q

What enzyme dephosphoylates myosin in smooth muscle?

A

Myosin Phosphatase

55
Q

What stimulates smooth muscle contraction?

A

Ach, epinephrine, hormonal stimulation, and muscle stretch.

56
Q

How does norepinephine> & epinephrine stimulate smooth muscle contraction? REVIEW THIS

BAD CARD lol im sorry

A

Noradrenaline/norepinephrine increases the tone of the smooth muscle/contraction of the reticular groove via **alpha-adrenergic receptors **and decreases its tone/relax via beta-adrenergic receptors.

Epinephrine binds both α and β adrenergic receptors to cause vasoconstriction and vasodilation. When activated, the α1 receptor triggers smooth muscle contraction in blood vessels in the skin, gastrointestinal tract, kidney, and brain, among other areas.

Epinephrine = (through IP3 in arterioles) or relaxation (through cAMP in bronchi).cAMP phos MLCK

*Ach causes depolarization in smooth muscle contraction
*Norepinephrine and epinephrine= cause repolarization in smooth muscle contraction

57
Q

Spike Potential

Smooth Muscle

A

Occurs in most types of unitary smooth muscles, can be caused by electrical stim, hormone secretion, trasmitter substances, stretch, spontaneous.

58
Q

Action Potential w/Plateau

Smooth Muscle

A

repolarization is delayed, prolonged contraction, found in ureter,uterus, etc

59
Q

Which as more calcium channels, skeletal or smooth muscle? Sodium?

A

Smooth m has more voltage gated calcium channels, but LESS sodium than skeletal. Ca ions act directly on smooth muscle..

60
Q

Slow Wave Potential

A

Some smooth muscle = self-excitator, associated with basic (slow wave) rhythm of membrane potential. Like the ocean, always waving.
This is bc of a local property of smooth muscles. If the waves get strong enough= action potential.

The Spikes= Action Potentials. These are caused by an influx of Ca+ ions. Repolarization is caused by influx of K+ and eventual closing of Ca channels and closing of K channels to bring it back to stage 1.

Threshold: 40mV. Anything past that is spikes/AP–>contraction.

The more depolarized the resting membrane potential becomes during slow waves, the higher the frequency.

61
Q

Muscle Stretch

A

When visceral smooth muscle is stretch sufficiently, spontneous action potentials are generated.

62
Q

Why can depolarization occur in multi-unit smooth muscle systems w/o generation of an action potential?

A

Local depolarization caused by a neurotransmitter itself spreads over the entire fiber= causes muscle contraction. No action potential needed.

63
Q

Describe the steps in a regular action potential

Physiology (10 decks)

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