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S1B5: Physiology > Skeletal Muscle > Flashcards

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
Q

Write down the qualities of one type of muscle fiber

A
26
Q

What is the size principle?

A

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

S1B5: Physiology (5 decks)

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