Transcript Muscle Tissue - Doctor Jade Main

Muscle Tissue
Muscle Tissue Classification
Skeletal Muscle
Cardiac Muscle
Intercalated
Disc
Smooth Muscle
Skeletal Muscle
• directly or indirectly
attached to bones of
skeleton
Functions
• movement
– simple-breathing to highly coordinated onesswimming
• posture & body position
– maintenance or stability
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constant muscle contraction holds the head
up
• store & move substances in the body
• maintains body temperature
– muscle contraction requires energy; when
energy is used some energy is converted to
heatkeeps body temperature within the
normal range
– when cold shivering occurs
Gross Anatomy
• entire muscle is surrounded by
epimysium
• fuses into connective tissue
sheets called fascia
• groups of muscle fibers are
arranged in bundles called
fascicles; wrapped in connective
tissue layer-perimysium
– contains blood vessels &
nerves
• endomysium surrounds each
individual muscle fiber
• connective tissue layers are
continuous through length of
muscle
• at end of muscle, collagen fibers
of epi-, peri- and endomysium
come together to form tendons &
aponeurosis
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Microscopic Anatomy
muscle cell myofibril or fiber is thin & very
long
Multinucleate-maybe hundreds present
– arranged around periphery just
beneath cell membrane
sarcolemma-plasma membrane
surrounds sarcoplasm or cytoplasm
– contains long protein bundles called
myofibrils, a great deal of glycogen
and a red pigment, myoglobin
Smooth endoplasmic reticulum-SR or
sarcoplasmic reticulum
– forms network around each myofibril
and periodically expands into
terminal cisternae
sarcolemma has tubular infoldings called
T (transverse) tubules which are
associated with two terminal cisternae
t tubule plus adjacent terminal cisternae is
a Triad
– stores & releases calcium needed for
contractions
– T tubules conduct action potential
through the entire muscle fiber
Myofibril Composition
• made of myofilaments
– arranged in repeating
patterns
– appear as striations
under a microscope
– two types: actin &
myosin
• one repeat is a sarcomere
– smallest, functional unit
of skeletal muscle
• narrow plates called Z
discs separate the
sarcomeres
• a sarcomere extends from
one Z disc to the next
Sarcomere Structure
• A band
• darker, middle part
• myosin & actin
• I Bands
• lighter areas
• actin only
• Z disc
• passes through middle of each I
band
• defines one sarcomere
• H zone
• either side of M line
• M line
• center of H zone
Proteins in Muscle Fibers
• Contractile Proteins
– actin
– myosin
• Regulatory Proteins
– tropomyosin
– troponin
• Structural Proteins
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titin
alpha actinin
myomesin
nebulin
dystrophin
Myosin
MYOSIN-THICK
FILAMENT
contractile protein
comprised of 2
subunits
twisted around one
another
forming long
coiled tail &
pair of heads
project toward m
line
Actin
• contractile protein
• comprises thin
filaments
• composed of two
intertwined strands of
fibrous (F) actincontractile protein
• each F-actin is made
up of subunits called
G-Actin
• each G-actin has an
active site which can
bind a myosin head
Regulatory Proteins
• Control contraction-turn it
on & off
• Tropomyosin
– winds around actin
– covers myosin binding
sites preventing actinmyosin interactions
• Troponin
– calcium binding protein
each
– bound to each
tropomyosin
• When calcium binds to
troponinchanges
shapepulls tropomyosin
off actinmyosin binding
site exposedcrossbridges
form
Structural Proteins
• Titin
– huge elastic molecule
– recoils after stretching
– anchors myosin to Z-disc
• Nebulin
– helps anchor thin filaments
to Z discs
– helps stabilize thick
filament
• Alpha actinin
– comprises z discs
• Myomesin
– forms M line
• Dystrophin
– under sarcolemma
– attaches actin to
membrane proteins
Sliding Filament Theory
• theory of how muscle contraction
takes place
• under microscope, during muscle
contraction
• H zone & I bands get smaller
• H zone almost disappears
• zones of overlap get larger
• Z lines move closer together
• width & length of A band remains
constant
• only make sense if thin filaments
slide to center of each sarcomere
• actin slides over myosin which
causes sarcomere to shorten
• ultimately entire muscle cell
shortens
Sliding Filament Theory
Contraction
• calcium binds to troponin
 tropomyosin is pulled
toward actin groove
• myosin binding site
uncovered
• myosin heads interact
with actin
• forming cross bridges
• like hinges
• myosin head pivots at its
base
• pulls on actin
• causing it to move to
center of sacromere
• muscle shortens
Muscle Cell Contraction
• Skeletal muscles only contract when
activated by motor neurons from
CNS
NEURON STRUCTURE
• Dendrites
– Receive
information
– Typically many
• Axons
– Send information
– Covered with
Myelin Sheath
– End in Terminal
Buttons
Neuromuscular Junction
• communication between
muscles & nerves occurs at
neuromuscular junction
• each branch of a motor nerve
fiber ends in a synaptic knob
• nestled in a depression on
sarcolemmamotor end
plate (MEP)
• exhibits many junctional
folds
• contains receptors
Neuromuscular Juncion
Neuromuscular Junction
• cells do not touch
• separated by a tiny
gap-synaptic cleft
• synaptic knobs contain
vesicles of
acetylcholine-ACH
• neurotransmitter
• the cleft & sarcolemma
contain ACHE or
acetylcholinesterase
– Breaks down ACH
Excitation Contraction Coupling
• Transfer of an impulse from somatic
motor neuron to muscle cell is
excitation contraction coupling
• 4 steps
• ACH release
• Activation of ACH receptors
• Production of Muscle Action Potential
• Termination of ACH activity
STEP 1 ACH release
• action potential
reaches synaptic
terminal
• opens calcium gates
• calcium enters neuron
causing synaptic
vesicles to fuse with
cell membrane which
releases ACH via
exocytosis into
synaptic cleft
• ACH diffuses across
cleft
STEP 2 Activation of ACH
Receptors
• ACH binds to
receptors on
motor end plate
• opens sodium
gates
• sodium rushes
into sarcoplasm
STEP 3 Production of Muscle
Action Potential
• positive charges of
sodium accumulate
• membrane potential of
cell moves toward zero
• as concentration of
sodium increases
threshold is reached
• muscle cell depolarizes
• Action potential begins
and spreads in all
directions
• invaginates at T tubules
• muscle cell contracts
STEP 4 Termination of ACH
Activity
• influx of calcium continues until
acetylcholinesterase degrades ACH
removing it from receptors
• component parts are recycled
• calcium is pumped back into the SR
• muscle cell relaxes
Muscle Cell Contraction
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arrival of action potential
releases ACH into cleft
binds to receptors
sodium rushes into cell
causes an Action
Potential in muscle cell
Muscle Cell Contraction
• action potential is
propagated across entire
membrane
• when reaches t
tubuletravels down t
tubules
• t tubules & terminal
cisternae of sarcoplasmic
reticulum form a triad
• triad releases calcium
from sarcoplasmic
reticulum
Muscle Cell Contraction
• calcium binds to
troponin
• changes its shape
• tropomyosin swings
away from active site
• exposes myosin
binding sites on actin
• cross-bridges form
• initiates contraction
• effect of calcium is
instantaneous
• contraction cycle
begins
Contraction Cycle Steps
• 1. ATP Hydrolysis
• 2. Attachment of
Myosin to Actin
forming CrossBridges
• 3. Power Stroke
• 4. Detachment of
Myosin from Actin
Step 1- ATP Hydrolysis
• each myosin head
must have an ATP
bound to it to initiate
contraction
• head contains
myosin ATPase
hydrolyzes
ATPADP + Pi &
energy
• ADP & Pi still
attached to myosin
head
Steps 2 & 3-Attachment of Myosin
to Actin & Power Stroke
• energized myosin
binds to exposed
active site on actin
forming a crossbridge
• myosin releases ADP
& phosphate
• flexes into a bent, low
energy position
bringing the thin
filament with it
• the power stroke
Step 4-Detachment of Myosin From Actin
• at end of power stroke myosin remains attached to actin until nyosin
binds another ATP
• upon binding more ATP, myosin releases actin and it is ready to
begin the process again by hydrolyzing the ATP
• each cycle shortens the sarcomere ~10 nm
• each myosin head continues to attach, pivot & detach as long as
calcium & ATP are available
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Relaxation
duration of muscle contractions depend on duration of stimulus at
neuromuscular junction
ACH does not last long-chewed up by ACHE
contraction continues only if more action potentials arrive at synaptic
terminal in rapid succession
muscle fiber & sarcoplasm return to normal or relax in two ways
– active transport of calcium across cell membrane into extracellular fluid
– active transport of calcium into the sarcoplasmic reticulum
• more important way
almost as soon as calcium is released-SR begins to absorb calcium from
surrounding sarcoplasm
here calcium binds to calsequestrin & is stored until stimulated again
as calcium in sarcoplasm decreases, calcium detaches from troponin
causing it to return to its original position recovering active sites with
tropomyosin
once contraction has ended sarcomere does not automatically return to its
original length
Sacromeres actively shorten but there is no active mechanism to reverse
the process
combination of elastic forces, opposing muscle contractions and
gravity return muscle to its uncontracted state
Tension Production
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muscle cells contract & shorten causing
them to pull on collagen fibers 
generates tension
collagen fibers resist building tension
– as muscle continues to pull on
collagen fibersfibers transmit force
and pull on something else
what happens depends on what fibers
are attached to and how muscle cells are
arranged
muscles are attached to at least 2
different structures
– usually bone & occasionally soft
tissue
as muscle contracts, one attachment
movesinsertion
other attachment remains stationary
origin
developing tension pulls object toward
source of tension
Tension Production
• tension produced by an individual muscle
fiber varies
• depends on
• resting length of fiber at time of
stimulation
– determines amount of overlap between
thin & thick filaments
• frequency of stimulation
– effects internal calcium concentration
• number of muscle fibers stimulated in
one muscle
Length-Tension Relationship
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amount of tension depends on how
stretched or contracted it was prior to being
stimulated
length-tension relationship
amount of tension produced by a muscle is
related to number of cross bridges
formed
number of cross bridges that can form
depends on degree of overlap between
thick & thin filaments
only myosin heads in zone of overlap can
bind to active sites on actin &produce
tension
Sarcomeres work most efficiently in an
optimal range of lengths
Outside optimal rangemuscle cannot
produce as much tension
optimal range is range where maximum
number of cross bridges can formmaking
most tension
when sarcomeres are short thick filaments
are jammed up against Z line
– cross bridges form but myosin heads
cannot pivotno tension production
sarcomeres with length longer than optimal
range has reduced zone of overlapless
cross bridges can formless tension
Frequency of Stimulation
• Increasing the number of nerve
impulses to the muscles will keep ACH
being released
• which will keep calcium being released
• which will keep cross bridges forming
• which will keep the muscle contracting
• which will cause the development of
more tension
Muscle Twitch
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one above threshold stimulus to
a muscle produces one
contraction/relaxation cycletwitch
vary in duration with type,
location, temperature &
environmental conditions
eye twitch-7.5msec
soleus (calf muscle) twitch100msec
too brief to be part of normal
activity
to show what a twitch looks like a
myogram is used
twitch can be divided into three
parts
1) latent period
2) contraction phase
3) relaxation phase
Muscle Twitch
• latent phase begins as stimulation of muscle
begins-lasts 2msec
• as tension rises to a peak contraction phase
begins (10-100msec)
• during relaxation phase tension decreases to
resting levels (10-100msdc)
Treppe
• twitches produce no
work
• sending more & more
stimulation to muscle
in short period of time
results in changes to
initial twitch
• when skeletal muscle
is stimulated for a
second time
immediately after a
relaxation phase
treppe contraction
develops
TREPPE
• myogram tracing shows a slightly higher tension than the first
tension
• tension increases over first 30-50 stimulations and thereafter
amount of tension remains constant
• increase in tension is due to increases in calcium in sarcoplasm
• stimuli are arriving so rapidly that calcium is not reabsorbed into the
SR
• thus there is more Ca in cytosol when the second stimulus arrives
• resulting in slightly more tension production & a slightly higher
tracing
Wave Summation
• as frequency of stimuli
increase before
previous twitch has
ended each new twitch
rides piggy back on
previous one
• wave summation
• result of one wave of
contraction being added
to another
• produces sustained
contraction called
incomplete tetanus
TETANUS
• at a still higher
frequencymuscl
e has no time to
relax between
stimuli
• twitches fuse into
a smooth,
prolonged
contraction called
complete
tetanus
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Tension
Production
tension developed depends on number of muscle
fibers involved
• each muscle fiber is innervated by one motor
neuron
• when nerve signal approaches end of axon-it
spreads to all of axon’s terminal branches &
stimulates all muscle fibers supplied by them
• makes all muscle fibers connected to neuron
contract at same time
• one nerve fiber & all muscle fibers innervated by
it is one motor unit
Motor Units
• some motor neurons
control few muscle fibers
• others control hundreds
• number of neurons
innervating a muscle
indicates how fine
movement can be in that
muscle
• eye muscles need to have
precise control
– neuron to muscle in
eye controls 4-6 fibers
• leg muscles do not need
precise control
– neuron to leg muscle
can control 1000-2000
muscle fibers
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MOTOR UNITS
neuron firescontracts all muscle
cells in one motor unit
greater tension can be be
generated by recruiting more motor
units
smooth & steady increase in
muscle tension is produced by
increasing number of active motor
units
– recruitment
peak tension occurs when all motor
units in a muscle contract to
tetanus
such powerful contractions do not
last long
sustained contractions are
maintained by asynchronous
recruitment
– motor units are activated on a
rotating basis
– some rest & recover while
others contract
Tension Production & Movement
• amount of tension produced in a skeletal
muscle depends on several factors
• before movement is possible, tension must
overcome resistance
– passive force opposing movement
– amount of resistance depends on
object’s weight, shape, friction and other
factors
• when tension is greater than resistance
object moves
Contraction Types
• contractions types are based
on pattern of tension
development
• Isometric
• Isotonic
–Concentric
–Eccentric
Isometric Contractions
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tension develops with no length change in the muscle
tension never exceeds resistance
occurs when you begin to use a muscle
occurs when you push against a locked door
– cross bridges formtension rises to a peakmuscle cannot
overcome resistance
• Example-carrying a bag of groceries-arm muscles are contracting to
hold the bag, but the arm itself is not moving
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Isotonic
Contractions
when tension in a muscle increases &
produces a change in muscle length
two types: eccentric & concentric
concentric contractions
– muscles shorten as it maintains
tension
eccentric contractions
– muscle lengthens as it maintains
tension
Examplebicep shortens then stretches as a
dumbell is curled
tension on muscle remains the same in
a muscle as length increases or
decreases
concentric is shortening (b) and
eccentric is lengthening (c)
To review-Isometric contraction is
when a muscle is used but it does not
shorten (a)
Both isotonic and isometric
contractions are used in normal
activities
Muscle Metabolism
• contracting
muscles use
enormous amounts
of ATP
• one muscle fiber
may have 15 billion
thick filaments
• during contraction
each filament
breaks down 2500
ATP molecules/sec
Muscle Metabolism
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ATP is also needed for
cross bridge release
to pump calcium back into SR
to restore sodium & potassium
levels to precontraction
conditions
cannot have all ATP needed for
contraction before contraction
begins
ATP stores are depleted in 6
sec.-time
enough for 8 twitches
for a cell is to continue to
contract more ATP must be
generated
muscle fiber generates ATP at
same rate it is used
ATP
• energy used to power
all activity in cells &
the body
• three high energy
phosphate bonds
• breaking off one
phostphate yields
about 7kcal of energy
• ATP  ADP + Pi +
7Kcal
Ways to Acquire ATP
• Creatine
Phosphate
• Glycolysisanerobic
cellular
respiration
• Aerobic Cellular
Respiration
Ways to Acquire ATP
Creatine Phosphate
• at rest muscle produce
more ATP than they use
• excess ATP is used to make
creatine phosphate
(phosphocreatine)
• in working muscles-creatine
kinase transfers a high
energy phosphate from
phosphocreatine to ADP 
creatine + ATP
• provides energy needed for
short burst of intense activity
• 1 minute of brisk walking or
6 second of sprinting
Glycolysis
• once creatine phosphate
stores have been used &
respiratory & cardiovascular
systems cannot deliver
oxygen to muscles fast
enough to use aerobic
respiration to produce ATP
• ATP is provided by
anaerobic cellular
respiration-glycolysis
• occurs in cytoplasm
• oxidizes glucose to 2
molecules of pyruvic acid
and 2 ATP molecules (net)
• produces enough ATP for
30-40 seconds of maximum
activity
Glycolysis
• without oxygen
pyruvic acidlactic
acid + ATP
• organic acid
• can lower blood pH
• eventually pH
changes alter
functional
characteristics of
enzymes
• muscle fibers cannot
continue to contract
• end resultmuscle
soreness & fatigue
Aerobic Respiration
• after 40 seconds or so
cardiopulmonary system catches
up  delivers oxygen to muscles
fast enough for aerobic
respiration
• requires oxygen
• occurs in mitochondria
• First-TCA (tri-carboxylic acid) or
Kreb’s Cycle
• Second-electron transport chain or
oxidative phosphorylation
• starting product -pyruvic acid
• muscles using aerobic respiration
can contract for long periods of
time
• 36 molecules of ATP are produced
• in exercise lasting 10 minutes or
more 90% of ATP is produced
aerobically
Metabolism Overview
Types of Muscle Fibers
•slow oxidative fibers
•fast glycolytic fibers
•fast oxidativeglycolytic fibers
Slow Oxidative Muscle Fibers
• called red fibers
• contain a great deal of mitochondria, blood capillaries &
myoglobin-red pigment like hemoglobin which binds oxygen
– provide dramatically higher oxygen supply
• gives fibers dark red color
– muscle dominated by slow twitch fibers is referred to as
dark meat in chicken
• contract slowly
– require 3X as long to contract after stimulation as fast
twitch fibers
• fatigue resistant
– specialized to contract for long periods of time
– keep contracting long after fast fibers fatigue
• diameters are half that of fast fibers
• less dependent on anaerobic metabolism
– obtain ATP via aerobic respiration
– used almost constantly to maintain posture, to stand and
to walk
Fast Glycolytic Fibers
• White fibers
• Muscles appear pale
– termed white muscle
• contract 0.01 sec. after stimulation
– 2-3X faster than slow twitch fibers
• faster speed leads to faster tension development
– muscles dominated by fast fibers display powerful
contractions
• have large diameters, densely packed myofibrils, large
glycogen reserves and few mitochondria
• use massive amounts of ATP
• rely on anaerobic respiration
– fatigue more rapidly due to lactic acid build up
Fast-Oxidative Glycolytic Fibers
• Intermediate fibers
• combine fast twitch response with aerobic
fatigue resistant metabolism
• contain large amount of myoglobin &
capillaries
– dark red in color
• get ATP by aerobic mechanisms
• fast due to presence of a faster type of
ATPase
• moderately resistant to fatigue
Thought questions: Why do chickens have white
breast meat and dark leg meat?
What does this say about the activities of the
associated muscles?
Why do ducks have dark breast meat?
Muscle Composition
• muscles are composed of all three fiber types
• proportion of each differs from muscle to
muscle
• no slow twitch fibers in eye or hand muscles
– need swift contractions
• people with different types & levels of
physical activity differ in the proportion of
each fiber type
• muscle performance & distribution of muscle
fibers is genetically determined
• proportions of different muscle fibers can
change with physical conditioning
Muscle Performance
• rated in terms of
• Power
– maximum amount of tension produced
• Endurance
– amount of time muscle can perform particular
activity
• two factors determine these performance
capabilities
• type of muscle fiber
• physical conditioning
– training of that muscle
Aerobic Endurance
• length of time muscle can contract
while supported by mitochondrial
activities
• determined by substrate availabilitybreak down of carbohydrates, lipids &
amino acids
• involves sustained low level muscle
activity-jogging
• training-alters characteristics of
muscle fibers
• fasts fibers will develop characteristics
of intermediate fibers
• improves performance of
cardiovascular system which delivers
oxygen & nutrients to muscles
• does not promote hypertrophy
Anaerobic Endurance
• length of time muscle contraction can be
supported by glycolysis & by existing
ATP & creatine phosphate reserves
• limited-amounts of ATP & creatine
phosphate, amounts of glycogen & ability
of muscles to tolerate lactic acid
• improve-frequent, brief, intensive
workouts
– weight lifting & body building
– produce muscle hypertrophy• repeated, exhaustive stimulation causes
muscle fibers to develop more
mitochondria, more glycolytic enzymes &
more glycogen
• muscle will develop more myofibrilshave more thin & thick filaments
• when muscles are not usedbecome
flaccid, smaller-atrophy
Muscular Strength &
Conditioning-Training
Smooth Muscle
• found in almost every
organ
• walls of hollow internal
structures, blood
vessels, stomach,
intestine, gallbladder &
urinary bladder
• important in
homeostasis
• contraction changes
shape of organs
• generate force to move
materials through the
lumens of organs
Smooth Muscle Structure
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long, slender, spindle-shaped
no striations, no myofibrils and no
sarcomeres
contains myosin & actin filaments
no t-tubules
SR forms loose network through
sarcoplasm
Actin is attached to dense bodies (like Z
discs)
intermediate fiber bundles are attached to
dense bodies
arranged so entire surface of actin is
covered by myosin heads
continuous line of myosin heads allows
actin to slide down myosin without
interruption producing tension
dense bodies & intermediate filaments
anchor thin filaments
when sliding they slide against each other
to produce contraction
Smooth Muscle Contraction
• dense bodies
are not found in
a straight line
• during
contraction
causes cell to
twist like a cork
screw
Types of Smooth Muscle
• Multiunit types
• Single-unit types or
Visceral Smooth
Muscle
Multiunit Smooth Muscles
• innervated like skeletal
muscle
• neural activity generates
an action potential which
is propagated over the
sarcolemma
• found-some large
arteries, pulmonary air
passages, piloerector
muscles and the iris
• cells contract or relax
depending on type of
neurotransmitter
released
Visceral Smooth Muscle
• arranged in sheets or layers
• adjacent cells connected by
gap junctions
• one muscle cell contracts
electrical impulse travels
to adjacent muscle cells
contraction spreads in
waves soon involving all
cells
• initial stimulus may be motor
neuron
• also contracts in response to
chemicals, hormones,
oxygen, CO2, stretching &
irritation
Excitation-Contraction Coupling
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trigger for contractioncalcium in sarcoplasm
calcium enters from extracellular fluid
more is released by the sarcoplasmic reticulum
calcium interacts with calmodulin, a calcium binding protein
which activates light chain myokinase to break down ATP
• starts contraction
• relaxation occurs when calcium is removed from cytosol
• accomplished by a Ca-Na antiport exchange & by Ca-ATPase