Module 5 Flashcards

1
Q

what is the difference between muscle action and muscle contraction?

A

Muscle action typically refers to concentric/eccentric contractions
Muscle contraction can refer to any contraction (concentric/eccentric/isometric)

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2
Q

what are the three types of muscle? how are they different?

A
  1. cardiac - has WAY more mitochondria (40-100times)
  2. smooth
  3. skeletal
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3
Q

Draw out the structure of skeletal muscle

A
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4
Q

what are the three layers of connective tissue in muscles?

A
  1. epimysium = superficial, surrounds muscle
  2. perimysium = middle layer, surrounds fascicles
  3. endomysium = the deepest CT, surrounds fibres
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5
Q

define sarcolemma and sarcoplasmic reticulum

A

sarcolemma: the thin elastic membrane that covers each fibre
sarcoplasmic reticulum: the tubular channel that surrounds fibres and acts as a road for speedy depolarization

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6
Q

What is the T tubule system

A

T tubule system: cnducts impulses from the cell surface into the SR

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7
Q

what is a myofibril

A

fibrils of skeletal and cardiac fibers consisting of myosin and actin filaments

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8
Q

what is the A, Z and I band?

A

Z line: dissects the I band and adheres to sarcolemma to provide structure (separates the sarcomeres)
A band: area with myosin
I band: area with only actin

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9
Q

what do tendons do

A

tendons connect the ends of muscle to the periosteum (outermost bone layer) and initiates adaptation by enlarging itself to create a stable union

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10
Q

how many nuclei do muscle fibers have?

A

idk but they are multinucleated

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11
Q

how do muscle fibres lie?

A

parallel to fiber’s long axis

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12
Q

what are myofibrils made of?

A

myofibrils contain smaller subunits of myofilaments

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13
Q

what is the myofibrillar complex?

A

the network of proteins that make up the contractile component of muscle fibres

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14
Q

for how much do myofilament’s actin and myosin account for the myofibril complex?

A

85% (the rest are from other proteins)

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15
Q

What other proteins aside from actin and myosin are important for muscle contraction?

A

tropomyosin, troponin, alpha and beta actinin, M protein and C protein

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16
Q

what causes the striated pattern in myofibrils?

A

the striped pattern is caused by layering of A and I bands. The A band is dark, I is light.

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17
Q

Describe the bands and lines in a sarcolemma

A

A band: portion of myosin filament (even if overlapped with actin)
I band: portion of actin filament ONLY
Z line: division between sarcolemmas, dissects I band
H zone: portion of myosin filament ONLY
M band: dissects the H zone, the middle of the sarcolemma

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18
Q

What divides sarcolemma?

A

Z line

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19
Q

what is the functional unit of a muscle fiber

A

sarcomere

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20
Q

what characteristic determines a muscle’s functional properties?

A

The length of its sarcomere

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21
Q

what is a collection of myofilaments (1000+)?

A

myofibril

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22
Q

what are myosin filaments?

A

myosin filament: contractile structure with polypeptide tails and globular heads

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23
Q

what are actin filaments?

A

actin filament: contractile structure of two twisted monomer chains bound by tropomyosin polypeptide chains

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24
Q

what is the shape that actin and myosin filaments form?

A

hexagon - actin surround myosin (6 actin to 1 myosin)

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25
Q

what is the ratio of actin to myosin filaments in a muscle

A

4:1

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26
Q

Give examples of muscles that are fusiform, unipennate, bipennate and multipennate

A

fusiform = biceps brachii
unipennate = extensor digitorum
bipennate = rectus femoris
multipennate = deltoid

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27
Q

Explain how pennation increases force production

A

when the fibres lay at an angle, it allows the fibres to remain short while the muscle attains considerable length. creates a larger cross sectional area because more sarcomeres can ‘pack’ into a given muscle volume. More fibers per area

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28
Q

muscles with greater pennation allow for greater ___ but less ______

A

greater force, less velocity

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29
Q

which fibre orientation is best for velocity, and which is best for force?

A

velocity = fusiform
force = pennate

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30
Q

describe the cross bridge mechanism

A

globular myosin heads extend perpendicularly to latch onto actin. ATP hydrolysis activates the heads, pulling the Z line towards the M line. Tropomyosin and troponin regulate make and end break contacts. myosin heads have opposite orientation at the thick filament ends

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31
Q

draw the cross bridge mechanism

A
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32
Q

what is the sliding filament model

A

the sliding filament model proposes that muscle shortens/lengthens due to thick and thin filaments sliding past each other without changing length

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33
Q

where is force produced in the sliding filament model

A

Z bands

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34
Q

What happens to the bands with shortening contraction

A

Z line pulled toward centre
actin moves into A band
no change in A band width
H zone can disappear

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35
Q

do cross bridges move synchronously or asynchronously

A

asynchronous. it allows for smooth contraction. about 50% of the cross bridges make contact with actin at a time

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36
Q

describe the isometric tension curve

A

idk if there is a pic on the slides. basically optimal force production occurs when actin is barely overlapped or barely has a gap

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37
Q

what are the events in muscle action

A

step 1 - AP generated, ACh diffuses
step 2 - depolarization
step 3 - calcium release
step 4 - calcium binds to actin
step 5 - cross bridge bind
step 6 - cross bridge release (contraction)
step 7 - cross bridge continues
step 8 - ATP hydrolysis, calcium moves back
step 9 - muscle relaxes

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38
Q

what determines if a fibre is relaxed or contracted

A

ATP and calcium. relaxed = ATP near cross bridge. Contracted = calcium and ATP utilized

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39
Q

describe step 1 of muscle action

A

ATP generated
terminal axon releases ACh, which diffuses across the synaptic cleft and attaches to receptors on sarcolemma

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40
Q

describe step 2 of muscle action

A

AP depolarizes the transverse tubules

41
Q

describe step 3 of muscleaction

A

depolarization of the T tubules causes calcium release from the lateral sacs of SR

42
Q

describe step 4 of muscle action

A

calcium binds to troponin and tropomyosin in the actin filaments. This releases the inhibition that prevented actin from combining with myosin

43
Q

describe step 5 of muscle action

A

actin combines with myosin ATP, activates myosin ATPase, which splits ATP. this reaction’s energy produces the cross bridge movement

44
Q

describe step 6 of muscle action

A

ATP binds to cross bridge, allowing detachment.

45
Q

describe step 7 of muscle action

A

cross bridge continues as long as calcium concentrations remains high enough to inhibit troponin-tropomyosin system

46
Q

describe step 8 of muscle action

A

when muscle stimulation ceases, calcium moves back to the lateral sacks via ATP hydrolysis. intracellular calcium concentration rapidly decreases

47
Q

describe step 9 of muscle action

A

calcium removal restores inhibitory action of troponin-tropomyosin. calcium is pumped back into the SR

48
Q

what two purposes does muscle deactivation serve?

A
  1. prevents any mechanical link between cross bridge and actin
  2. inhibits myosin ATPase activity to prevent ATP splitting
49
Q

what does the length tension curve describe?

A

the relationship between length of sarcomere and the amount of tension developed

50
Q

what is the ratio of fiber length to muscle length

A

between 0.2 and 0.6

51
Q

How do fibers in parallel vs series affect force and velocity?

A

parallel = more force under low velocity, hits 0 force early on
series = half the force under low velocity, hits 0 force later

52
Q

how do we differentiate the fiber types

A
  1. ATP production mechanism
  2. motor neuron innervation
  3. type of myosin heavy chain
53
Q

what ratio of type 1 and 2 fibers contribute during near max aerobic and anaerobic activities (basketball, swimming, hockey)

A

even

54
Q

describe the characteristics of the fast twitch fiber

A
  • high ATP transmission
  • high myosin ATPase activity
  • rapid Ca release and update
  • high rate of cross bridge turnover
  • high contraction speed
55
Q

describe the characteristics of type 1 fibers

A
  • low myosin ATPase activity
  • aerobic system
  • slow Ca regulation
  • large and numerous mitochondria
  • fatigue resistant
56
Q

how do we take muscle biopsy in humans?

A

needle is inserted, plunger is used to drive a circular guillotine into the muscle, and a small portion is cut out. syringe is used to generate suction

57
Q

what fiber type is higher in endurance athletes vs power athletes

A

endurance = more type 1
power athletes = more type 2

58
Q

what gender typically has higher cross sectional area, and diversity in fibres?

A

more CA = men
more diversity = women

59
Q

what are the two divisions of the nervous system

A

central = brain and spinal cord
peripheral = nerves
- somatic
- autonomic
- symp
- parasymp

60
Q

define motor unit and motor pool

A

motor unit: an alpha motor neuron and the fibers that it innervates (only contains one type of fiber)
motor neuron pool: all alpha neurons that innervate one muscle

61
Q

define anterior motor neuron

A

The motor neuron that projects from the anterior dorsal horn. Sends efferent information to muscle

62
Q

define neuromuscular junction

A

NMJ: the interface between motor neuron terminal ends and the fibre

63
Q

draw out the NMJ

A
64
Q

what is the synaptic cleft?

A

serves as the site for neural impulse transmission

65
Q

Is ACh release excitatory or inhibitory?

A

excitatory

66
Q

describe temporal and spatial summation

A

temporal = repeated stimulation
spatial = convergence

67
Q

describe the types of motor units by the typical three characteristics

A

Type 2x = fast twitch, high force, fast fatigue
type 2a = fast twitch, moderate force, fatigue resistant
type 1 = slow twitch, low force, fatigue resistant

68
Q

Whats the big 3 for classifying motor units

A

twitch, tension and fatiguability

69
Q

what is meant when we say motor units are adaptable?

A

with aerobic training, fast twitch fibers can be as fatigue resistant as type 1 fibres. surgical innervation of fast twitch fiber with slow motor neuron can alter the fibres characteristics. long term low frequency stimulation can convert muscle fibres

70
Q

what is the all or none principle

A

the principle that a stimulus strong enough to trigger a motor neuron AP will activate all fibers in a unit to contract synchronously. the unit will not exert force gradation, it either elicits an action or it does not

71
Q

what is gradation of force

A

the exertion of different amounts of force via two mechanisms
1. increased recruited motor units
2. increased motor unit discharge frequency

72
Q

what is the size principle

A

states that motor units will be recruited in an orderly fashion from smallest to largest. allows for fine tuning and smooth contraction

73
Q

Which skill is more synchronous in its contraction? weight lifters or endurance runners?

A

weight lifters. they are more synchronous. endurance runners are more asynchronous to allow for recovery before firing again

74
Q

define fatigue

A

fatigue: decline in force capacity with repeated stimulation in a given time period. occurs from disruption in the connection between CNS and the fiber

75
Q

what four components affect muscle fatigue

A

CNS, PNS, NMJ, and muscle fibre

76
Q

what are some substrate-related reasons for fatigue

A

PCr depletion, changes in myosin ATPase, impaired glycolytic energy transfer, disturbed T tubule, ionic imbalances

77
Q

what determines muscle strength

A

muscle size (#of sarcomeres in parallel), muscle activation (# of active fibres + unit firing rate), specific force (fiber type), biomechanics (moment arm length?)

78
Q

How can we reverse muscle fatigue?

A

rest

79
Q

describe central vs peripheral fatigue

A

central = seen at high levels of motor input, transmission, motoneurons and neural signals
peripheral = seen at NMJ and in inhibition of excitation contraction coupling process

80
Q

what are some easy explanations for muscle fatigue?

A

acidosis = high concentrations of hydrogen and phosphorous impact power stroke and decreases sarcolemma calcium sensitivity
lactic acid = dissipates into hydrogen ions

81
Q

How does hydrogen and inorganic phosphate effect calcium?

A

They make it more difficult for calcium. Hydrogen acidity can inhibit calcium binding, and phosphate can bind to calcium

82
Q

what are some more difficult explanations for muscle fatigue?

A

reactive oxygen species = more so in longer duration exercises
superoxide = a byproduct of oxidative phosphorylation, which reduces to H2O2 and then OH (unstable). This effects sarcolemma calcium sensitivity and release

83
Q

What happens to H and Pi levels with type 1 vs 2 fibres

A

type 1 = decreased H and Pi
type 2 = increased H and Pi

84
Q

what factors change how muscles fatigue

A
  1. muscle fibre composition
  2. type and intensity - central fatigue more present in endurance, peripheral more present in high intensity. isometric vs dynamic contractions
  3. available oxygen - lowering oxygen = higher fatigue. increasing FiO2 decreases fatigability
85
Q

what is the central fatigue hypothesis?

A

CFH is based on the assumption that during prolonged exercise, the synthesis and metabolism of monoamines (serotonin, dopamine, noradrenaline) are influenced. There is increased brain serotonergic activity which augments lethargy, loss of drive, and reduction in unit recruitment

86
Q

explain the three portions of central fatigue

A
  1. excitatory drive to lower neurons - afferent signals from receptors of muscles depress the firing rate of efferent signals
  2. motor neuron excitability - AP increases to match work rate intensity. with sustained contractions, the MUFR starts to decrease
  3. neuromuscular transmission - prolonged exercise decreases choline availability, which is a precursor for ACh
87
Q

What are electrophysiological considerations and contractile-biochemical considerations in muscle fatigue?

A

EPC in central fatigue includes the brain and alpha motor neuron along with the fibre
CBC in peripheral fatigue includes the actual muscle fibre

88
Q

what product does not have a role in skeletal muscle fatigue?

A

lactic acid

89
Q

define peripheral fatigue

A

refers to the fatigue distal from the motor unit, and involves processes associated with mechanical/cellular changes in the muscular system

90
Q

Summarize the less obvious factors of peripheral fatigue

A
  1. circulation - decreased Sa O2 and cardiac output
  2. contractile elements - decreased Ca release, actin-myosin cross bridge
  3. Muscle - increased H NH4 and Pr
  4. substrate - decreased glucose, glycogen PC
91
Q

What are the four factors contributing to peripheral fatigue?

A
  1. Contractile mechanism - Pi competes with Ca and decreases cross bridge formation
  2. Excitation-contraction coupling - Pi and H release and decrease sarcolemma Ca sensitivity
  3. Excitability of sarcolemma - chronic depolarization, causing net K efflux, in turn requiring larger depolarization to excite
  4. Supply of metabolic energy - low glycogen = low muscle function
92
Q

How can we confirm muscle fatigue?

A
  1. decline in performance of max effort
  2. sub max effort with brief max tests
  3. sub max effort until task failure
93
Q

How do we examine muscle fatigue?

A

EMG! it increases upon beginning the exercise, and with fatigue there is an increase in EMG but no increase in force production.

94
Q

What is interpolation in fatigue

A

interpolation is a technique that uses electric stimulation and voluntary contraction to see muscle behaviour. if it changes, there is central fatigue present

95
Q

what does lower twitch force indicate?

A

peripheral fatigue

96
Q

What are the central fatigue sites?

A
  1. higher centres (brain)
  2. spinal motor neurons
  3. motoneuron excitability
  4. NM transmission
97
Q

what are the peripheral fatigue sites

A
  1. Twitch
  2. interpolation
98
Q

Why is inorganic phosphate dangerous for muscle contraction?

A

because it competes with calcium for troponin binding. it decreases cross-bridge formation and can act as the rate limiting step