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Biomedical Physiology > Muscle Physiology > Flashcards

Muscle Physiology Flashcards

1
Q

anchors entire myofibril array to cell membrane

A

Dystrophin

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2
Q

nebula

A

spans the entire length of the this filament; thought to measure correct length of filament and appropriately hold the thin filament, cutting the thin filament to the right length, acts like a ruler

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3
Q

Attaches the thick filaments to the Z line and holds it apporpriately in the myofibril.
Stabilizes both thin and thick filaments.
Connects the Z line to the M line, has elasticity to maintain sarcomere shape

A

Titin

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4
Q

Actin is present as what two different morphologies?

A

G-actin - monomeric, globular

F-actin - strands, filamentous, the helical structure with myosin binding sites

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5
Q

Not attached to actin, but runs along the groove of actin, held in place by troponin

A

tropomyosin

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6
Q

globular, at the end of each tropomyosin, has a binding site for Ca++, block the binding site on actin for myosin

A

troponin

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7
Q

What are the three components of troponin?

A

TnT - binds to tropomyosin
TnI - binds it to actin
TnC - binds Ca++

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8
Q

Type I muscle fibers

A

Slow Oxidative “SO”
contract slowly and relax slowly
resistant to fatigue
predominate in antigravity muscles, such and the back and buttocks

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9
Q

Why are type I (and type II to some some extent) reddish in pigment?

A

myoglobin, related to hemoglobin and stores O2

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10
Q

What does “oxidative” mean when referring to muscle types?

A

Oxidative means mitochondria are present, there are many mitochondria in SO muscle (type I)

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11
Q

Type IIa muscle fibers

A 
"fast oxidative"
contract and relax quickly
fairly resistant to fatigue
some mito
use much ATP
contain some myoglobin
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12
Q

Type IIb muscle fibers

A 
"fast glycolytic"
very fast contractions
fatigue easily
not many mito
white in appearnace bc they lack much myoglobin
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13
Q

How does myosin itself contribute to strength of contraction?

A

Therefore, the greater the number of cross-bridges in contact with the actin filament at any given time, the greater the force of contraction.Therefore, the greater the number of cross-bridges in contact with the actin filament at any given time, the greater the force of contraction.

Hall, John E.. Guyton Physiology : Guyton and Hall Textbook of Medical Physiology (12th Edition). Saint Louis, MO, USA: Elsevier - Health Sciences Division, 2010. ProQuest ebrary. Web. 4 February 2016.
Copyright © 2010. Elsevier - Health Sciences Division. All rights reserved.

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14
Q

What is the ratchet theory (or walk along) of contraction?

A
  1. Before contraction begins, the heads of the crossbridges bind with ATP. The ATPase activity of the myosin head immediately cleaves the ATP but leaves the cleavage products, ADP plus phosphate ion, bound to the head. In this state, the conformation of the head is such that it extends perpendicularly toward the actin filament but is not yet attached to the actin.
  2. When the troponin-tropomyosin complex binds with calcium ions, active sites on the actin filament are uncovered and the myosin heads then bind with these, as shown in Figure 6-8.
  3. The bond between the head of the cross-bridge and the active site of the actin filament causes a conformational change in the head, prompting the head to tilt toward the arm of the cross-bridge. This provides the power stroke for pulling the actin filament. The energy that activates the power stroke is the energy already stored, like a “cocked” spring, by the conformational change that occurred in the head when the ATP molecule was cleaved earlier.
  4. Once the head of the cross-bridge tilts, this allows release of the ADP and phosphate ion that were previously attached to the head. At the site of release of the ADP, a new molecule of ATP binds. This binding of new ATP causes detachment of the head from the actin.
  5. After the head has detached from the actin, the new molecule of ATP is cleaved to begin the next cycle, leading to a new power stroke. That is, the energy again “cocks” the head back to its perpendicular condition, ready to begin the new power stroke cycle.
  6. When the cocked head (with its stored energy derived from the cleaved ATP) binds with a new active site on the actin filament, it becomes uncocked and once again provides a new power stroke.

Hall, John E.. Guyton Physiology : Guyton and Hall Textbook of Medical Physiology (12th Edition). Saint Louis, MO, USA: Elsevier - Health Sciences Division, 2010. ProQuest ebrary. Web. 4 February 2016.
Copyright © 2010. Elsevier - Health Sciences Division. All rights reserved.

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15
Q

What is ATP needed for during muscle contraction?

A

1) The walk along of the myosin head against the actin filament
2) Ca++ pumps to relive sarcoplasm from xs Ca++. Pumped back into the sarcoplasmic reticulum and terminal cisternae.
3) Na+/K+ pumps to reestablish RMP after AP

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16
Q

So, ATP is the currency of muscle contraction, but where does that come from?

A

Muscle stores (1-2sec), rephosphorylation by PCr(5-8 sec), Glycolysis (1 min) and glycogen breakdown, oxidative metabolism (2-4 hours, 95% of muscle source of ATP)

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17
Q

If you have a muscle that needs fine motor control, what will the motor unit look like?

A

Motor unit will be one neuron to 3-4 muscle cells. Muscle that only do groos movements will be 1 neuron to ~100 muscle fibers

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18
Q

What are the two types of increasing force of muscle contraction?

A

multiple fiber summation/recruitment/motor unit summation
AND
temporal summation/frequency summation/wave summation

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19
Q

Where is ACHase located?

A

synaptic cleft

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20
Q

SNARE complex:

Which protein is found attached to the vesicle?

A

synaptobrevin and synaptotagmin (Mendonca said that synptotagmin was not on the vesicle)

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21
Q 
SNARE complex:
Which protein(s) are associated with the plasma membrane of the neuron? [facing inward]
A

syntaxin and SNAP25

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22
Q

SNARE complex:

What ion causes synaptobrevin, syntaxin, and SNAP25 to intermigle with each other?

A

Ca++

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23
Q

SNARE complex:

Which ion associates with which protein (where) to finish off exocytosis of NT?

A

Ca++, synaptotagmin on vesicle membrane

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24
Q

What happens when the ACH gated CG Na+ channels open?

A

As shown in Figure 7-3 B , the principal effect of opening the acetylcholine-gated channels is to allow large numbers of sodium ions to pour to the inside of the fiber, carrying with them large numbers of positive charges. This creates a local positive potential change inside the muscle fiber membrane, called the end plate potential. In turn, this end plate potential initiates an action potential that spreads along the muscle membrane and thus causes muscle contraction.
Hall, John E.. Guyton Physiology : Guyton and Hall Textbook of Medical Physiology (12th Edition). Saint Louis, MO, USA: Elsevier - Health Sciences Division, 2010. ProQuest ebrary. Web. 4 February 2016.
Copyright © 2010. Elsevier - Health Sciences Division. All rights reserved.

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25
Q

How does curare work?

A

COMPETITIVE INHIBITOR

blocks the gating action of acetylcholine on the acetylcholine channels by competing for the acetylcholine receptor sites.
Hall, John E.. Guyton Physiology : Guyton and Hall Textbook of Medical Physiology (12th Edition). Saint Louis, MO, USA: Elsevier - Health Sciences Division, 2010. ProQuest ebrary. Web. 7 February 2016.
Copyright © 2010. Elsevier - Health Sciences Division. All rights reserved.

It attaches to the ACH receptor but does not cause an action potential. Works postsynaptically. “nondepolarizing blocker” TUBADIL

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26
Q

Myasthenia graves

A

autoimmune disease where antibodies attack postsynaptic Ach receptors
neostigmine is drug to treat, Neostigmine inhibits Achase, leving more Ach in the synaptic cleft than usual, overwhelming the weak Ach receptors, allowing them to function normally

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27
Q

What is the resting membrane potential of muscle cells?

A

-80 to -90 mV

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28
Q

Is the fluid in the T-tubule ECF of ICF?

A

extracellular fluid, they are internal extensions of the cellular membrane

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29
Q

Where is the DHP receptor?

A

T-tubule

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30
Q

Where is the ryanodine receptor?

A

Terminal cisternae

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31
Q

Which drugs are Achase inihbitors?

A

physostigmine, neostigmine, insecticides (organophosphates), nerve gases

These increase the half life of ACH

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32
Q

Succinylcholine (ANECTINE)

A

binds to ACH receptors and allows 1 AP, then blocks it, “depolarizing blocker” used to relax pharynx in a surgical situation

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33
Q

What pathology is caused by a sensitivity to Succinylcholine/suxamethonium?

A

malignant hyperthermia, the SR RyR get locked open, and Ca++ is uncontrollably released. Normally the DHP would plug the RyR as soon as the AP left, but not the case here.

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34
Q

Botox

A

a toxin produced by C. botulinum that blocks the release of NT on the presynaptc side of the cleft, interferes with the SNARE complex

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35
Q

Tetanus toxiod

A

interferes with inhibitory neurons in the CNS, interferes with GABA secretion that inhibits pathways to muscle secretion

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36
Q

muscel relaxers

A

inhibition of CNS neurons that control skeletl muscle contraction

37
Q

The part of the A band that only contains thick filaments

A

H zone

38
Q

The part of the muscle fibril that is only thin filaments and titin

A

I band

39
Q

Muscle fibril:

zone where thick filaments and thin filaments overlap

A

A band

40
Q

The region within the H zone within the A band where the thick filaments link together

A

M line

41
Q

The area that joins two sarcomeres, defines the limits of one sarcomere

A

Z line

42
Q

from Z line to Z line

A

sarcomere

43
Q

What gets smaller when a muslce contracts?

A

Sarcomere (z line to z line)

I band, H zone

44
Q

How do you know if the Nernst potential is positive or negative?

A

the sign of the potential is positive (+) if the ion diffusing from inside to outside is a negative ion, and it is negative (−) if the ion is positive.

Hall, John E.. Guyton Physiology : Guyton and Hall Textbook of Medical Physiology (12th Edition). Saint Louis, MO, USA: Elsevier - Health Sciences Division, 2010. ProQuest ebrary. Web. 7 February 2016.
Copyright © 2010. Elsevier - Health Sciences Division. All rights reserved.

45
Q

A positive ion flow from inside to outside causes _____ within the membrane.

A negative ion flow from inside to outside the membrane causes _______ within the membrane.

A negative ion flow from outside to inside the membrane causes _______ within the membrane.

A positive ion flow from outside to inside the membrane causes _______ within the membrane.

A

electronegativity

electropositivity

electronegativity

electropositivity

46
Q

In which direction does the Na+/K+ pumps send those ions?

A

Na out, K in

47
Q

In addition to the large proteins on the inside of the cell that contribute to the overall negative charge, what other part of membrane dynamics adds to this effect?

A

3 Na+ out for every 2 K+ in, overall more positives outside

48
Q

What are the main players in maintaining RMP?

A

K leak channels, Na leak channels, K+/Na+ ATPase pump

49
Q

What are the main players in AP?

A

voltage gated Na and voltage gated K

50
Q

What drug and what toxin blocks the voltage gated Na channels?

A

lidocaine, tetrodotoxin and saxitoxin

51
Q

Absolute refractory period

A

is the period during which another action potential cannot be elicited, no matter how large the stimulus.
■ coincides with almost the entire duration of the action potential.
■ Explanation: Recall that the inactivation gates of the Na+ channel are closed when the membrane potential is depolarized. They remain closed until repolarization occurs.
No action potential can occur until the inactivation gates open.

52
Q

relative refractory period

A

begins at the end of the absolute refractory period and continues until the membrane potential returns to the resting level.
■ An action potential can be elicited during this period only if a larger than usual inward current is provided.
■ Explanation:TheK+conductanceishigherthanatrest,andthemembranepotentialis closer to the K+ equilibrium potential and, therefore, farther from threshold; more inward current is required to bring the membrane to threshold.

53
Q

What is an example of a ligand gated receptor?

A

Nicotinic receptor for Ach at NMJ

54
Q

excitatory neurotransmitters

A

ACh, norepinephrine, epinephrine, dopamine, glutamate, and serotonin.

55
Q

inhibitory neurotransmitters

A

GABA and glycine

56
Q

Drugs/toxins that work centrally

A

tetanus (GABA secretion that inhibits in pathways to muscle contraction, inhibitory neurons) Muscles are in isometric contraction, causes too much excitement, spastic contractions

muscle relaxers - fexeril, skelaxin, soma

57
Q

VR K+ channel blocker

A

Dendrotoxin, blocks K, makes it hard to depolarize, found in mamba snakes, agonist to contraction

58
Q

Neurotransmitter release inhibitor

A

works pre-synaptically

BOTOX

59
Q

Neurotransmitter release agonist

A

black widow spider venom (alpha -latrotoxin), causes massive release of Ach, this massive release of NT causes the Na channels to open without closing, massive depolarization

60
Q

Synaptic cleft drugs

A 
Ach-ase inhibitors, increase the half life of Ach, a good way to treat myesthenia graves
the "stigmines"
neostigmine 
physostigmine
ESERINE
organophosphates
war gases

In normal patients, causes convulsions

61
Q

CR Na channel blocker/ aka Ach receptor blocker

A

Curare(TUBADIL, D-tubocurare) blocks the Ach receptor. Works post-synaptically, non-depolarizing blocker

Succinylcholine (ANECTINE, SUXAMETHONIUM), binds to CR Na channels, allows 1 AP, then blocks the channel

62
Q

How would you reverse the effects of suxamethonium?

A

neostigmine(physostigmine)

63
Q

CR Na channel AGONIST

A

nicotine, binds to CG NA nuerotransmitter receptor aka nicotinic receptor, is a mimetic drug of Ach

64
Q

What is the cell ID glycocalyx?

A

glycoprotein

65
Q

Water can traverse the phospholipid bilayer

A

TRUE, lil breaks in the surface

66
Q

VG Ca++ channels are found at the

A

terminal cisternae (80% of Ca++ comes from here) and the sarcolemma (only a few in the sarcolemma) and the motor end plate

67
Q

tropomyosin binds

A

troponin

68
Q

multi-unit smooth muscle

A

each cell is innervated by one motor neuron, iris of the eye, arrector pili, blood vessel SM

69
Q

unitary smooth muscle

A

syncytial or visceral or single unit, arranged in sheets or bundles, connected by gap junctions which transmit ion signal

70
Q

Does smooth muscle have troponin?

A

NOPE, they also do not have RyR

71
Q

What is the ratio of thin to thick filaments in smooth muscle?

A

12-15 thin: 1 thick

72
Q

In smooth muscel, actin is attached to

A

intermediate filaments

73
Q

calcium-calmodulin mechanism of contraction

A
  1. The calcium ions bind with calmodulin.
  2. The calmodulin-calcium initiars a protein kinase cascade allowing myosin kinase to be P, complex then joins with and activates myosin light chain kinase, a phosphorylating enzyme.
  3. One of the light chains of each myosin head, called the regulatory chain, becomes phosphorylated in response to this myosin kinase. When this chain is not ­ phosphorylated, the attachment-detachment cycling of the myosin ­ head with the actin filament does not occur.But when the regulatory chain is phosphorylated, the head has the capability of binding repetitively with the actin filament and proceeding through the entire cycling process of intermittent “pulls,” the same as occurs for skeletal muscle, thus causing muscle contraction.
74
Q

the latch

A

prolonged muscle contraction with little energy expenditure in smooth muscle

75
Q

Voltage gated K channels are found at

A

Nodes of Ranvier
Sarcolemma
T tubules

76
Q

Myosin is fitted how into the sarcomere?

A

Titin attaches it to the Z disc, the M line in the A band is the atttachment in the middle

77
Q

Which is reponsible for the termination of Ca++ release into the muscle fiber ICF?

A

The DHP receptor uncorks the RyR and lets the Ca++ flow out. The DHP chnages conformation and plugs it back after the action potential has passed.

78
Q

Does anaerobic metabolism occurs ONLY in oxygen debt?

A

no, can run when oxygen is present

79
Q

Does smooth muscle have tropomyosin?

A

yes, but no troponin

80
Q

Are dense bodies anchored to actin or intermediate filaments?

A

intermediate filaments

81
Q

What is the actin of smooth muscle attached to?

A

intermediate filaments and myosin

82
Q

Is the spread of Ca++ slow or fast in smooth muscle?

A

slow

83
Q

Why is Ca++-calmodulin binding to myosin light chain kinase important anyway?

A

MLCK phosphorylates light chains in the myosin heads and increases myosin ATPase activity

84
Q

Smooth muscel cells

A

can occur in sheets because of gap junctions

85
Q

What causes the myosin head to act as an ATPase?

A

binding the myosin binding site, when the P splits off, the myosin to do the power stroke

86
Q

After the power stroke what happens?

A

lose the ADP, bind another, new ATP

When it gains a new ATP, it releases the actin, this ATP is what generates the next power stroke

87
Q

How does the ADP in the myosin head become ATP in smooth muscle?

A

myosin light chain kinase

88
Q

light chain myosin phosphatase

A

this is what gets rid of the phosphate from the kinase, always there, once MLCK is dephosphorylated, the contraction stops, LCMP and MLCK are in titration competition between each other

89
Q

In smooth muscle, what is the default mechanism?

A

might chain myosin phosphatase

Biomedical Physiology (14 decks)

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