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Intro Bio II Exam 2 > Muscle > Flashcards

Muscle Flashcards

1
Q

Striated muscles

A

Skeletal, cardiac

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2
Q

Multinucleated muscles

A

Skeletal only

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3
Q

Motor unit

A

Group of muscle fibers that function together and the somatic motor neuron that controls them. All muscle fibers in a motor unit are of the same type and this is determined by the somatic neuron during development. Motor units can contain as little as a few fibers. All fibers in the same motor unit fire together and are of the same fiber type.

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4
Q

Antagonistic muscle pairs

A

Ex: bicep & tricep; skeletal muscles largely exist in antagonistic pairs

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5
Q

Muscle origin

A

Part of the muscle closest to the trunk or more stationary

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6
Q

Muscle insertion

A

Part of the muscle that is more distal or mobile

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7
Q

Ligaments

A

Connect two bones

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8
Q

Tendons

A

Connect muscle to bone

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9
Q

Muscle “growth”

A

Satellite cells are muscle stem cells that contribute extra nuclei to skeletal muscles for muscle “growth”

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10
Q

Components of the sarcomere

A

Sarcomere = basic structural unit of skeletal muscle

Myofibrils are made up of back to back sarcomere.

Sarcomere is composed of thick (myosin) and thin (actin) filaments. Thick filaments are stabilized by titin and nebulous helps align actin filaments.

Each end of the sarcomere is the Z disk. The center of the sarcomere is the M line.

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11
Q

Sliding filament theory

A

Thick and thin filaments slide past each other in muscle contraction shortening the distance between the M line and Z disk. The myosin heads form crossbridges with actin of the thin filament.

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12
Q

Function of the t-tubule

A

Brings action potentials into the interior of the muscle fiber

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13
Q

Protein that blocks myosin-actin binding sites

A

Tropomyosin

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14
Q

Protein that sits atop tropomyosin and moves tropomyosin when bound to Ca2+

A

Troponin

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15
Q

Relationship between myosin and actin in the relaxed state

A

Myosin head is cocked and weakly bound to actin

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16
Q

Relationship between myosin and actin in power stroke

A

Myosin is bound strongly to actin causing actin filament to move in power stroke

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17
Q

Events that lead to the firing of an AP at the neuromuscular junction

A

Somatic neuron releases ACh which binds to ligand-gated Na+ channels in sarcolemma of motor end plate. Na+ flows into the cell, depolarizing it and causing more voltage-gated Na+ channels to open. Further depolarization causes an AP which travels down the t-tubule to the DHP (dihydropyridine L-type calcium channel).

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18
Q

How does an AP lead to an increase in [Ca2+] in the cytosol?

A

DHP is stimulated by the AP to “tug” on RyR (ryanodine receptor-channel) which causes the release of Ca2+ from the sarcoplasmic reticulum. Ca2+ then binds to troponin and muscle contraction begins.

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19
Q

What causes a decrease in [Ca2+] in the cytosol which allows the muscle fiber to relax?

A

Sarcoplasmic Ca2+-ATPase pumps Ca2+ back into the sarcoplasmic reticulum

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20
Q

What occurs during the latent period between muscle fiber AP and development of tension during muscle twitch?

A

Ca2+ releases, binds to troponin, troponin moves tropomyosin

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21
Q

Types & causes of muscle fatigue

A

CNS fatigue - largely psychological
PNS fatigue - failure of excitation-contraction coupling, acidosis, elevated inorganic phosphate slows release of inorganic phosphate from myosin or binds to Ca2+, ion imbalances which change sodium potassium pump activity

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22
Q

Ways that muscle cells make ATP

A

Substrate-level phosphorylation using creative phosphate
Oxidative phosphorylation
Substrate-level phosphorylations of glycolysis

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23
Q

Slow twitch vs fast twitch

A

Slow - oxidative ATP synthesis which is slower but generates more ATP, requires more oxygen so more vascularized & contains more myoglobin, smaller diameter allows more efficient oxygen diffusion

Fast - glycolytic & creative ATP synthesis which is faster but generates less ATP, not dependent on oxygen so not as vascularized/lighter in color b/c less myoglobin/ larger diameter due to glycogen stores; fatigues more quickly

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24
Q

Fastest source of energy in the muscle fiber

A

ATP and CP stores

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25
Q

Intermediate source of energy in the muscle fiber

A

ATP from glycolysis

26
Q

Slowest but most sustainable source of energy in the muscle fiber

A

ATP from oxidative phosphorylation

27
Q

In which type of muscle fiber would you expect to find more mitochondria?

A

Slow-twitch

28
Q

Which type of muscle fiber do you expect to undergo glycolytic then oxidative phosphorylation as energy needs continue?

A

Fast-twitch oxidative-glycolytic (intermediate)

29
Q

Which muscle fibers are most easily fatigued?

A

Fast-twitch

30
Q

Why does too much actin/myosin overlap result in reduced fiber tension?

A

TBD

31
Q

Why does too little actin/myosin overlap result in reduced fiber tension?

A

Too few crossbridge linkages to generate much force

32
Q

Muscle twitches can undergo ______ summation

A

Temporal (not spatial)

33
Q

What determines how long a muscle is contracted?

A

[Ca2+] is continually high in the cytosol

34
Q

Tetanus & difference between infused and complete tetanus

A

Tetanus - Continuous maximum muscle tension

Unfused - brief moments of slight relaxation occur during this period
Complete - no relaxation - complete maximum tension until muscle fatigue causes the muscle to lose tension despite continuing stimuli

35
Q

How to lift heavy :)

A

Recruit more motor units

36
Q

Isotonic vs isometric contractions

A

Isotonic - muscle contracts, shortens, and creates enough force to move a load

Isometric - muscle contractions, does NOT shorten, force does NOT move the load

Elastic tendons compensate for muscle shortening in isometric contractions

37
Q

Types of smooth muscle + examples

A

Phasic that is usually relaxed; ex: esophagus
Phasic that cycles between contraction and relaxation; ex: intestine

Tonic that is usually contracted; ex: sphincter
Tonic that contracts variably; ex: vascular smooth muscle

38
Q

Contracted smooth muscle appears _____

A

Bulky instead of shortened

39
Q

Why are single unit smooth muscle cells connected by gap junctions?

A

Allows the signal from the autonomic neuron varicosity to travel between cells so they all contract as a unit. Ex: small intestine

40
Q

Why are multi-unit smooth muscle cells electrically independent?

A

Each cell can be stimulated independently which allows for more precise movements. Ex: eye

41
Q

Which muscle cells have the longest contraction-relaxation cycle?

A

Smooth (then cardiac, and skeletal is fastest)

42
Q

Slow wave potential vs pacemaker potential

A

Periodic subthreshold depolarization which may eventually reach threshold causing an AP

Periodic suprathreshold depolarization which causes an AP to fire every time. Present in cardiac and smooth muscle cells.

43
Q

Steps involved in smooth muscle contraction

A
  1. Signal arrives for Ca2+ to enter the cell (vague, but roll with it)
  2. Entry of Ca2+ initiates release from the SR (aka calcium spark)
  3. Ca2+ binds to calmodulin
  4. Calmodulin activates MLCK (kinase)
  5. MLCK phosphorylates the myosin head and increases myosin ATPase activity
  6. Crossbridge cycling is enabled
44
Q

How does smooth fiber myosin differ from skeletal fiber myosin?

A

Smooth fiber myosin does not have an ATP binding site

45
Q

Why does smooth muscle have lower ATP requirements than skeletal muscle?

A

TBD

46
Q

Troponin exists in which muscle fiber types?

A

Skeletal and cardiac, not smooth

47
Q

Steps involved in smooth muscle relaxation

A
  1. Ca2+ is removed from the cytosol by: a) primary active transport into SR, b) primary active transport into ECF, c) secondary active transport using Na+ gradient into ECF
  2. Ca2+ is released from calmodulin (law of mass action)
  3. MLCK activity decreases
  4. MLCP removes phosphates from myosin heads and decreases myosin ATPase activity
  5. Cross-bridge cycling decreases
48
Q

Why do cardiac muscle cells have larger t-tubules?

A

Spread the depolarization faster

49
Q

Why do cardiac muscle cells have intercalated disks?

A

Contain demsmosomes and gap junctions which help in cell-to-cell communication and thus coordinated muscle contraction and provide mechanical strength to the small cardiac fibers

50
Q

Why do cardiac muscle cells have smaller SR?

A

Some Ca2+ comes from outside of the cell

51
Q

Pacemaker cells

A

A patch of cells independent of the CNS which fire action potentials at a given rate and depolarize the cardiac fiber

52
Q

Process of excitation-contraction coupling in cardiac muscle

A
  1. Depolarization/Na+ entry —> fires AP
  2. Depolarization opens DHP Ca2+ channels in T-tubules
  3. Small amount of Ca2+ Enters cell binding to RyR in SR membrane causing it to open
  4. Ca2+ flows into cytosol
  5. Ca2+ binds troponin, enables crossbridge cycling/sliding filaments
  6. Ca2+ pumped back into SR/ECF via primary/secondary active transport
  7. Membrane is repolarized when K+ exits cell and ends AP
53
Q

Biggest difference between cardiac and skeletal excitation-contraction coupling

A

DHP physically tugs on RyR in skeletal muscle while in cardiac muscle, DHP allows a trigger amount of Ca2+ into the cell to bind to RyR

54
Q

Why does cardiac muscle have a long refractory period and action potential?

A

Influx of Ca2+ contributes to the formation of the AP

TBD

55
Q

What activates the myosin head for cross-bridge cycling?

A

ATP!

56
Q

What breaks the bond between myosin head and actin filament to end cross bridge cycling?

A

ATP!

57
Q

What is on the myosin head when in the cocked position?

A

ADP and inorganic phosphate

58
Q

What is released from the myosin head to bind it more strongly to actin?

A

inorganic phosphate

59
Q

What is released from the myosin head to make the head pivot, performing the full cross bridge?

A

ADP

60
Q

What is the cause of rigor mortis?

A

Tension requires ATP…but so does relaxation! Lack of ATP means that myosin heads remain bound to actin, so your muscles tense up completely. That’s why a corpse is called a ‘stiff’.

61
Q

Tight binding in rigor state for myosin head

A

Myosin is tightly bound to actin, but has already pivoted and not yet cocked. NO ATP, NO Pi, NO ADP. NOTHING!

Intro Bio II Exam 2 (8 decks)

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