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Ex Phys > Neuromuscular Nervous System > Flashcards

Neuromuscular Nervous System Flashcards

1
Q

What are the three types of muscles?

A
  • skeletal
  • cardiac
  • smooth
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2
Q

Skeletal muscle:

A
  • voluntary
  • there are over 600
  • moves the skeleton
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3
Q

Cardiac muscle:

A
  • involuntary
  • only in the heart
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4
Q

Smooth muscle:

A
  • involuntary
  • in the walls of blood vessels and internal organs
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5
Q

Skeletal muscle functions:

A
  • movement
  • posture
  • stabilize joints
  • heat
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6
Q

Muscle structure:

A
  • tendon
  • periosteum (outer most layer of the bone)
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7
Q

Muscle structure:

A
  • epimysium
  • perimysium
  • endomysium
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8
Q

Epimysium

A
  • surrounds entire muscle
  • fascia of fibrous connective tissue
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9
Q

Perimysium

A
  • surrounds individual bundles of muscle fibers
  • bundles call fascicles
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10
Q

Endomysium:

A
  • surrounds each muscle fiber
  • fine layer of connective tissue
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11
Q

Muscle fiber structure:

A
  • sarcolemma
  • myofibril
  • sarcoplasm
  • transverse tubules (t-tubules)
  • sarcoplasmic reticulum
  • sarcomeres
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12
Q

sarcolemma:

A
  • thin elastic membrane surrounding the muscle fiber
  • includes z-line, m-line, h-zone, a-band, I-band
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13
Q

Myofibril

A
  • contain contractile proteins
  • actin and myosin
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14
Q

Sarcoplasm

A
  • serves as cytoplasm of muscle cell
  • has unique features: glycogen storage, mitochondria
  • what feeds/provides energy for muscle movement
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15
Q

Transverse tubules (t-tubules)

A
  • extends inward from the sarcolemma
  • carry action potential deep into muscle fiber
  • balloon wraps around finger analogy
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16
Q

Sarcoplasmic reticulum

A
  • Ca2+ storage
  • at rest this is where calcium should be sitting
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17
Q

sarcomeres

A
  • functional unit of the muscle cell
  • basic contractile element of skeletal muscle
  • end-to-end for full myofibril length
  • to make most efficient: stack sarcomeres parallel so they transmit signal across entire fiber
  • red “E” parts and everything in between
  • thick and thin filaments
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18
Q

Look at z-disc to determine:

A

how many sarcomeres are present

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19
Q

What is the z-disc?

A

dark band which is end border of one sarcomere

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20
Q

A-band:

A
  • dark area in mid region
  • overlap between thick and thin filaments
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21
Q

I-bands

A
  • lighter areas
  • only contains thin filament
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22
Q

H-zone

A
  • middle of A-band
  • hard to see on micro view
  • only contain myosin heads
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23
Q

M-line

A
  • middle of sarcomere
  • no distinctive marking
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24
Q

Actin (thin filaments)

A
  • projects between myosin filaments
  • contains active sites that bind to myosin
  • composed of three proteins
  • anchored at z-disc
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25
Q

What three proteins compose actin (thin filaments)?

A
  • actin: contains myosin-binding site
  • tropomyosin: covers active site at rest
  • troponin (anchored to actin): moves tropomyosin
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26
Q

Myosin (thick filament)

A
  • about 2/3 of muscle protein is myosin
  • two intertwined filaments
  • globular heads
  • titin as stabilizer
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27
Q

globular heads:

A
  • “myosin head”
  • protrude 360 degrees from thick filament axis
  • will interact with actin filaments for contraction
  • heads will flutter which drives shortening of sarcomere
  • two heads present
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28
Q

Titin

A
  • stabilizer for myosin
  • anchors thick filament to z-disc
  • muscle injury will disrupt titins which causes thick filaments to fall over
  • more likely damaging in muscle injury
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29
Q

Motor unit

A

a single alpha motor neuron and all the muscle fibers it innervates

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30
Q

Synapse (Neuromuscular cleft)

A

gap between the neuron and sarcolemma

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31
Q

neuromuscular junction

A
  • consists of synapse between alpha motor neuron and muscle fiber
  • serves as the site of communication between neuron and muscle
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32
Q

motor end plate

A
  • pocket formed around motor neuron by sarcolemma
  • other side that would receive the signal and start new propagation of muscle signal
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33
Q

Muscle actions

A
  • static
  • dynamic
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34
Q

static muscle action:

A
  • muscles generate force without movement taking place
  • measurement of effort at a single joint angle at a time
  • muscle length remains the same (isometric)
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35
Q

dynamic muscle action:

A
  • apply force to move an object/body segment
  • measurement of effort through a range of joint angles
  • muscle length changes during movement
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36
Q

Muscle shortening:
Muscle lengthening:

A

concentric
eccentric

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37
Q

after someone has had an injury what muscle action do you start with?

A

static because you won’t irritate the muscle by changing its length

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38
Q

Muscle concentric action

A
  • a muscle performs work by shortening
  • this action pulls on tendons attached to the bone and movement occurs
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39
Q

When we say “i want to lift my arm up” what happens?

A

we pull sarcomeres in on each other, shorten sarcomeres up gives us length change of overall muscle

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40
Q

Sliding filament theory:

A
  • relaxed state
  • contracted state
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41
Q

relaxed state of sliding filament theory

A
  • no actin interaction occurs at binding site
  • myofilaments overlap a little
  • go through periods of relaxed state where calcium is basically locked up and no contraction is happening (micro level: brighter mid section)
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42
Q

contracted state of sliding filament theory

A
  • when activated, myosin binds with actin
  • myosin head pulls actin toward sarcomere center (power stroke)
  • filaments slide past each other
  • sarcomeres, myofibrils, muscle fiber all shorten
  • pulling fibers over each other (power stroke)
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43
Q

H-zone from relaxed to contracted

A
  • shortens
  • area that contains only myosin heads reduced
44
Q

I-band from relaxed to contracted

A
  • smaller
  • area that contains only actin (thin filaments)
45
Q

A-band relaxed to contracted

A
  • stays constant
  • just length of thick filament
  • never changes
46
Q

M-line relaxed to contracted

A
  • no change
  • middle of sarcomere
47
Q

describe the central governor theory and its importance during fatigue

A
  1. central control center regulates exercise performance
  2. reduces motor output to exercising muscle
  3. protects against catastrophic disruptions of homeostasis
  4. basically tells muscle to stop working so hard
48
Q

define cardiac output, what two factors contribute to cardiac output?

A
  1. the amount of blood pumped by the heart each minute
  2. stroke volume and HR
49
Q

The process why which a nerve stimulus initiated in the brain causes a muscle contraction:

A

brain > nerve > muscle > contraction

50
Q

Muscle contraction: excitation-contraction coupling

A
  1. action potential (AP): reaches muscle fiber
  2. Calcium release: Ca2+ is released
  3. Troponin activated: Ca2+ binds to troponin
  4. cross-bridge: myosin head attaches to actin, cross bridges formed
  5. power stroke: myosin head pulls actin inward, using “power stroke”
  6. reset: myosin detaches from actin, resets
51
Q

step 1: AP arrives at axon terminal

A
  • ACh is released and the muscle membrane is depolarized
  • calcium pushes vesicles to outer edge
  • once bound, AP forms on sarcolemma or muscle membrane
  • AP goes both ways so it gets the whole muscle
52
Q

step 2: calcium released

A
  • Ca2+ released from SR
  • AP comes down and in t-tubule there is another specialized receptor which is voltage gated
  • calcium leaves the sarcoplasmic reticulum and floods muscle cell
  • calcium will continue to flood out
  • when calcium exits, it binds with tropomyosin
53
Q

step 3: calcium activates troponin

A
  • at rest, tropomyosin covers myosin-binding site, blocking actin-myosin attraction
  • Ca2+ binds to troponin, configuration changes
  • physically moves tropomyosin; exposing binding sites
  • myosin head can now form cross bridge with actin
54
Q

step 4: cross-bridge

A
  • myosin heads bind to actin, forming a cross bridge
55
Q

step 5: myosin moves actin

A
  • myosin head moves actin toward the M-line called the power stroke
  • action requires ATP
  • moves from energized to non-energized position
  • ATP was already bound, which is why it was energized
56
Q

step 6: reset

A
  • myosin head detaches from myosin-actin binding sites
  • myosin head moves back to the initial position
  • requires ATP
  • reset to keep process moving
  • New ATP comes into play, attaches to myosin head which signals “release” from actin site (causes de-coupling of cross bridge)
57
Q

Muscle relaxation: Ca2+ uptake

A
  • as long as neural impulses arrive and Ca2+ concentration remain high, force generation continues
  • when the impulse stops, calcium levels drop and force decreases as Ca2+ is pumped back into SR
  • once Ca2+ drop below a critical level, thin filament inhibition again resumes
  • last step in muscle relaxation
58
Q

energy for muscle contraction

A
  • muscular action requires energy (chemical (ATP) > mechanical (contractions))
  • myosin contains the binding site for ATP
  • enzyme located on myosin head (ATPase) splits ATP into adenosine diphosphate (ADP), inorganic phosphate (Pi) - “hydrolyzes” ATP - and energy
  • energy released during this process is used to drive muscle contraction
  • ATP > ADP + Pi + energy
59
Q

source of ATP

A
  • phosphocreatine (PC)
  • glycolysis
  • oxidative phosphorylation
60
Q

Muscle fiber types

A
  • three muscle fiber types exist in human skeletal muscle and differ in their function properties
61
Q

contractile properties of muscle fiber types

A
  • maximal specific force production (labeled specific force production)
  • speed of contraction (Vmax)
  • maximal power output = force x shortening velocity
  • fatigue resistance
  • muscle fiber efficency
62
Q

Nonathletes fiber type and performance

A
  • approx 50% slow and 50% fast fibers
  • of fast-twitch fibers: 25% IIa and 25% IIx
  • older adults typically lose their fast fibers
63
Q

Power athletes fiber type and performance

A
  • higher percentage of fast fibers
  • e.g. elite sprinters (70-75% type II)
64
Q

endurance athletes fiber type and performance

A
  • higher percentage of slow fibers
  • e.g. distance runners (70-80% type I)
65
Q

Ratio of fiber type and performance is largely driven by:

A

genetics

66
Q

fiber type is not the only variable that determines the success of an athlete:

A
  • cardiovascular function
  • motivation
  • training habits
  • muscle size
67
Q

size principle:

A

smallest alpha motor neuron recruited first: smaller cell volume means the same stimulus has a greater impact on its resting potential

68
Q

types of motor units:

A
  • type I (slow) (smallest)
  • type IIa (fast, fatigue resistant) (intermediate size)
  • tyoe IIx (fastest, fatigable) (largest)
69
Q

recruitment pattern during incremental exericse

A

type I > type IIa > type IIx

70
Q

speed of myosin ATPase varies

A
  • type I - slow myosin ATPase = slow contraction cycling
  • type II - fast myosin ATPase = fast contraction cycling
71
Q

sarcoplasmic reticulum fiber type characteristics

A
  • type II more highly developed SR
  • calcium more quickly available; pumped faster (fast fibers)
72
Q

Motor units fiber type characteristics

A
  • type I - small cell body <300 fibers
  • type II - larger cell body >300 fibers
73
Q

How are muscle fibers typed?

A
  • muscle biopsy
  • immunohistochemical staining
  • gel electrophoresis
74
Q

muscle biopsy

A
  • small piece of muscle removed
  • may not be representative of entire body
75
Q

immunohistochemical staining

A
  • selective antibody binds to unique myosin isoforms
  • fiber types differentiated by differences in color
76
Q

gel electrophoresis

A
  • identify myosin isoforms by separating myosin isoforms on gel
77
Q

What affects the force and speed of muscle contraction?

A
  • types and number of motor units recruited (activated)
  • increase motor units = increase force
  • increase type II fibers = increase force and velocity
  • length-tension relationship (sarcomere length)
  • frequency of stimulus
  • force-velocity relationship
78
Q

muscle twitch

A
  • contraction as the result of a single depolarization (caused by a stimulus)
  • latent period (action potential arrived but contraction has not started)
  • contraction
  • relaxation
79
Q

speed of contraction is faster in type II fibers

A
  • SR releases Ca2+ at a faster rate
  • faster myosin ATPase activity
80
Q

Summation

A
  • multiple stimuli occur quickly enough that the muscle cannot fully relax between stimuli and the force from one twitch is added to the force from the previous twitch
81
Q

tetanus

A
  • summation where stimuli occur fast to prevent any relaxation between stimuli (causes smooth contraction)
82
Q

Force-velocity relationship

A
  • high force lifts can only happen slowly
  • low force lifts can be fast
83
Q

high force lifts can only happen slowly

A
  • need of more actin and myosin cross-bridge connection at any one point in time to maintain and generate force
84
Q

low force lifts can be fast

A
  • fewer cross-bridge connections are needed at one point in time to maintain force
  • more myosin heads can let go at any one point in time while maintaining the required force
  • allows for faster cross bridging cycle to occur
85
Q

satellite cells

A
  • play a key role in muscle growth and repair
  • a single nuclei can only maintain (produce proteins for) a finite volume
  • satellite cells merge with the much fiber and become new nuclei for that fiber
86
Q

muscle fatigue

A
  • fatigue is defined as a decline in muscle power output
  • cause of muscle fatigue dependent upon exercise intensity and duration
  • central fatigue
87
Q

high-intensity short-duration exericse

A

accumulation of lactate, H+, ADP, Pi, and free radicals

88
Q

long-duration exercise

A

muscle factors:
- accumulation of free radicals
- electrolyte imbalance
- glycogen depletion

89
Q

central fatigue

A
  • reduced nerve transmission to muscle
  • current research suggests that fatigue is related to both central and peripheral factors
90
Q

muscle cramps

A
  • erratic, involuntary muscle contractions
91
Q

causes of muscle cramps

A
  • electrolyte depletion theory
  • altered neuromuscular control theory
92
Q

electrolyte depletion theory

A

sodium loss via sweating causes spontaneous muscle contractions due to loss of normal resting membrane potential

93
Q

altered neuromuscular control theory

A
  • muscle fatigue causes abnormal activity of the muscle spindle and golgi tendon organ
  • leads to abnormal firing of alpha motor neurons
94
Q

adaptations to resistance training

A
  • neural adaptations responsible for early gains in strength
  • evidence that neural adaptations occur
95
Q

neural adaptations responsible for early gains in strength

A

strength gains during first 8 weeks of training are largely due to nervous system adaptations

96
Q

evidence that neural adaptations occur

A
  • muscular strength increases in first two weeks of training without increase in muscle fiber size
  • phenomenon of “cross education” - training of one limb results in increases of strength in untrained limb
97
Q

neural adaptations include:

A
  • increased neural drive
  • increased number motor units recruited
  • increased firing rate of motor units
  • increased motor unit synchronization
  • improved neural transmission across neuromuscular juction
98
Q

training adaptations to muscle mass

A
  • hyperplasia
  • hypertrophy
99
Q

hyperplasia

A

increased number of fibers
- unclear if hyperplasia occurs in humans

100
Q

hypertrophy

A
  • increased cross-sectional area of muscle fibers
  • hypertrophy is likely the dominant factor in resistance training-induced increases in muscle mass
  • hypertrophy due to increased muscle proteins (that is actin and myosin)
  • leads to an increase in maximal force generating capacity
101
Q

muscle soreness

A
  • delayed onset muscle soreness (DOMS)
  • eccentric exercise causes more damage than concentric exercise
  • slowly begin a specific exercise over 5 to 10 training sessions to avoid DOMS
102
Q

Delayed onset muscle soreness (DOMS)

A
  • appears 24 to 48 hours after strenuous exercise
  • due to microscopic tears in muscle fibers or connective tissue
103
Q

steps leading to DOMS

A
  • strenuous muscle contraction results in muscle damage
  • membrane damage occurs
  • calcium leaks out of SR and collects in mitochondria
  • results in inflammatory process
  • edema and histamines stimulate pain receptors
104
Q

muscle injury

A
  • repeated lengthening contractions can cause nerve damage to the muscle fiber
  • during lengthening contractions, actin filaments are pulled apart in the opposite direction by an external force on the muscle
  • streaming of Z-lines
105
Q

muscle atrophy

A
  • limb immobilization
  • changes occur in a matter of hours
  • during first 6 hours: decreased rate of protein synthesis and “use it or lose it”
  • decreased strength
  • affects both type I and II fibers
  • muscles can recover when activity is resumed

Ex Phys (10 decks)

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