Muscle Flashcards

1
Q

What are the different Muscle tissue types ?

A

Skeletal, Smooth, and Cardiac

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2
Q

What is the whole muscle surrounded by ?

A

Epimysium

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3
Q

What are bundles of muscle called ?

A

Fascicles or Fasciculi

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4
Q

What are the Fascicle surrounded by ?

A

Perimysium

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5
Q

What do Fascicle consist of ?

A

Individual muscle cells (muscle fibers)

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6
Q

What are muscle fibers surrounded by ?

A

Endomysium

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7
Q

What are muscle fibers made up of ?

A

– Consists of myofibrils divided into sarcomeres

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8
Q

What is the cell membrane of muscle fibers called ? (Fuses with tendon and conducts action potential.

A

Plasmalemma

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9
Q

What is the role of Plasmalemma ?

A

– Fuses with tendon
– Conducts action potential
– Maintains pH, transports nutrients

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10
Q

What is the cytoplasm of muscle fibers called ?

A

Sarcoplasm

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11
Q

What are the unique features of sarcoplasm ?

A

glycogen storage, myoglobin

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12
Q

What are Transverse Tubules (T-tubules)

A

– Extensions of plasmalemma
– Carry action potential deep into muscle fiber

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13
Q

What is the Sarcoplasmic Reticulum ?

A

– Calcium (Ca2+) storage

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14
Q

How many myofibrils are to a single muscle fiber ?

A

Hundreds to thousands

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15
Q

What are sarcomeres ?

A

– Basic contractile element of skeletal muscle
– End to end for full myofibril length

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16
Q

How are sarcomeres identified ?

A

Distinctive striped appearance (striations)

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17
Q

What are the different striations of the sarcomeres ?

A

– A-bands: red/blue stripes (both colors)
– I-bands: light/pink stripes (gaps)
– H-zone: middle of A-band
– M-line: middle of H-zone

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18
Q

What is the thin protein filament of sarcomeres ?

A

Actin
– Show up lighter under microscope (red)
– I-band contains only actin filaments

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19
Q

What are the other proteins of the thin filaments ?

A

– Tropomyosin: covers active site at rest
– Troponin: anchored to actin, moves tropomyosin

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20
Q

What is the thick protein filament of sarcomeres ?

A

Myosin (thick filaments)
– Show up darker under microscope (blue)
– A-band contains both actin and myosin filaments
– H-zone contains only myosin filaments

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21
Q

Where is Actin (thin filaments) anchored ?

A

Anchored at Z disk

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22
Q

What is the third myofilament ?

A

Titiin

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23
Q

What does titin do ?

A
  • Acts like a spring (stiffness
    increases with muscle
    activation and force
    development).
    – Extends from Z-disk to M-band.
  • Stabilizes sarcomeres and
    centers myosin.
  • Prevents overstretching
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24
Q

What innervates muscle fibers ?

A

a-Motor Neurons

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25
Q

What’s important to keep in mind about motor units ?

A

– Single α-motor neuron + all
fibers it innervates
– More operating motor units =
more contractile force

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26
Q

What is the sequence of events that fibers contract through called ?

A

“excitation-contraction coupling”

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27
Q
A

Muscle -> Fascicle -> Muscle Fiber -> Myofibril -> Sarcomeres -> protein filaments

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28
Q

What are the steps through “excitation-contraction coupling” ?

A
  1. Action potential (AP) starts in brain
  2. AP arrives at axon terminal, releases acetylcholine (ACh)
  3. ACh crosses synapse, binds to ACh receptors on plasmalemma
  4. AP travels down plasmalemma, T-tubules
  5. Triggers Ca2+ release from sarcoplasmic reticulum (SR)
  6. Ca2+ enables actin-myosin contraction
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29
Q

What happens after action potential arrive at sarcoplasmic reticulum from T tubule ?

A

– SR sensitive to electrical charge
– Causes mass release of Ca2+ into sarcoplasm

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30
Q

What happens after Ca2+ binds to troponin on thin filament ?

A

– At rest, tropomyosin covers myosin-binding site
– Troponin-Ca2+ complex moves tropomyosin
– Myosin binds to actin, forming a cross-bridge,
allowing a contraction to occur

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31
Q

How is the muscle at the relaxed state ?

A

– No actin-myosin interaction at binding site
– Myofilaments overlap a little

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32
Q

How is the muscle at the contracted state ?

A

– Myosin head pulls actin toward sarcomere center
(power stroke)
– Filaments slide past each other
– Sarcomeres, myofibrils, muscle fiber all shorten

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33
Q

What happens in muscle contraction state after power stroke ends ?

A

– Myosin detaches from active site
– Myosin head rotates back to original position
– Myosin attaches to another active site farther down

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34
Q

How does muscle contraction state end ?

A

– Z-disk reaches myosin filaments

Or

– AP stops, Ca2+ gets pumped back into SR

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35
Q

Where does ATP bind to so its energy can be used for muscle contraction ?

A
  • Binds to myosin head
    – ATPase on myosin head
    – ATP = ADP + Pi + energy
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36
Q

What causes rigor mortis ?

A

Lack of ATP production

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37
Q

How does muscle relaxation occur ?

A
  • AP ends, electrical stimulation of SR stops
  • Ca2+ pumped back into SR
    – Stored until next AP arrives
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38
Q

Referring to muscle relaxation what happens without Ca 2+ ?

A
  • troponin and tropomyosin
    return to resting conformation
    – Covers myosin-binding site
    – Prevents actin-myosin cross-bridging
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39
Q

What is a muscle biopsy ?

A

– Small (10-100 g) piece of muscle removed
– Frozen, sliced, examined under microscope

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40
Q

What fiber has slow form of myosin ATPase ?

A

Type 1

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41
Q

What fiber has fast form of myosin ATPase ?

A

Type 2

42
Q

How are type 1 fiber described ?

A

High aerobic endurance
* Efficiently produce ATP from oxidation of fat and carbohydrate
* Can maintain exercise for prolonged periods
* Require oxygen for ATP production
* Recruited most often during low-intensity
– aerobic exercise (e.g., marathon running)
– daily activities (walking)
– posture

43
Q

When is peak tension in type 1 fibers ?

A

– Peak tension in 110 ms (slow twitch)
– ~50% of fibers in an average muscle

44
Q

When is peak tension in type 2 fibers ?

A

– Peak tension in 50 ms (fast twitch)
– Type IIa (~25% of fibers in an average muscle)
– Type IIx (~25% of fibers in an average muscle)

45
Q

How are type 2 fiber described ?

A
  • Type II fibers in general
    – Poor aerobic endurance, fatigue quickly
    – Produce ATP through anaerobic pathways
  • Type IIa
    – More force, faster fatigue than type I
    – Short, high-intensity endurance events (1,600
    m run)
  • Type IIx
    – Seldom used for everyday activities
    – Short, explosive sprints (100 m)
46
Q

How do Type 1 compare to Type 2 in Variable speed of myosin ATPase ?

A

– Fast myosin ATPase = fast contraction cycling.
– Slower myosin ATPase = slower contraction cycling.

47
Q

How do Type 1 compare to Type 2 in Sarcoplasmic reticulum ?

A

– Type II fibers have a more highly developed SR.
– Ca2+ release is faster

48
Q

How do Type 1 compare to Type 2 in motor units ?

A

– Type I motor unit: smaller neuron, <300 fibers
– Type II motor unit: larger neuron, >300 fibers

49
Q

How do Type 1 compare to Type 2 in Peak power ?

A

– Type IIx > type IIa > type I

50
Q

What are muscle Fiber type determinants ?

A
  • Each person has unique ratios.
  • Genetic factors
    – Most influential in determining percentage
  • Arm and leg ratios are similar in one
    person.
    – Type I predominates in endurance athletes.
    – Type II predominates in power athletes.
  • Soleus is type I in everyone.
  • Aging: muscles lose type II motor units
51
Q

What is muscle fiber recruitment also called ?

A

motor unit recruitment
– When a motor unit is recruited,
ALL of its fibers are activated

52
Q

What is the method of muscle fiber recruitment for altering force production ?

A

– Less force: fewer or smaller
motor units (type I)
– More force: more or larger
motor units (type II)

53
Q

What is the orderly recruitment (Size Principle) ?

A
  • Recruitment order:
    – First: Smallest (type I) motor units
    – Next: Midsized (type IIa) motor units
    – Last: Largest (type IIx) motor units
  • Recruited in same order each time
54
Q

What is the Principle of orderly recruitment
(size principle) ?

A

order of recruitment
of motor units directly related to size
of α-motor neuron

55
Q

How do thresholds change in motor units ?

A
  • Smaller MUs are low-threshold, recruited first
  • Progressively higher threshold MUs are
    recruited based on the increasing demands of
    the activity
56
Q

What are the types of dynamic contraction ?

A

– Concentric
– Eccentric

57
Q

What is dynamic contraction ?

A

– Muscle produces force and changes length
– Joint movement produced

58
Q

How is concentric contraction described ?

A
  • Muscle shortens while
    producing force
  • Sarcomere shortens,
    filaments slide toward center
59
Q

How is eccentric contraction described ?

A
  • Muscle lengthens while
    producing force
  • Cross-bridges form but
    sarcomere lengthens
  • Ex) lowering heavy weight
60
Q

How is Static (isometric) contraction described ?

A

– Muscle produces force but does not change length
– Joint angle does not change
– Myosin cross-bridges form and recycle, no sliding

61
Q

What are the dependents of the amount of force developed ?

A
  1. Number and type of motor units activated
  2. Size of the muscle
  3. Frequency of stimulation of each motor unit
  4. Muscle fiber and sarcomere length
  5. Speed of contraction
62
Q

When is more force generated and how is it related to the type of fibers ?

A

More force generated when more motor units
activated
* Type I motor units = less fibers = less cross-bridges = less force
* Type II motor units = more fibers = more cross-bridges = more force

63
Q

How can a motor unit exert varying level of force ?

A

Single motor unit can exert varying levels of force
dependent on frequency of stimulation

64
Q

What are the frequency of stimulations called regarding motor units based on rate coding ?

A

– Twitch: contractile response to single electrical stimulus
– Summation: consecutive stimuli for greater force
– Tetanus: continued stimulation resulting in peak force

65
Q

What is rate coding ?

A
  • Process of varying levels is rate coding
66
Q

What happens if fibers are too short or too stretched ?

A

Too short or too stretched = little or no force develops

67
Q

Why is having fibers at optimal length important ?

A

Fibers have optimal length for force production
* Optimal sarcomere length = optimal overlap of
actin/myosin
– Maximizes cross-bridge interaction

68
Q

Why is speed important to producing force ?

A
  • Concentric: maximal force development decreases at higher speeds
  • Eccentric: maximal force development increases at higher speeds
69
Q

After 3 to 6 months of resistance training

A

– 25 to 100% strength gain
– Learn to more effectively produce force
– Learn to produce true maximal movement

70
Q

Strength gains similar as a percent of initial
strength

A

– Young men experience greatest absolute gains
versus young women, older men, children
– Due to incredible muscle plasticity

71
Q

Hypertrophy

A

Muscle size increase = Muscle Strength Increase

72
Q

Atrophy

A

Muscle size Decrease = Muscle Strength Decrease

73
Q

Strength gains result from…..

A

– Altered neural control
– Increase Muscle size

74
Q

What has to occur for strength gain ?

A

neural adaptations via plasticity

75
Q

Strength gain can occur without hypertrophy

A

True

76
Q

What factors are important for strength gains ?

A

– Increase motor unit recruitment
– Decrease autogenic inhibition
– Reduced coactivation

77
Q

How are motor units generally recruited?

A

asynchronously; not all engaged at the same instant

78
Q

Resistance training = synchronous recruitment

A

Synchronous recruitment = strength gains

79
Q

Synchronicity = more motor units fire at the same time

A

This improves rate of force development and increase capability to exert force.

80
Q

What are Normal intrinsic inhibitory mechanisms ?

A

– Inhibit muscle contraction if tendon tension too high
– Prevent damage to bones and tendons

81
Q

Why does training decrease inhibitory impulses ?

A

So muscles can generate more force.

82
Q

What may reducing coactivation do ?

A

Cause strength gain

83
Q

What do antagonist (coactivation) normally do ?

A

Oppose agonist force.

84
Q

Definition of muscle hypertrophy.

A

Increase in muscle size.

85
Q

What is Transient hypertrophy (after exercise bout) ?

A

– Due to edema formation from plasma fluid
– Disappears within hours

86
Q

What is Chronic hypertrophy (long term)?

A

– Structural change in muscle
– Fiber hypertrophy

87
Q

How is chronic hypertrophy maximized ?

A

– High-velocity eccentric training
– Disrupts sarcomere Z-lines (protein remodeling)

88
Q

What may Fiber Hypertrophy be the result of ?

A
  • More actin, myosin filaments
  • More myofibrils
  • More sarcoplasm
  • More connective tissue
89
Q

Resistance training = Increase in protein synthesis

A

– During exercise: synthesis decreases , degradation increases
– After exercise: synthesis increases , degradation decreases

90
Q

How does Testosterone facilitates fiber hypertrophy ?

A

– Natural anabolic steroid hormone
– Massive doses of anabolic steroids + resistance
training = large increases in muscle mass

91
Q

We don’t gain muscle fiber (hyperplasia). We increase our fiber size. What does hyperplasia ?

A

Animals

92
Q

Short term increase in muscle strength is due to what ?

A

– Neural factors critical in first 8 to 10 weeks
– Substantial Increase in 1RM
– Due to increase in voluntary neural activation

93
Q

Long-term Increase in muscle strength is due to what ?

A

– Hypertrophy major factor after first 10 weeks
– Associated with significant fiber hypertrophy
– Net Increase protein synthesis takes time to occur

94
Q

What does Reduction or cessation of activity do to muscle ?

A

major change in muscle structure and function

95
Q

How much is muscle reduced in immobilization in the first 6 hrs ?

A

– Lack of muscle use = reduced protein synthesis

96
Q

How much is muscle reduced in immobilization in First week ?

A

-strength loss of 3 to 4% per day
– DECREASE Size/atrophy
– DECREASE Neuromuscular activity

97
Q

How are the effects of immobilization reversed ?

A
  • Recover when activity is resumed
    – But recovery period longer than immobilization
98
Q

What happens in detraining ?

A

Leads to decrease in 1RM
– Strength losses can be regained (~6 weeks)
– New 1RM matches or exceeds old 1RM

99
Q

What happens after muscle goal met ?

A

Once training goal met, maintenance
resistance program prevents detraining
- maintain intensity but reduce frequency

100
Q

Fiber type alterations Training regimen may not outright change fiber type but …..

A

– Type II become more oxidative with aerobic training
– Type I become more anaerobic with anaerobic training

101
Q

Type IIx = type IIa transition common in RT (Fiber Type Alterations)

A

– 20 weeks of heavy RT program showed
* Static strength Increase, cross-sectional area increases
* Percent type IIx decrease, percent type IIa Increase

102
Q

Increases in strength dependent primarily on
neural adaptations

A

True