Muscular System Flashcards

1
Q

Overview of muscle tissue

A

• Types: Different cells, location,
different control
1. Skeletal muscle
2. Smooth muscle
3. Cardiac muscle
• Terminology: muscle fibers,
“myo”, “mys”, “sarco” pertain to
muscle

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2
Q

Properties of skeletal muscle tissue

A

• Electrically excitable
– Respond to certain stimuli by
producing action potentials
– Stimulated by chemical
neurotransmitters released by
nervous system
• Respond with mechanical contraction
– Develops tension as proteins slide past each other

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3
Q

Skeletal muscle tissue

A

• Location: (general)
– In skeletal muscles attached to
skeleton
– Most abundant
• Cells: very large! (muscle fibers)
– long and slender
– multinucleated
– striated (striped); dark- light bands
– Amitotic
• Voluntary control
– Subject to conscious control
• Somatic motor nervous system
– Some subconscious control:
diaphragm, reflexes, postural
muscles

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4
Q

Location

A

Attached to skeleton

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5
Q

Control

A

Voluntary- somatic
motor nervous system

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6
Q

Shape of fibers (cells)

A

Elongated, cylindrical,
blunt ends: FIBERS

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7
Q

Striations

A

Yes

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8
Q

of nuclei/cell

A

Many

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9
Q

Location of nuclei

A

Periphery

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10
Q

Function

A

Movement, heat,
posture

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11
Q

Functions of skeletal muscle

A

• Composition of muscle as organ:
– Skeletal muscle tissue, connective
tissue, nerves, blood vessels
• Functions:
– Movement of skeleton
– Maintain body posture
– Support and protect soft tissue
– Guard entrances and exits
– Thermoregulation
– Communication
– Energy storage…lots of proteins

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12
Q

Skeletal muscle connective tissue

A

• Major connective tissue: fascia
– Tough sheet of connective tissue
• Below superficial fascia
(subcutaneous fat layer)
– Functions:
• Anchors to surrounding
tissue
• Separates individual muscles
• Binds together muscle
groups of similar function
• Fills spaces between muscles
• Contains nerves and blood,
lymph vessels supplying
muscle

• 3 more connective tissue
layers internal to fascia
– Epimysium: surrounds
whole muscle
– Perimysium: surrounds
fascicle (fiber bundles)
• “grain” of the meat
– Endomysium: surrounds/
between individual
muscle fibers
• Contains myosatellite
cells
• Nerve supply and extensive
blood vessel branches
throughout

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13
Q

Skeletal muscle tissue attachments

A

• Indirect attachment to
bones: epi-, peri-, and
endomysium come together
– Tendons: bundle
attached to bone
periosteum or fascia of
other muscles
– Aponeurosis: sheet
maybe to >1 bone
• Direct attachments: collagen
fibers fused directly to bone
periosteum or cartilage
perichondrium

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14
Q

Nerve and blood supply

A

• Nervous system controls skeletal
muscle activity
– Somatic motor neurons – nerve
cells from brain/spinal cord that
stimulate skeletal muscle fibers
within muscle
• 1 muscle fiber controlled by
only 1 nerve cell axon (nerve
ending)
• 1 axon controls multiple fibers
• Blood supply is extensive!
– Need rich blood supply!
• Oxygen, nutrients in (artery)
– Make, use lots of ATP!!!
• Waste, heat out (vein)

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15
Q

Skeletal muscle and fibers

A

• Skeletal muscle (organ) with epimysium around it
• Muscle made of fascicles with perimysium around them
• Fascicles made of bundles of muscle fibers (cells) with endomysium
around them

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16
Q

Skeletal muscle cells- muscle fibers!!

A

• Large, multinucleate, non-dividing
– Myoblast fusion forms multinucleated muscle fibers
– Purpose of many nuclei?
– Limited repair possible -myosatellite cells (in endomysium)
Some:
100μm wide
12 in. long !!

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17
Q

Skeletal muscle fiber structure

A

• Sarcolemma: plasma membrane
– Characteristic transmembrane potential, negative ICF vs. ECF
– Electrically excitable cells
• Transverse (T) tubules: invaginations (folding in) of sarcolemma
– Quick spread of action potential (electrical signal) allows for
synchronous muscle fiber contraction

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18
Q

Muscle fiber structure

A

• Sarcoplasm: cytoplasm
– Nuclei!
– Mitochondria (ATP)
– Myofibrils: protein filament bundles
– Glycogen!
– Myoglobin: O2 storage,
pigmented
Muscle fiber structure
– Sarcoplasmic reticulum
• Muscle cell ER
• Stores Ca2+, keeps
cytoplasmic Ca2+ low
• Terminal cisternae:
enlarged SR ends
against T tubules
• Triad: 2 terminal
cisternae +
1 T-tubule

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19
Q

Skeletal muscle fiber structure

A

• Myofibril
– Contractile organelle of
skeletal muscle fiber
– Parallel to each other
– SR and T tubules encircle
– Other organelles squeezed
in between myofibrils
• Myofibril contains 2 types of
myofilaments (protein
filaments)
– Thin filaments w/ actin
– Thick filaments w/myosin

• Sarcomeres of myofibril
– Smallest contractile unit of
skeletal muscle fiber myofibril
– Repeating units of actin and
myosin myofilaments
– Boundaries formed by Z lines
– Dark – light areas = striations

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20
Q

Anatomy of a sarcomere

A

• Sarcomere ends are called Z discs /lines
• Striations within sarcomere:
– Darker area: A band
• Thick myosin filaments present
• H- zone – center of A band
containing only myosin
– M-line: Middle of H zone
• Zone of overlap: thin actin and
thick myosin filaments overlap
– Lighter area: I band
• Z line/disc
• Thin actin filaments
• No thick myosin filaments

• Sarcomere:
– Z disc to Z disc
– 2- ½ I bands
– 1- A band

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21
Q

Thin actin filaments

A

• Actin: contractile protein
– Attached to Z discs
– Actin molecules each
have active site for
myosin binding
• Tropomyosin: regulatory
protein
– In resting muscle: Covers
myosin binding sites on
actin
• Troponin: regulatory protein
with 3 parts for binding:
– Tropomyosin
– Actin
– Ca 2

22
Q

Thick myosin filaments

A

• Myosin: contractile protein
– Motor protein
– Head and tail
• Tail: interacts with
other myosin
molecules
• Head: two globular
subunits (ATPase)
– “Business end”
– Binds ATP, uses
for energy
– Forms cross-
bridges with actin
during
contraction

23
Q

Structural protein

A

• Titin (connectin):
– Extends from Z line to M line through thick myosin- stabilizes thick
filament
– Provides some elasticity: like elastic SPRING
Titin

24
Q

Contraction: filaments sliding

A

• Contraction = cross bridge formation
– Myosin heads bind actin, pull actin
filaments
• Thin actin filaments slide past
thick myosin towards M line
• Amount of overlap changes, but
thin and thick filaments do not
change length!
– H, I bands: become smaller→
disappear
– Zones of overlap – larger
– Z lines- closer
– A band width: same
• Shorter sarcomeres= shorter myofibrils=
shorter muscle fiber= contraction!

25
Q

Requirements
for
contraction

A
  1. Neuron stimulation of
    muscle fiber
  2. Generation, spread of
    electrical current (action
    potential) along muscle
    fiber sarcolemma
  3. Rise in muscle fiber
    intracellular Ca2+ -triggers
    contraction
    Excitation-contraction
    coupling
26
Q

Transmembrane potential

A

• Transmembrane potential:
– Uneven (+/-) charges across sarcolemma
membrane - negative inside sarcoplasm vs
outside
– Muscle fiber stimulated by neuron activity: Na+
moves in, K+ moves out = change in
transmembrane potential
– Excitation (action potential produced)-
contraction coupling

27
Q

Neuromuscular junctions

A

• Neural control of skeletal muscle
contraction
– Axon of somatic motor neuron in
brain, spinal cord extends out to
skeletal muscle fiber
• Action potential (electrical
signal) travels along axon of
neuron
• Converted to chemical signal
(ACh) to stimulate muscle fiber
• Produces action potential
(electrical signal) in muscle fiber
which results in contraction
– Neuromuscular junction (NMJ):
• Communication site between
neuron- muscle cell

• Neuromuscular junction (NMJ): (type of synapse- communication site
between neuron and another cell (ie. muscle fiber, neuron))
1. Axon terminal (neuron)
• Synaptic vesicles with chemical neurotransmitter: acetylcholine (ACh)
2. Synaptic cleft: small liquid-filled space between neuron and muscle fiber
3. Motor end plate (muscle cell sarcolemma)
• One muscle fiber controlled by only one motor neuron
• Sarcolemma in folds

28
Q

Muscle excitation

A

• Excitation: electrical
change (action
potential) in the
neuron axon leads
to action potential in
the muscle fiber
1. Neuronal action
potential (electrical
signal) arrives at
neuron’s axon
terminal:
– Causes Ca2+ entry
into terminal

  1. Ca2+ entering neuron axon terminal causes release of acetylcholine
    (chemical signal) from neuron axon terminal into cleft
    – Electrical signal (AP) has been turned into chemical signal (ACh)
    – ACh diffuses across synaptic cleft to motor end plate
    – ACh binds to ACh receptors on protein ion channel in muscle fiber
    sarcolemma (motor end plate)
  2. When Ach binds sarcolemma protein ion channel (type of ligand-gated
    ion channel) –channel open
    – A lot of Na+ moves in, some K+ moves out – why?
    – Extracellular Na+ > intracellular Na+ inside muscle fiber SO………… Na+
    rushes into sarcoplasm!! = depolarization (more + charge inside fiber)
  3. Na+ entry starts action
    potential (AP) in sarcolemma
    – Na+ entry causes more
    voltage sensitive Na+
    channels to open
    – Forms AP and spreads along
    sarcolemma (propagation)
    • Continues in one
    direction as more
    voltage sensitive ion
    channels open
    – AP spread (excitation) will
    lead to sliding of actin and
    myosin filaments
    (contraction): Excitation-
    contraction coupling!! (stay
    tuned)
29
Q

Ca2+ : the coupler!

A

• Both Ca2+ and energy (ATP) needed for contraction
• Calcium in general
– Intracellular cytoplasmic [Ca2+] kept low
– Stored in sarcoplasmic reticulum (SR)….terminal cisternae
– Important for muscle contraction: released from terminal cisternae into
sarcoplasm

30
Q

Excitation-
contraction
coupling

A

• AP moves along sarcolemma and
down T-tubules
– AP causes Ca2+ channels in
sarcoplasmic reticulum to
open
– Ca2+ released from SR
terminal cisternae
– Large amount of Ca2+ enters
sarcoplasm at zones of
overlap
• Excitation coupled to
contraction: effect of Ca2+

31
Q

Muscle fiber
contraction

A

• Resting sarcomere before
contraction starts
– Myosin head energized
(cocked position)
– Energy stored in head as
a result of prior ATP
breakdown
• Will be used to
power contraction
– Tropomyosin covers
myosin binding sites on
actin

  1. Contraction cycle start
    – Ca2+ from SR terminal cisternae
    released within zone of overlap
  2. Active sites exposed
    – Ca2+ binds troponin
    • Changes troponin shape
    • Tropomyosin rolled off
    myosin binding sites on
    actin
    • Allows actin and myosin to
    interact
  3. Cross bridge formation:
    “attach”
    – Myosin heads (which
    were in cocked position
    from previous cycle) bind
    to exposed active sites on
    actin
    – Form cross-bridges
  4. Powerstroke: “pull”
    – ADP and Pi released
    – Cocked myosin head
    pivots
    – Pulls on actin, slides actin
    past myosin filaments
    towards M line
  5. Cross bridge detaches:
    “release”
    – Another ATP binds to
    myosin to cause cross-
    bridge release
    – Myosin and actin link
    broken
    – If active sites on actin still
    exposed: bind another
    myosin
  6. Myosin reactivation: “reset”
    – ATP split by ATPase in
    myosin head →energy
    used to re-cock myosin
32
Q

End of muscle excitation: relaxation

A

• Neural stimulus ends
• AChE breaks down ACh
• Membrane returns to normal
resting transmembrane
potential
End of muscle excitation: relaxation

33
Q

Relaxation

A

• SR Ca2+ channels close, Ca2+ returns to SR
– Ca2+ pumped (requires ATP!) into
terminal cisternae
– Takes longer than release: relaxation
takes longer than contraction
• Troponin-tropomyosin return to normal
– Active sites covered, no cross bridges
• Rigor mortis?
• Note: ATP needed for contraction and
relaxation!

34
Q

Tension –
length
relationship

A

• Starting sarcomere length affects tension (force of contraction) produced
• Affects number of cross bridges that can form
• Optimal starting sarcomere length? – 100% resting length and moderate
range around (80-120% resting length) -allows optimal overlap of filament
• Starting sarcomere length too short or too long? – can not form optimal #
of cross bridges, affects filaments sliding/tension

35
Q

Twitch

A

• Understand contraction of muscle fiber
to understand contraction of skeletal
muscle!!
• Muscle twitch: contraction of muscle
fiber (or skeletal muscle)
– In response to motor neuron
stimulation
– Produces tension: pulling force
• Measure of force of muscle
contraction
– Single twitch: not enough tension to
perform work (ie. move object
(load))

36
Q

Twitch contraction in a muscle fiber

A

• Latent period
– No tension yet but excitation!
– AP spreads, SR releases Ca2+
• Contraction period
– Tension (force of contraction)
peaks
– Ca2+ binding troponin
– Myosin binding sites on actin
exposed- cross bridges form
– If tension> load, muscle
shortens
• Relaxation period- longer
– Ca2+ pumped into SR
– Cross bridges detach,
tropomyosin covers active sites
– Tension returns to resting

37
Q

Factors that affect
fiber tension

A

• Amount of tension produced by 1
muscle fiber varies, depends on:
– Frequency of stimulation –
affects Ca2+ in cytosol
– How stretched muscle was
before stimulation: length-
tension relationship
• Resting produces optimal #
of x-bridges
– Temperature: “warming up”
benefits

38
Q

Frequency of stimulation

A

• Repeated stimulation (frequency of stimulation) of muscle fiber by motor
neuron results in twitches with greater tension: Wave summation
– Waves of contraction add together
– No time to pump all Ca2+ back into SR, Ca2+ increases with each stimulus
• Types of wave summation:
– Incomplete (unfused) tetanus: lower rate of stimulation, partial
relaxation occurs
– Complete (fused) tetanus: high rate of stimulation, no relaxation
before next stimulation

39
Q

Skeletal muscle
tension

A

• Amount of tension in whole muscle,
depends on:
– Amount of tension in individual fibers
(frequency of stimulation)
– # of muscle fibers contracting at same
time (recruitment)

40
Q

Motor
units

A

• Motor unit: Somatic motor neuron + all muscle fibers it controls (more
than 1 fiber!)
• Fibers not clustered together- spread throughout entire muscle
• Motor units differ in # of muscle fibers
– Size of motor unit reflects control
• Few fibers= precise control, less force (eye)
• Many fibers= less control, more force (leg)
• In 1 muscle = mixture of motor units

41
Q

Motor unit
recruitment
and tension

A

• Motor unit recruitment:
increase in # of active motor
units
– Lifting a feather – few
motor units recruited
– Lifting a box of books –
more motor units
stimulated

42
Q

Muscle relaxation

A

• Remember what happens at muscle fiber level!
• Muscle returns to original length:
1. Elastic forces
• Recoiling
• Pull of tendons, ligaments
2. Opposing muscle contractions: antagonistic pairs
3. Gravity

43
Q

Energy for muscle activity at rest

A

• Resting muscle fibers:
– Low ATP demand – some ATP storage but not significant (5-6 sec)
– Fatty acids used
– Some glucose stored as glycogen
– ATP used to convert creatine to creatine phosphate: quick “energy”
storage

44
Q

Energy for peak activity (max exertion)

A

• Glucose = energy source
• 5-6 seconds (like 50m dash) – immediate energy needed!
– Immediate energy source: ATP and Creatine phosphate (CP)
• 50-60 seconds (like 400m run) – short term, quick energy needed!
– High demand for ATP, but oxygen diffusion into mitochondria slow
– Most from CP and anaerobic glycolysis, little from aerobic metabolism
– Drawbacks: ↑ lactic acid produced, pH ↓, inefficient ATP production,
rapid fatigue results

45
Q

Energy for moderate activity

A

• Mins- hrs (moderate pace long run)- long term, continual energy needed
– Increased demand for ATP, no excess ATP made
– Mitochondria meets demand if O2 supply sufficient – aerobic
metabolism of glycogen!
– O2 consumption ↑, blood flow to muscles ↑ to meet demand
– If glycogen low, other nutrients used
– Glycogen, lipids and amino acid depleted? = muscle fatigue

46
Q

Muscle fatigue

A

• Muscle contraction can not
continue even with nervous
stimulation
– Not well understood!- CNS or
muscle level?
– Lactic acid, H+ build up: pH ↓
– Ca2+ release and uptake
– Decreased O2 available
– Energy sources depleted (CP,
glycogen, other substrates)
– Hyperthermia
– Psychological basis

47
Q

Muscle recovery

A

• Return body to pre-exercise conditions
– Lactic acid recycled to pyruvate – make ATP, rebuild glycogen
– Excess post-exercise oxygen consumption (EPOC) – “O2 debt”
• Increased amount of O2 inhale to help return
• The more ATP required for recovery, the more O2 needed
• Correct blood pH: lactic acid recycled, CO2 exhaled
• Replace O2 on hemoglobin in blood, myoglobin in muscle
– Heat elimination
• Delayed onset muscle soreness (DOMS) – small muscle tears? Injury to
tendons, body adapts after and becomes stronger

48
Q

Skeletal muscle fiber types

A

• Typed by:
– Time to reach peak tension (fast vs. slow)
– Major metabolic pathways for forming ATP (glycolytic vs. oxidative)
• Types:
– Fast glycolytic: (fast fibers)
• WHITE muscle fibers
– Slow oxidative (slow fibers)
• RED (dark) muscle fibers

• Red Slow-oxidative
– Slow contraction
– Small diameter fibers- fewer myofibrils
– Less forceful contractions
– More mitochondria-red
– Extensive blood supply- dark
• More O2 - Aerobic metabolism
– More myoglobin: red
• Red-colored O2-binding/ releasing
protein
– Slow to fatigue: prolonged sustained
contractions for hours= endurance
• Maintain posture, marathon running
(endurance)

• White Fast-glycolytic
– Majority in body
– Largest diameter, most
myofibrils: powerful
– Faster contractions
– Less myoglobin, fewer blood
vessels, few mitochondria
– Lots of glycogen for
glycolysis: anaerobic
– Fatigue easily
– Best suited for strong,
powerful, short contractions
• Anaerobic exercise:
weight lifting, sprinting,
swing bat

49
Q

Muscles and fiber types

A

• White muscles: pale
– Fast fibers more abundant
– Speed
– Turkey breast “white meat”
• Red muscle: reddish
– Slow fibers more abundant
– Endurance
– Turkey legs “dark meat”
• Humans:
– One muscle usually mixture
– % genetically determined
– But fibers in motor unit = SAME!… Refer back to motor unit
recruitment
– Aerobic physical conditioning can affect muscle fiber performance

50
Q

Physical conditioning

A

• Anaerobic conditioning
– Short duration, high intensity,
frequent: i.e. weight lifting, sprint
training
– Promote strength, speed and power
– Contraction of fast-glycolytic fibers
– Adaptations cause muscles to get
bigger (hypertrophy) – due to ↑ # of
fiber myofibrils NOT fibers!
?
• Aerobic conditioning
– Longer activity, moderate intensity, endurance training (ie. marathon)
– Must be supported by oxidative phosphorylation (O2, mitochondria)
– Adaptations to support metabolism, some fast fibers physiologically be
more like slower fibers
– No hypertrophy