Skeletal Muscle Flashcards

1
Q

Identify the sections of the Sarcomere

A
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2
Q

What are the major components of the Thin filament?

A
  • Actin: 2 strands F actin in a helix
  • Tropomyosin: in parallel with acitn strand
  • Troponin: aligned with tropomyosin
    • Troponin T: binds troponin to tropomyosin
    • Troponin I: physically blocks the interaction between myosin and actin
    • Troponin C: binding site for Ca2+ initiates contraction
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3
Q

What is the name for the midpoint of myosin?

A

M line = midpoint myosin & projects in both directions to interact with the actin

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4
Q

What happens to the length of the A band during contraction?

I band?

A

A band does not shorten (just myosin)

I band shortens b/c as the overlap between thin and thick filaments increases, the section of only thin filament shortens

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5
Q

What is the name of the protein that

  1. connects Z line to M line and acts as “spring”, contributing to passive elasticiyt of muscle; centers the A band
  2. runs from Z line along the actin filament; stabilizes actin
  3. connects actin filaments to Z disc
  4. large structural molecule tha tconnects actin filaments to beta dystroglycan in sarcolemma by syntrophins
    • associted w/ transmembrane sarcoglycans alpha, beta, gamma and delta
    • provides structural scaffold for myofibrils
A
  1. Titin (connectin)
  2. Nebulin
  3. alpha-actinin
  4. Dystrophin
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6
Q

What disease can result from disruption of the dystrophin-glycoptorein complex?

A

Muscular dystophy

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7
Q

What is the name of the process by which electrical activation of the muscl leads to contraction adn mechanical work?

A

Excitation-contraction coupling

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8
Q

What neurotransmitted is released to the pre-synaptic membrane? What type of receptor is located here?

What neurotransmitted is released to the post synaptic membrane of skeletal muscle?
What type of receptor is located here?

A

Pre synaptic: ACh to N1 (Nm)

Post synaptic: ACh to N1 (Nm)

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9
Q

What happens to the excess ACh after the synapse?

A

it is rapidly degraded and cleared

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10
Q

What is the muscle membrane potential?

What neurotransmitter elicits an action potential?

How long is the duration of the action potential?

How long is the duration of the contraction?

A

-90mV

Acetylcholine

Action potential: 3-5ms

Contraction: 20-100 ms

muscle cells have short refractory period

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11
Q

What are the invagination of the sarcolemma into the muscle?

What is the purpose of these structures?

What structures are located on either side of these invaginations?

A

T tubules

permits rapid transmission of action potentials into the muscle

Terminal cisternae

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12
Q

What is the name of the receptors located inside the T-tubule ?

What sarcoplasmic reticulum receptor do they directly interact with? What is the impact of this?

A

(calcium sensitive) DHPR (dihydropyridine receptors)

Ryanadine receptor, which opens a channel to allows calcium to enter the intracellular space

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13
Q

What happens to the Ca2+ once it is released from the sarcoplasmic reticulum?

A

it binds ot troponin C, weakens the interaction between troponin I and actin, and causes a conformational change that moves the troponin-tropomyosin complex

which uncovers the actin binding site & allows formation of actin-myosin cross-bridges

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14
Q

Describe the cross-bridge cycle

What if there is no ATP?

A
  • Formation cross-bridge causes Pi to be released, followed by ADP
    • which results in conformational change in the myosin head that causes movement of the thin filament relative to myosin in “power stroke”
    • ATP binds to the free site & causes detachment of myosin head
    • ATP is hydrolyzed to Pi adn ADP causing the myosin head to “re-cock”

With not ATP there is no release of hte actin/myosin crossbridge

this result in Rigor Mortis (muscles stiff)

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15
Q

What is the name of the transporter responsible for the quick Ca2+ uptake by the sarcoplasmic reticulum?

What happens as intracellular calcium levels begin to drop?

What happens if Ca2+ transport into the SR is inhibited?

A

SERCA

Ca2+ detaches from Troponin C ending the actin-myosin interaction

If Ca2+ is inhibited, the muscle remains in “contracture”

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16
Q

What are the components of the parallel elastic elements?

What are the components of the series elastic elements?

A
  • Parallel: sarcolemma, intracellular components, connective tissue
  • Series: tendons and regions within myosin
17
Q

What changes during internal shortening?

What changes during external shortening?

A

internal: contractil elements
external: muscle itself

18
Q

What happens when sarcomere length is increased?

What about increasing muscle length?

A

it increases developed tension; peak tension is achieved at optimal sarcomere length

increasing muscle length increases both passive tension and active tension to a maximum. However, after a certain length, active tension decreases as you move past optimal sarcomere length.

19
Q

What measure is the same for all loads?

What measure changes as sarcomere length changes?

A

“max velocity” of shotening (Vmax) is the same for all loads

the rate of shortening is higher as you are at a more optimal sarcomere length compared to shorter sarcomere lengt; Optimal length for force production is related to actin-myosin overalp

20
Q

What must happen to achieve external shortening?

what increases as load increases?

A

the deveoped tension must exceed the elastic elements

sarcomere length increases as load increases

21
Q

Identify the following types of contractions

  1. single contractile event
  2. no external shortening; the load is greater than the ability ot create tension (velocity = zero)
  3. external shortening; the load is less than the ability to create tension
  4. muscle contraction wiht external lengthening
A
  1. Twitch contraction
  2. Isometric contraction
  3. Isotonic contraction (concentric contraction)
  4. eccentric contraction
22
Q

What is the definition of a motor unit?

A

a single alpha motot neuron adn all the muscle fibers it innervates

one action potential in the motor neuron will elicit contraction in all muscle fibers in the motor

  • small motor unit: smaller alpha motot neurons and fewer muscle fibers; less force
  • large motor unit: larger alpha moto neurons with more and larger muscle fibers; progressively more force
23
Q

With relation to EPSPs at the motor neuron cell body, what is it called to increase the number of inputs? What is it called to increase the frequency of inputs?

A
  • Spatial summation: increased number of inputs
  • Temporal summation: increased frequency of inputs
24
Q

What happens with increasing frequency of stimulation?

A

temporal summation

as rate of contraction icnreases, there is still Ca2+ in the cytosol, which results in greater contractile force

muscle doesn’t fully relax before next stimulation

can be incomplete or complete (fused) tetany

25
Write down the qualities of one type of muscle fiber
26
What is the size principle?
As CNS inputto motor neurons increases, motor units are recruited in an ordered manner form smallest to largest, and force development increases progressively * asynchronous recruitment * permits development smooth, graded increases in muscle tension