Chapter 10
Muscle Tissue
Lecture Outline
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INTRODUCTION
• Motion results from alternating contraction (shortening) and
relaxation of muscles; the skeletal system provides leverage
and a supportive framework for this movement.
• The scientific study of muscles is known as myology.
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Chapter 10
Muscle Tissue
• Alternating contraction
and relaxation of cells
• Chemical energy
changed into
mechanical energy
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OVERVIEW OF MUSCLE TISSUE
• Types of Muscle Tissue
• Skeletal muscle tissue is primarily attached to bones. It is
striated and voluntary.
• Cardiac muscle tissue forms the wall of the heart. It is
striated and involuntary.
• Smooth (visceral) muscle tissue is located in viscera. It is
nonstraited (smooth) and involuntary.
• Table 4.4 compares the different types of muscle.
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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 TISSUE
• Each skeletal muscle is a separate organ composed of cells
called fibers.
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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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Connective Tissue Components
• Tendons and aponeuroses are extensions of connective
tissue beyond muscle cells that attach muscle to bone or
other muscle.
• A tendon is a cord of dense connective tissue that attaches
a muscle to the periosteum of a bone (Figure 11.22).
• An aponeurosis is a tendon that extends as a broad, flat
layer (Figure 11.4c).
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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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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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Sarcolemma, T Tubules, and Sarcoplasm
• Skeletal muscle consists of fibers (cells) covered by a
sarcolemma (Figure 10.3b).
– The fibers contain T tubules and sarcoplasm
– T tubules are tiny invaginations of the sarcolemma that
quickly spread the muscle action potential to all parts of
the muscle fiber.
• Sarcoplasm is the muscle cell cytoplasm and contains a
large amount of glycogen for energy production and
myoglobin for oxygen storage.
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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
– near the muscle proteins that use ATP during contraction
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Myofibrils and Sarcoplasmic Reticulum
• Each fiber contains myofibrils that consist of thin and thick
filaments (myofilaments) (Figure 10.3b).
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Myofibrils & Myofilaments
• Muscle fibers are filled with threads called myofibrils
separated by SR (sarcoplasmic reticulum)
• The sarcoplasmic reticulum encircles each myofibril. It is
similar to smooth endoplasmic reticulum in nonmuscle cells
and in the relaxed muscle stores calcium ions.
• 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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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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Sarcomere
• Figure 10.5 shows the relationships of the zones, bands,
and lines as seen in a transmission electron micrograph.
• Exercise can result in torn sarcolemma, damaged myofibrils,
and disrupted Z discs (Clinical Application).
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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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Thick & Thin Myofilaments Overlap
Dark(A) & light(I) bands (electron microscope)
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Muscle Proteins
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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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Structural Proteins
• Structural proteins keep the thick and thin filaments in the
proper alignment, give the myofibril elasticity and
extensibility, and link the myofibrils to the sarcolemma and
extracellular matrix.
– Titin helps a sarcomere return to its resting length after a
muscle has contracted or been stretched.
– Myomesin forms the M line.
– Nebulin helps maintain alignment of the thin filaments in
the sarcomere.
– Dystrophin reinforces the sarcolemma and helps transmit
the tension generated by the sarcomeres to the tendons.
• Table 10.1 reviews the type of proteins in skeletal muscle.
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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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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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Overview: From Start to Finish
Basic Structures
• Nerve ending
• Neurotransmitter
• Muscle membrane
• Stored Ca+2
• ATP
• Muscle proteins
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How Does Contraction Begin?
1. Nerve impulse reaches an axon terminal & synaptic vesicles
release acetylcholine (ACh)
2. ACh diffuses to receptors on the sarcolemma & Na+
channels open and Na+ rushes into the cell
3. A muscle action potential spreads over sarcolemma and
down into the transverse tubules
4. SR releases Ca+2 into the sarcoplasm
5. Ca+2 binds to troponin & causes troponin-tropomyosin
complex to move & reveal myosin binding sites on actin--the
contraction cycle begins
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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
& there is a high Ca+2 level near the filaments.
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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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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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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 site on the
actin
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Overview: From Start to Finish
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•
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•
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Nerve ending
Neurotransmittor
Muscle membrane
Stored Ca+2
ATP
Muscle proteins
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Length-Tension Relationship
• The forcefulness of muscle contraction depends on the
length of the sarcomeres within a muscle before contraction
begins.
• Figure 10.10 plots the length-tension relationships for
skeletal muscle.
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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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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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Neuromuscular Junction (NMJ) or Synapse
• NMJ = myoneural junction
– end of axon nears the surface of a muscle fiber at its motor end
plate region (remain 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
1. Arrival of nerve impulse at nerve terminal causes release of ACh from
synaptic vesicles
2. ACh binds to receptors on muscle motor end plate opening the gated ion
channels so that Na+ can rush into the muscle cell
3. Inside of muscle cell becomes more positive, triggering a muscle action
potential that travels over the cell and down the T tubules
4. The release of Ca+2 from the SR is triggered and the muscle cell will
shorten & generate force
5. Acetylcholinesterase breaks down the ACh attached to the receptors on
the motor end plate so the muscle action potential will cease and the
muscle cell will relax.
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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
– aerobic cellular respiration
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MUSCLE METABOLISM
• Creatine phosphate and ATP can power maximal muscle
contraction for about 15 seconds and is used for maximal
short bursts of energy (e.g., 100-meter dash) (Figure
10.13a).
– Creatine phosphate is unique to muscle fibers.
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MUSCLE METABOLISM
• The partial catabolism of glucose to generate ATP occurs in
anaerobic cellular respiration (Figure 10.13b). This system
can provide enough energy for about 30-40 seconds of
maximal muscle activity (e.g., 300-meter race).
• Muscular activity lasting more than 30 seconds depends
increasingly on aerobic cellular respiration (reactions
requiring oxygen). This system of ATP production involves
the complete oxidation of glucose via cellular respiration
(biological oxidation) (Figure 10.13c).
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Creatine Phosphate: Details
• 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: Details
• 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
• Factors that contribute to fatigue
– central fatigue is feeling of tiredness and a desire
to stop (protective mechanism)
– insufficient release of acetylcholine from motor
neurons
– depletion of creatine phosphate
– decline of Ca+2 within the sarcoplasm
– insufficient oxygen or glycogen
– buildup of lactic acid and ADP
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The Motor Unit
• Motor unit = one somatic motor neuron & all the skeletal muscle cells
(fibers) it stimulates (10 cells to 2,000 cells)
– 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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CONTROL OF MUSCLE TENSION
• A twitch contraction is a brief contraction of all the muscle
fibers in a motor unit in response to a single action potential.
• A record of a muscle contraction is called a myogram and
includes three periods: latent, contraction, and relaxation
(Figure 10.15).
• The refractory period is the time when a muscle has
temporarily lost excitability with skeletal muscles having a
short refractory period and cardiac muscle having a long
refractory period.
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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
– the twitch contraction lasts from 20 to 200 msec
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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
– 5 msec for skeletal & 300 msec for cardiac muscle
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Frequency of Stimulation
• Wave summation is the increased strength of a contraction
resulting from the application of a second stimulus before
the muscle has completely relaxed after a previous stimulus
(Figure 10.16a, b).
• A sustained muscle contraction that permits partial
relaxation between stimuli is called incomplete (unfused)
tetanus (Figure 10.16c); a sustained contraction that lacks
even partial relaxation between stimuli is called complete
(fused) tetanus (Figure 10.16d).
• The process of increasing the number of active motor units
is called recruitment (multiple motor unit summation).
– It prevents fatigue and helps provide smooth muscular
contraction rather than a series of jerky movements.
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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 with no
relaxation between stimuli will result
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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 posture & supports objects in a fixed position
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TYPES OF SKELETAL MSUCLE FIBERS
• On the basis of structure and function, skeletal muscle fibers
are classified as
– slow oxidative,
– oxidative-glycolytic, or
– fast glycolytic fibers.
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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
• 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)
– anaerobic movements for short duration; used for weight-lifting
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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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Distribution and Recruitment of Different Types of
Fibers
• Although the number of different skeletal muscle fibers does
not change, the characteristics of those present can be
altered by various types of exercise.
• The use of anabolic steroids by athletes to increase muscle
size, strength, and endurance has been shown to have very
serious side effects, some of which are life-threatening.
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Anabolic Steroids
• Similar to testosterone
• Increases muscle size, strength, and endurance
• 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 MUSCLE TISSUE - Overview
• Cardiac muscle tissue is found only in the heart wall (see
Chapter 20).
– Its fibers are arranged similarly to skeletal muscle fibers.
– Cardiac muscle fibers connect to adjacent fibers by
intercalated discs which contain desmosomes and gap
junctions (Figure 4.1e).
– Cardiac muscle contractions last longer than the skeletal
muscle twitch due to the prolonged delivery of calcium
ions from the sarcoplasmic reticulum and the
extracellular fluid.
– Cardiac muscle fibers contract when stimulated by their
own autorhythmic fibers.
• This continuous, rhythmic activity is a major physiological
difference between cardiac and skeletal muscle tissue.
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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 of O2
• Larger mitochondria generate ATP aerobically
• Extended contraction is possible due to slow Ca+2 delivery
– Ca+2 channels to the extracellular fluid stay open
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SMOOTH MUSCLE
• Smooth muscle tissue is nonstriated and involuntary and is
classified into two types: visceral (single unit) smooth
muscle (Figure 10.18a) and multiunit smooth muscle (Figure
10.18b).
– Visceral (single unit) smooth muscle is found in the walls
of hollow viscera and small blood vessels; the fibers are
arranged in a network and function as a “single unit.”
– Multiunit smooth muscle is found in large blood vessels,
large airways, arrector pili muscles, and the iris of the
eye. The fibers operate singly rather than as a unit.
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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 the Smooth Muscle
• Sarcoplasm of smooth muscle fibers contains both thick and
thin filaments which are not organized into sarcomeres.
• Smooth muscle fibers contain intermediate filaments which
are attached to dense bodies. (Figure 10.19)
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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
• In smooth muscle, the regulator protein that binds
calcium ions in the cytosol is calmodulin (in place of
the role of troponin in striated muscle);
– calmodulin activates the enzyme myosin light chain
kinase, which facilitates myosin-actin binding and
allows contraction to occur at a relatively slow rate.
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Smooth Muscle Tone
• The prolonged presence of calcium ions in the cytosol of
smooth muscle fibers provides for smooth muscle tone,
a state of continued partial contraction.
• Smooth muscle fibers can stretch considerably without
developing tension; this phenomenon is termed the
stress-relaxation response.
• Useful for maintaining blood pressure or a steady
pressure on the contents of GI tract
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DEVELOPMENT OF MUSCLE
• With few exceptions, muscles develop from mesoderm
(Figure 6.13a)
• Skeletal muscles of the head and extremities develop from
general mesoderm; the remainder of the skeletal muscles
develop from mesoderm of somites (Figure 10.20a).
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Fusion of Myoblasts into Muscle Fibers
• Mature muscle cells developed from 100 myoblasts that fuse together in
the fetus. (multinucleated)
• Mature muscle cells are not known to divide.
• Muscle growth is a result of cellular enlargement (hypertrophy) & not cell
division (hyperplasia)
• Satellite cells retain the ability to regenerate new cells.
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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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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 can form from stem cells in BV walls
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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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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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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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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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end
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