Download muscle as a tissue

Chapter 10
Muscle Tissue
• Alternating
contraction and
relaxation of cells
• Chemical energy
changed into
mechanical energy
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3 Types of Muscle Tissue
• Skeletal muscle
– attaches to bone, skin or fascia
– striated with light & dark bands visible with scope
– voluntary control of contraction & relaxation
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3 Types of Muscle Tissue
• Cardiac muscle
– striated in appearance
– involuntary control
– autorhythmic because of built in pacemaker
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3 Types of Muscle Tissue
• Smooth muscle
–
–
–
–
attached to hair follicles in skin
in walls of hollow organs -- blood vessels & GI
nonstriated in appearance
involuntary
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Functions of Muscle Tissue
• Producing body movements
• Stabilizing body positions
• Regulating organ volumes
– bands of smooth muscle called sphincters
• Movement of substances within the body
– blood, lymph, urine, air, food and fluids, sperm
• Producing heat
– involuntary contractions of skeletal muscle (shivering)
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Properties of Muscle Tissue
• Excitability
– respond to chemicals released from nerve cells
• Conductivity
– ability to propagate electrical signals over membrane
• Contractility
– ability to shorten and generate force
• Extensibility
– ability to be stretched without damaging the tissue
• Elasticity
– ability to return to original shape after being stretched
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Skeletal Muscle -- Connective Tissue
• Superficial fascia is loose connective tissue & fat
underlying the skin
• Deep fascia = dense irregular connective tissue around
muscle
• Connective tissue components of the muscle include
– epimysium = surrounds the whole muscle
– perimysium = surrounds bundles (fascicles) of 10-100
muscle cells
– endomysium = separates individual muscle cells
• All these connective tissue layers extend beyond
the
muscle
belly
to
form
the
tendon
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Connective Tissue Components
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Nerve and Blood Supply
• Each skeletal muscle is supplied by a nerve,
artery and two veins.
• Each motor neuron supplies multiple muscle cells
(neuromuscular junction)
• Each muscle cell is supplied by one motor neuron
terminal branch and is in contact with one or two
capillaries.
– nerve fibers & capillaries are found in the
endomysium between individual cells
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Fusion of Myoblasts into Muscle Fibers
• Every mature muscle cell developed from 100 myoblasts
that fuse together in the fetus. (multinucleated)
• Mature muscle cells can not divide
• Muscle growth is a result of cellular enlargement & not
cell division
• Satellite cells retain the ability to regenerate new cells.
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Muscle Fiber or Myofibers
• Muscle cells are long, cylindrical & multinucleated
• Sarcolemma = muscle cell membrane
• Sarcoplasm filled with tiny threads called myofibrils &
myoglobin (red-colored, oxygen-binding protein)
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Transverse Tubules
• T (transverse) tubules are invaginations of the sarcolemma
into the center of the cell
– filled with extracellular fluid
– carry muscle action potentials down into cell
• Mitochondria lie in rows throughout the cell
–Tortora
near
the muscle proteins that use ATP during contraction10-12
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Myofibrils & Myofilaments
• Muscle fibers are filled with threads called myofibrils
separated by SR (sarcoplasmic reticulum)
• Myofilaments (thick & thin filaments) are the contractile
proteins of muscle
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Sarcoplasmic Reticulum (SR)
• System of tubular sacs similar to smooth ER in
nonmuscle cells
• Stores Ca+2 in a relaxed muscle
• Release of Ca+2 triggers muscle contraction
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Atrophy and Hypertrophy
• Atrophy
– wasting away of muscles
– caused by disuse (disuse atrophy) or severing of the
nerve supply (denervation atrophy)
– the transition to connective tissue can not be reversed
• Hypertrophy
– increase in the diameter of muscle fibers
– resulting from very forceful, repetitive muscular
activity and an increase in myofibrils, SR &
mitochondria
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Filaments and the Sarcomere
• Thick and thin filaments overlap each other in
a pattern that creates striations (light I bands
and dark A bands)
• The I band region contains only thin filaments.
• They are arranged in compartments called
sarcomeres, separated by Z discs.
• In the overlap region, six thin filaments
surround each thick filament
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Thick & Thin Myofilaments
• Supporting proteins (M line, titin and Z disc help
anchor the thick and thin filaments in place)
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Overlap of Thick & Thin Myofilaments
within a Myofibril
Dark(A) & light(I) bands visible with an electron microscope
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Exercise-Induced Muscle Damage
• Intense exercise can cause muscle damage
– electron micrographs reveal torn sarcolemmas,
damaged myofibrils an disrupted Z discs
– increased blood levels of myoglobin & creatine
phosphate found only inside muscle cells
• Delayed onset muscle soreness
– 12 to 48 Hours after strenuous exercise
– stiffness, tenderness and swelling due to
microscopic cell damage
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The Proteins of Muscle
• Myofibrils are built of 3 kinds of protein
– contractile proteins
• myosin and actin
– regulatory proteins which turn contraction on & off
• troponin and tropomyosin
– structural proteins which provide proper alignment,
elasticity and extensibility
• titin, myomesin, nebulin and dystrophin
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The Proteins of Muscle -- Myosin
• Thick filaments are composed of myosin
– each molecule resembles two golf clubs twisted together
– myosin heads (cross bridges) extend toward the thin filaments
• Held in place by the M line proteins.
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The Proteins of Muscle -- Actin
• Thin filaments are made of actin, troponin, & tropomyosin
• The myosin-binding site on each actin molecule is covered
by tropomyosin in relaxed muscle
• The thin filaments are held in place by Z lines. From one
Z line to the next is a sarcomere.
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The Proteins of Muscle -- Titin
• Titan anchors thick filament to the M line and the Z disc.
• The portion of the molecule between the Z disc and the
end of the thick filament can stretch to 4 times its resting
length and spring back unharmed.
• Role in recovery of the muscle from being stretched.
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Other Structural Proteins
• The M line (myomesin) connects to titin and adjacent
thick filaments.
• Nebulin, an inelastic protein helps align the thin filaments.
• Dystrophin links thin filaments to sarcolemma and
transmits the tension generated to the tendon.
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Sliding Filament Mechanism Of Contraction
• Myosin cross bridges
pull on thin filaments
• Thin filaments slide
inward
• Z Discs come toward
each other
• Sarcomeres shorten.The
muscle fiber shortens. The
muscle shortens
• Notice :Thick & thin
filaments do not change in
length
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How Does Contraction Begin?
• Nerve impulse reaches an axon terminal &
synaptic vesicles release acetylcholine (ACh)
• ACh diffuses to receptors on the sarcolemma &
Na+ channels open and Na+ rushes into the cell
• A muscle action potential spreads over
sarcolemma and down into the transverse tubules
• SR releases Ca+2 into the sarcoplasm
• Ca+2 binds to troponin & causes troponintropomyosin complex to move & reveal myosin
binding sites on actin--the contraction cycle begins
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Excitation - Contraction Coupling
• All the steps that occur from the muscle action potential
reaching the T tubule to contraction of the muscle fiber.
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Contraction Cycle
• Repeating sequence of events that cause the
thick & thin filaments to move past each other.
• 4 steps to contraction cycle
–
–
–
–
ATP hydrolysis
attachment of myosin to actin to form crossbridges
power stroke
detachment of myosin from actin
• Cycle keeps repeating as long as there is ATP
available & high Ca+2 level near thin filament
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Steps in the Contraction Cycle
• Notice how the myosin head attaches and pulls on the thin
filament with the energy released from ATP
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ATP and Myosin
•
•
•
•
•
•
Myosin heads are activated by ATP
Activated heads attach to actin & pull (power stroke)
ADP is released. (ATP released P & ADP & energy)
Thin filaments slide past the thick filaments
ATP binds to myosin head & detaches it from actin
All of these steps repeat over and over
– if ATP is available &
– Ca+ level near the troponin-tropomyosin complex is high
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Overview: From Start to Finish
•
•
•
•
•
•
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Nerve ending
Neurotransmittor
Muscle membrane
Stored Ca+2
ATP
Muscle proteins
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Relaxation
• Acetylcholinesterase (AChE) breaks down ACh
within the synaptic cleft
• Muscle action potential ceases
• Ca+2 release channels close
• Active transport pumps Ca2+ back into storage in
the sarcoplasmic reticulum
• Calcium-binding protein (calsequestrin) helps hold
Ca+2 in SR (Ca+2 concentration 10,000 times
higher than in cytosol)
• Tropomyosin-troponin complex recovers binding
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site
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Rigor Mortis
• Rigor mortis is a state of muscular rigidity
that begins 3-4 hours after death and lasts
about 24 hours
• After death, Ca+2 ions leak out of the SR
and allow myosin heads to bind to actin
• Since ATP synthesis has ceased,
crossbridges cannot detach from actin until
proteolytic enzymes begin to digest the
decomposing cells.
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Length of Muscle Fibers
• Optimal overlap of thick & thin filaments
– produces greatest number of crossbridges and the
greatest amount of tension
• As stretch muscle (past optimal length)
– fewer cross bridges exist & less force is produced
• If muscle is overly shortened (less than optimal)
– fewer cross bridges exist & less force is produced
– thick filaments crumpled by Z discs
• Normally
– resting muscle length remains between 70 to 130% of
the optimum
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Length Tension Curve
• Graph of Force of contraction
(Tension) versus Length of
sarcomere
• Optimal overlap at the top
of the graph
• When the cell is too stretched
and little force is produced
• When the cell is too short, again
little force is produced
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Neuromuscular Junction (NMJ) or Synapse
• NMJ = myoneural junction
– end of axon nears the surface of a muscle fiber at its motor
end& plate
separated by synaptic cleft or
gap)
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Structures of NMJ Region
• Synaptic end bulbs are
swellings of axon terminals
• End bulbs contain synaptic
vesicles filled with
acetylcholine (ACh)
• Motor end plate membrane
contains 30 million ACh
receptors.
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Events Occurring After a Nerve Signal
• Arrival of nerve impulse at nerve terminal causes release
of ACh from synaptic vesicles
• ACh binds to receptors on muscle motor end plate
opening the gated ion channels so that Na+ can rush into
the muscle cell
• Inside of muscle cell becomes more positive, triggering a
muscle action potential that travels over the cell and down
the T tubules
• The release of Ca+2 from the SR is triggered and the
muscle cell will shorten & generate force
• Acetylcholinesterase breaks down the ACh attached to the
receptors on the motor end plate so the muscle action
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potential
will
cease
Pharmacology of the NMJ
• Botulinum toxin blocks release of neurotransmitter
at the NMJ so muscle contraction can not occur
– bacteria found in improperly canned food
– death occurs from paralysis of the diaphragm
• Curare (plant poison from poison arrows)
– causes muscle paralysis by blocking the ACh receptors
– used to relax muscle during surgery
• Neostigmine (anticholinesterase agent)
– blocks removal of ACh from receptors so strengthens
weak muscle contractions of myasthenia gravis
–
also
an antidote
for curare after surgery is finished
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Muscle Metabolism
Production of ATP in Muscle Fibers
• Muscle uses ATP at a great rate when active
• Sarcoplasmic ATP only lasts for few
seconds
• 3 sources of ATP production within muscle
– creatine phosphate
– anaerobic cellular respiration
– anaerobic cellular respiration
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Creatine Phosphate
• Excess ATP within resting muscle used to form creatine
phosphate
• Creatine phosphate 3-6
times more plentiful
than ATP within muscle
• Its quick breakdown
provides energy for
creation of ATP
• Sustains maximal contraction for 15 sec (used for 100
meter dash).
• Athletes tried creatine supplementation
– gain muscle mass but shut down bodies own synthesis (safety?)
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Anaerobic Cellular Respiration
• ATP produced from glucose
breakdown into pyruvic acid
during glycolysis
– if no O2 present
• pyruvic converted to lactic acid
which diffuses into the blood
• Glycolysis can continue
anaerobically to provide ATP
for 30 to 40 seconds of
maximal activity (200 meter
race)
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Aerobic Cellular Respiration
• ATP for any activity lasting over 30 seconds
– if sufficient oxygen is available, pyruvic acid enters the
mitochondria to generate ATP, water and heat
– fatty acids and amino acids can also be used by the mitochondria
• Provides 90% of ATP energy if activity lasts more than 10
minutes
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Muscle Fatigue
• Inability to contract after prolonged activity
– central fatigue is feeling of tiredness and a
desire to stop (protective mechanism)
– depletion of creatine phosphate
– decline of Ca+2 within the sarcoplasm
• Factors that contribute to muscle fatigue
– insufficient oxygen or glycogen
– buildup of lactic acid and ADP
– insufficient release of acetylcholine from motor
neurons
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Oxygen Consumption after Exercise
• Muscle tissue has two sources of oxygen.
– diffuses in from the blood
– released by myoglobin inside muscle fibers
• Aerobic system requires O2 to produce ATP
needed for prolonged activity
– increased breathing effort during exercise
• Recovery oxygen uptake
– elevated oxygen use after exercise (oxygen debt)
– lactic acid is converted back to pyruvic acid
– elevated body temperature means all reactions faster
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The Motor Unit
• Motor unit = one somatic motor neuron & all the skeletal
muscle cells (fibers) it stimulates
– muscle fibers normally scattered throughout belly of muscle
– One nerve cell supplies on average 150 muscle cells that all
contract in unison.
• Total strength of a contraction depends on how many
motor
units are activated & how large the motor units
are
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Twitch Contraction
• Brief contraction of all fibers in a motor unit in response to
– single action potential in its motor neuron
– electrical stimulation of the neuron or muscle fibers
• Myogram = graph of a twitch contraction
– the action potential lasts 1-2 msec
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– Tortora
the twitch
contraction
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Myogram of a Twitch Contraction
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Parts of a Twitch Contraction
• Latent Period--2msec
– Ca+2 is being released from SR
– slack is being removed from elastic components
• Contraction Period
– 10 to 100 msec
– filaments slide past each other
• Relaxation Period
– 10 to 100 msec
– active transport of Ca+2 into SR
• Refractory Period
– muscle can not respond and has lost its excitability
– Tortora
5 msec
for skeletal
& 300 msec for cardiac muscle
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Wave Summation
• If second stimulation applied after the refractory period
but before complete muscle relaxation---second
contraction is stronger than first
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Complete and Incomplete Tetanus
• Unfused tetanus
– if stimulate at 20-30 times/second, there will be only partial
relaxation between stimuli
• Fused tetanus
– if stimulate at 80-100 times/second, a sustained contraction
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with no relaxation between stimuli will result
Explanation of Summation & Tetanus
• Wave summation & both types of tetanus
result from Ca+2 remaining in the
sarcoplasm
• Force of 2nd contraction is easily added to
the first, because the elastic elements
remain partially contracted and do not delay
the beginning of the next contraction
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Motor Unit Recruitment
• Motor units in a whole muscle fire asynchronously
– some fibers are active others are relaxed
– delays muscle fatigue so contraction can be sustained
• Produces smooth muscular contraction
– not series of jerky movements
• Precise movements require smaller contractions
– motor units must be smaller (less fibers/nerve)
• Large motor units are active when large tension is
needed
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Muscle Tone
• Involuntary contraction of a small number of
motor units (alternately active and inactive in a
constantly shifting pattern)
– keeps muscles firm even though relaxed
– does not produce movement
• Essential for maintaining posture (head upright)
• Important in maintaining blood pressure
– tone of smooth muscles in walls of blood vessels
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Isotonic and Isometric Contraction
• Isotonic contractions = a load is moved
– concentric contraction = a muscle shortens to produce force and
movement
– eccentric contractions = a muscle lengthens while maintaining
force and movement
• Isometric contraction = no movement occurs
– tension is generated without muscle shortening
– maintaining
& supports objects in a fixed position 10-55
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Variations in Skeletal Muscle Fibers
• Myoglobin, mitochondria and capillaries
– red muscle fibers
• more myoglobin, an oxygen-storing reddish pigment
• more capillaries and mitochondria
– white muscle fibers
• less myoglobin and less capillaries give fibers their pale color
• Contraction and relaxation speeds vary
– how fast myosin ATPase hydrolyzes ATP
• Resistance to fatigue
–
different metabolic reactions used to generate ATP
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Classification of Muscle Fibers
• Slow oxidative (slow-twitch)
– red in color (lots of mitochondria, myoglobin & blood vessels)
– prolonged, sustained contractions for maintaining posture
• Fast oxidative-glycolytic (fast-twitch A)
– red in color (lots of mitochondria, myoglobin & blood vessels)
– split ATP at very fast rate; used for walking and sprinting
• Fast glycolytic (fast-twitch B)
– white in color (few mitochondria & BV, low myoglobin)
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–Tortora
anaerobic
Fiber Types within a Whole Muscle
• Most muscles contain a mixture of all three fiber
types
• Proportions vary with the usual action of the
muscle
– neck, back and leg muscles have a higher proportion
of postural, slow oxidative fibers
– shoulder and arm muscles have a higher proportion
of fast glycolytic fibers
• All fibers of any one motor unit are same.
• Different fibers are recruited as needed.
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Anabolic Steroids
• Similar to testosterone
• Increases muscle size, strength, and endurance
• Many very serious side effects
–
–
–
–
–
–
liver cancer
kidney damage
heart disease
mood swings
facial hair & voice deepening in females
atrophy of testicles & baldness in males
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Anatomy of Cardiac Muscle
•
•
•
•
Striated , short, quadrangular-shaped, branching fibers
Single centrally located nucleus
Cells connected by intercalated discs with gap junctions
Same arrangement of thick & thin filaments as skeletal
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Cardiac versus Skeletal Muscle
• More sarcoplasm and mitochondria
• Larger transverse tubules located at Z discs,
rather than at A-l band junctions
• Less well-developed SR
• Limited intracellular Ca+2 reserves
– more Ca+2 enters cell from extracellular fluid
during contraction
• Prolonged delivery of Ca+2 to sarcoplasm,
produces a contraction that last 10 -15 times
longer than in skeletal muscle
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Appearance of Cardiac Muscle
• Striated muscle containing thick & thin filaments
• T tubules located at Z discs & less SR
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Physiology of Cardiac Muscle
• Autorhythmic cells
– contract without stimulation
• Contracts 75 times per min & needs lots O2
• Larger mitochondria generate ATP aerobically
• Sustained contraction possible due to slow Ca+2
delivery
– Ca+2 channels to the extracellular fluid stay open
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Two Types of Smooth Muscle
• Visceral (single-unit)
– in the walls of hollow
viscera & small BV
– autorhythmic
– gap junctions cause fibers
to contract in unison
• Multiunit
– individual fibers with own
motor neuron ending
– found in large arteries,
large airways, arrector pili
muscles,iris & ciliary body
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Microscopic Anatomy of Smooth Muscle
• Small, involuntary muscle cell -- tapering at ends
• Single, oval, centrally located nucleus
• Lack T tubules & have little SR for Ca+2 storage
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Microscopic Anatomy of Smooth Muscle
• Thick & thin myofilaments
not orderly arranged so lacks
sarcomeres
• Sliding of thick & thin
filaments generates tension
• Transferred to intermediate
filaments & dense bodies
attached to sarcolemma
• Muscle fiber contracts and
twists into a helix as it shortens
-- relaxes by untwisting
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Physiology of Smooth Muscle
• Contraction starts slowly & lasts longer
– no transverse tubules & very little SR
– Ca+2 must flows in from outside
• Calmodulin replaces troponin
– Ca+2 binds to calmodulin turning on an enzyme
(myosin light chain kinase) that phosphorylates the
myosin head so that contraction can occur
– enzyme works slowly, slowing contraction
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Smooth Muscle Tone
• Ca+2 moves slowly out of the cell
– delaying relaxation and providing for state of
continued partial contraction
– sustained long-term
• Useful for maintaining blood pressure or a
steady pressure on the contents of GI tract
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Regulation of Contraction
• Regulation of contraction due to
– nerve signals from autonomic nervous system
– changes in local conditions (pH, O2, CO2, temperature
& ionic concentrations)
– hormones (epinephrine -- relaxes muscle in airways &
some blood vessels)
• Stress-relaxation response
– when stretched, initially contracts & then tension
decreases to what is needed
– stretch hollow organs as they fill & yet pressure
remains fairly constant
–Tortora
when
empties,
rebounds & walls firm up10-69
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Regeneration of Muscle
• Skeletal muscle fibers cannot divide after 1st year
– growth is enlargement of existing cells
– repair
• satellite cells & bone marrow produce some new cells
• if not enough numbers---fibrosis occurs most often
• Cardiac muscle fibers cannot divide or regenerate
– all healing is done by fibrosis (scar formation)
• Smooth muscle fibers (regeneration is possible)
– cells can grow in size (hypertrophy)
– some cells (uterus) can divide (hyperplasia)
– new
fibers
form from stem cells in BV walls10-70
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Developmental Anatomy of the
Muscular System
• Develops from mesoderm
• Somite formation
– blocks of mesoderm give rise
to vertebrae and skeletal
muscles of the back
• Muscles of head & limbs
develop from general
mesoderm
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Aging and Muscle Tissue
• Skeletal muscle starts to be replaced by fat
beginning at 30
– “use it or lose it”
• Slowing of reflexes & decrease in maximal
strength
• Change in fiber type to slow oxidative fibers may
be due to lack of use or may be result of aging
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Myasthenia Gravis
• Progressive autoimmune disorder that blocks the
ACh receptors at the neuromuscular junction
• The more receptors are damaged the weaker the
muscle.
• More common in women 20 to 40 with possible line
to thymus gland tumors
• Begins with double vision & swallowing difficulties
& progresses to paralysis of respiratory muscles
• Treatment includes steroids that reduce antibodies
that bind to ACh receptors and inhibitors of
acetylcholinesterase
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Muscular Dystrophies
• Inherited, muscle-destroying diseases
• Sarcolemma tears during muscle contraction
• Mutated gene is on X chromosome so problem
is with males almost exclusively
• Appears by age 5 in males and by 12 may be
unable to walk
• Degeneration of individual muscle fibers
produces atrophy of the skeletal muscle
• Gene therapy is hoped for with the most
common
form
= Duchenne muscular dystrophy
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Abnormal Contractions
• Spasm = involuntary contraction of single
muscle
• Cramp = a painful spasm
• Tic = involuntary twitching of muscles
normally under voluntary control--eyelid or
facial muscles
• Tremor = rhythmic, involuntary contraction
of opposing muscle groups
• Fasciculation = involuntary, brief twitch of
a motor unit visible under the skin
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