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Physiology > Unit 8: Muscle Physiology > Flashcards

Unit 8: Muscle Physiology Flashcards

1
Q

During embryonic development, huge skeletal fibres are formed by fusion of what component?

A

Myoblasts

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2
Q

What are the contractile elements of skeletal muscle?

A

Myofibrils

*Consist of thick and thin filaments

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3
Q

What protein make up thick filaments?

A

Myosin

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4
Q

What proteins make up thin filaments?

A

Actin

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5
Q

What are the 2 man components of connective tissue that covers muscle?

A

Collagen & Elastin

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6
Q

What are the 3 layers of connective tissue?

A
  1. Epimysin
  2. Perimysin
  3. Endomysin
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7
Q

What is a dark (A band) ?

A
  • Arranged of stacks of thick filaments along thin filaments that overlap the ends of the thick filaments.
  • Contains an M line, a series of proteins that holds the thick filaments in place.
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8
Q

What is the H zone of an (A band)?

A

-Contain an H zone (middle ear of the A band- that has no thin filaments)

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9
Q

What is a light I Band?

A

-Consists of thin filaments that do not project into the A band.

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10
Q

What is a Z line?

A

–>The middle of each I band has a vertical Z line, and the area between the 2 Z lines is called a sacromere, the functional unit of skeletal muscle.

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11
Q

What are the 2 crucial sites needed for myosin-actin interaction?

A

1) Actin-myosin binding site

2) Myson ATPase site (ATP splitting)

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12
Q

What are the 3 thin filament proteins?

A

1) Actin
2) Tropomyosin
3) Troponin

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13
Q

Why can’t muscle contraction occur in a relaxed muscle?

A

-Tropomyosin and troponin block the binding site.

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14
Q

Basic muscle contraction process.

A

The binding of Troponin to Ca2+ which allows for the movement of tropomyosin, no longer blocking the binding site. This allows actin and myosin to bind, and the muscle can contract.

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15
Q

What is the sliding filament mechanism?

A

-The THIN FILAMENTS SLIDE INWARD, over the thick filaments, towards the A bands center during contraction.
Z lines are pulled closer together, and sacromeres shorten.
*All sacromere’s shorten at once, and the muscle fibre simultaneously shortens.
->Known as concentric contraction
*Thick filaments remain unchanged.

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16
Q

What are the mechanisms of a Power Stroke?

A

When actin and myosin make contact at a cross bridge, the bridge changes shape- bending inward towards the sacromere like the stroking of an oar.

  • The power stroke pulls thin filaments inward.
  • repeated cycles complete the shortening process.
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17
Q

How is an actin-myosin interaction stopped?

A

-At the end of the cross bridge, the myosin-actin link breaks. The cross bridge returns to its original shape, ready for another actin to bind the myosin head.

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18
Q

What is the term “excitation-contraction” for muscles?

A

excitation- generation of action potentials in the muscle fibre

contraction- actin-myosin binding that causes sacromeres to shorten

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19
Q

What are Transverse Tubules (T Tubules) ?

A

Carry action potentials generated throughout the muscle fiber

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20
Q

What is the Sarcoplasmic Reticulum?

A

-Segments are wrapped around each A/I band, and have sac like regions called LATERAL SACS.

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21
Q

What are Lateral Sacs?

A

-Store calcium, and a spread of an action potential down a T tubule leads to the release of calcium from the sarcoplasmic reticulum into the cytosol.

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22
Q

What is the role of Calcium in the contraction of muscles?

A

Ca2+ is what moves tropomyosin during cross bridge activity, allowing actin and myosin to bind.

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23
Q

How is the myosin ATPase site involvement in the myosin-actin cross bridge?

A
  • The breakdown of ATP occurs before actin and myosin meet.
  • Pi and ADP are released (ATP is used) when the myosin and actin interaction occurs, after calcium has been released.
  • ->When Pi and ADP are released, the myosin ATPase site is free for attachment of another ATP molecule.
  • This allows for the bending back of the cross bridge and the cycle can continue.
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24
Q

How does the cycle continue ?

A

The new bound ATP is split by ATPase, energizing the myosin cross bridge once again, and on binding with another actin, the cross bridge bend to make a power stroke, and so on.

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25
Q

Why does Rigor Mortis occur?

A
  • Actin and Myosin once bound, are stuck in place… They can’t detach because their is no fresh ATP.
  • ->The thick and thin filaments stay in place, causing muscle stiffness.
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26
Q

What is the Latent period of muscle contraction?

A

-The lag in between a skeletal muscle fibres action potential, and the contractile appartus’ response.

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27
Q

What is the Contraction Time of muscle contraction?

A

The time from contraction onset until peak tension occurs.

*Occurs until all Ca2+ is used up from the lateral sacs.

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28
Q

What is the Relaxation Time of muscle contraction?

A

The time from peak tension until relaxation is complete

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29
Q

What is the Refractory period of muscle contraction?

A

The period following contraction where excitation is impossible.

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30
Q

What is a twitch?

A

–>A single action potential in a muscle fibre that produces a weak, brief contraction.

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31
Q

How is gradation of a contraction determined?

A
  1. The number of muscle fibers contracting

2. The tension developed by each fibre.

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32
Q

What is Fatigue?

A

Inability of a muscle to maintain tension at a given level.
*Asynchronous recruitment of motor neurons can take place (switching off to give others a break- can only occur at submaximal contractions)

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33
Q

What is Twitch Summation?

A
  • A muscle fiber undergoes an action potential, and is re stimulated with another action potential before it has completely relaxed from the first twitch.
  • Twitches are added together.
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34
Q

What is Tetanus?

A
  • A muscle fiber is stimulated so rapidly that it does not have a chance to relax at all between the 2 stimuli.
  • 3-4x stronger than a regular contraction.
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35
Q

How is twitch summation maintained?

A

Availability of calcium

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36
Q

What is Optimal Muscle Length?

A

The length at which maximal force can be achieved on a subsequent tetanic contraction.

37
Q

What are series-elastic components?

A

Stretchy spring like components

–>Connective tissue and tendons

38
Q

What is an origin?

A

Stationary part of the muscle (doesn’t move)

39
Q

What is an insertion?

A

Skeletal part of the muscle (moves)

40
Q

What is an Isotonic Contraction?

A

Muscle fibre tension remains CONSTANT as the muscle fibres change length.

41
Q

What is an Isometric Contraction?

A

The muscle fibre is PREVENTED FROM SHORTENING, so tension develops at constant muscle fiber length.

42
Q

What is Dynamic Contraction?

A

The whole muscle changes length

43
Q

What is Concentric Contraction?

A

Produces tension during a shortening motion (z-lines move closer together)

44
Q

What is an Essentric Contraction?

A

Produces tension while strengthening, STRETCHES Z LINES.

45
Q

What processes in Muscle Contraction Require ATP?

A
  1. Splitting of ATP
  2. Binding of fresh ATP
  3. Active Transport of Calcium back into the SR during muscle relaxation.
46
Q

What is Creatine Phosphate?

A

High energy molecule!
produces ATP from pi!
*Catalyzed by creatine kinase

47
Q

What is the advantage of a tissue abundant with myoglobin?

A

Higher affinity for tissue to carry oxygen, as well as other nutrients.

48
Q

What is Muscle Fatigue?

A

When a muscle can no longer respond to stimulation with the same degree of contractile ability (during exercise)

49
Q

What is Central Fatigue?

A

Occurs when the CNS no longer adequately activates the motor neurons supplying working muscle cells.

50
Q

What is Neuromuscular Fatigue?

A

The inability of active motor neurons to synthesize Ach rapidly enough to sustain chemical transmission of action potentials from the motor neurons to the muscles.

51
Q

Slow Twitch Fibres ?

A

Type 1

52
Q

Fast Twitch Fibres?

A

Type 2

53
Q

Slow Oxidative Fibers (Type 1)

A
  • high myoglobin content

- produce energy by oxidative processes

54
Q

Fast Oxidative Fibres (Type 2)

A
  • High myoglobin content

- Produce energy by oxidative processes

55
Q

Fast Glycolytic Fibres (Type 2b)

A
  • Low myoglobin content

- Produce energy by anaerobic processes

56
Q

What are Higher % of fast glycolytic good for?

A

-Sprinting

57
Q

What are Higher % of slow-oxidative good for?

A

-Marathon running

58
Q

What is Muscular Hypertrophy?

A
  • An increase in the mass or girth or a muscle and can induced by a number of stimuli.
  • MUST affect protein-pattern expression
59
Q

True or False: Fast- glycolytic fibres can change diameter in response to short, regular shifts of high intensity exercise.

A

True.

–>Oxidative fibres CAN’T change size

60
Q

What is muscle atrophy?

A

Decrease in muscle mass
Can occur in 2 ways
1. Disuse Atrophy: Occurs when a muscle is not used for a long period of time, even though the nerve supply is still intact.
2. Denervation Atrophy: Occurs after the nerve supply to a muscle is lost.

61
Q

Control of Motor Movement:

A

1) Input from afferent neurons
2) Input from the primary motor cortex
3) Input from the brain stem as part of a multi neuronal motor system.

62
Q

What are Muscle Spindles?

A

Distributed throughout the muscle fibres as the fleshy part of the muscle.
-Consists of intrafusal fibres surrounded by extrafusal fibres (contain myofibrils)

63
Q

What are Intrafusal Fibres?

A

Consist of non-contractile elements with contractile elements on the ends.

64
Q

What are Gamma Motor Neurons?

A

-Innervate a muscles spindle INTRAFUSAL FIBRES

65
Q

What are Alpha Motor Neurons?

A

-Innervate a muscles spindles EXTRAFUSAL FIBRES

66
Q

What are Primary (Annulospiral Endings?)

A
  • Type of afferent sensory ending that is wrapped around the central portion of the intrafusal fibres.
  • Detect changes in length and speed when strecthing occurs.
67
Q

What are the Secondary (Flower-Spray) Endings?

A
  • Clustered at the end of segments of many intrafusal fibres.
  • ->Sensitive ONLY to changes in length during stretching.
68
Q

What are muscle spindles mainly involved in?

A

Stretch Reflex

69
Q

What are the mechanisms of “Knee Jerk” reflex?

A

Tapping of the patellar tendon passivley stretches the quadracep muscle, activating intrafusal spindle fibres.
–>Results in a knee jerk contraction

70
Q

What are the Golgi Tendon Organs?

A

-Monitor changes in muscle tension

71
Q

What are the 3 filaments in smooth muscle?

A
  • Thick myosin filaments
  • Thin actin filaments
  • Filaments of intermediate size for support
72
Q

What are smooth muscle cells lacking that is responsible for their unstriated look?

A
  • ->Lack of sacromeres, therefore they lack Z lines

* Do contain dense bodies which contain similar protein constituents as Z lines.

73
Q

Do smooth muscle cells have T tubules?

A

No!

74
Q

If T tubules don’t exist in smooth muscle cells, how does myosin interact with actin?

A
  • ->The myosin light chain MUST be Phosphorylated to interact with actin.
  • ->Calcium binds Calmodulin, creating a complex that activates myosin kinase, which in turn phosphorylates myosin. (chemical change- not a physical change)
  • *Calcium is removed at the end to allow for a slow contraction rate.
75
Q

How are cardiac muscle fibres connected?

A

-Intercalated discs, which form a unique network through STRONG desmosomes and tight junctions.

76
Q

How is Multiunit Smooth muscle stimulated?

A
  • Consists of multiple discrete units that function independently of one another & must be stimulated separately by nerves to contract (neurogenic)
  • ->Stimulated by the autonomic nervous system
77
Q

What system innervates skeletal muscle?

A

The somatic nervous system

78
Q

Where is most single unit smooth muscle tissue found?

A

Visceral tissue

  • ->Found within the walls of hollow tissues and organs
  • fibre’s become excited and contract as a single unit
  • Electrically linked by gap junctions
79
Q

What is it called when interconnected muscle cells function electrically and mechanically as a unit?

A

Functional Syncytium

80
Q

What is special about single unit smooth muscle?

A

It is self excitable

81
Q

What is a Pacemaker Potential?

A

-The membrane potential gradually depolarizes on its own because of passive ionic fluxes accompanying membrane permeability.

82
Q

What is a Slow-Wave Potential?

A
  • Gradually alternating hyperpolarizations and depolarizing swings in potential are caused by automatic cycling changes in the rate of sodium transported across the membrane.
  • Spontaneously threshold causes action potentials
83
Q

What is Myogenic activity?

A
  • Once an action potential is generated by a self-excitable cell smooth muscle cell (single unit), it is contracted by the remaining nonpacemaker cells to contract in functional syncytium.
  • ->Spreads via gap junctions WITHOUT nervous input
84
Q

In smooth muscle, what does an increase in Ca2+ result in?

A

More cross bridge activity.

85
Q

In skeletal muscle, what does an increase in Ca2+ result in?

A

*Only a certain amount of Ca2+ is needed to trigger an action potential, which permits ALL cross bridges to cycle.

86
Q

What determines how sensitive smooth muscle cells are to neurotransmitters and hormones?

A

-The cells distribution of cholinergic and androgenic receptors.

87
Q

What is the resting length for smooth muscle?

A

Much less than optimal length (Lo)

–>Can be stretched considerably before reaching its optimal length.

88
Q

Which is faster? Smooth muscle or skeletal muscle contractions?

A

Skeletal muscle contractions

*ATPase splitting is much slower in smooth muscle

Physiology (12 decks)

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