Download Chapter 11: Muscular Tissue

3 Types of Muscle Tissue
• Skeletal muscle
Chapter 11
– attaches to bone, skin or fascia
– striated with light & dark bands visible with scope
– voluntary control of contraction & relaxation
Muscle Tissue
2
1
3 Types of Muscle Tissue
3 Types of Muscle Tissue
• Cardiac muscle
• Smooth muscle
– striated in appearance
– involuntary control
– autorhythmic because of built in pacemaker
–
–
–
–
3
attached to hair follicles in skin
in walls of hollow organs -- blood vessels & GI
nonstriated in appearance
involuntary
4
Properties of Muscle Tissue
Functions of Muscle Tissue
• Excitability
– respond to chemicals released from nerve cells
• Producing body movements
• Stabilizing body positions
• Regulating organ volumes
• Conductivity
– ability to propagate electrical signals over membrane
• Contractility
– bands of smooth muscle called sphincters
– ability to shorten and generate force
• Movement of substances within the body
• Extensibility
– blood, lymph, urine, air, food and fluids, sperm
– ability to be stretched without damaging the tissue
• Producing heat
• Elasticity
– involuntary contractions of skeletal muscle (shivering)
– ability to return to original shape after being stretched
5
6
Connective Tissue Components
SKELETAL MUSCLE TISSUE
• Connective tissue components of the muscle include
• Each skeletal muscle is a separate organ
composed of cells called fibers
– 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
7
8
Connective Tissue Components
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
• An aponeurosis is a tendon that extends as a
broad, flat layer
9
10
Muscle Fiber or
Myofibers
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.
• Muscle cells are long,
cylindrical &
multinucleated
• Sarcolemma = muscle
cell membrane
• Sarcoplasm filled with
tiny threads called
myofibrils & myoglobin
(red-colored, oxygenbinding protein)
– nerve fibers & capillaries are found in the endomysium
between individual cells
11
12
Transverse
Tubules
Sarcolemma, T Tubules, and Sarcoplasm
• Skeletal muscle consists of fibers (cells) covered by
a sarcolemma
• 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
• 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
13
Myofibrils,
Sarcoplasmic
Reticulum &
Myofilaments
• Muscle fibers are filled with long organelles called myofibrils
• The sarcoplasmic reticulum (SR) encircles each myofibril
14
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
– similar to smooth ER in nonmuscle cells
– stores calcium ions in the relaxed muscle
– release of Ca+2 triggers muscle contraction
• Myofibrils consist of myofilaments (thick & thin filaments)
– the contractile proteins of muscle
15
16
Thick & Thin Myofilaments
Thick & Thin Myofilaments Overlap
• Supporting proteins (M line, titin and Z disc help
anchor the thick and thin filaments in place)
Dark(A) & light(I) bands (electron microscope)
17
18
The Proteins of Muscle -- Myosin
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
• Thick filaments are composed of myosin
– each molecule resembles two golf clubs twisted together
– myosin heads (cross bridges) extend toward the thin
filaments
19
20
Sliding Filament Mechanism Of Contraction
The Proteins of Muscle -- Actin
• Myosin cross bridges
pull on thin filaments
• Thin filaments slide
inward
• Z Discs come toward
each other
• Sarcomeres shorten
• Thin filaments are made of actin, troponin, &
tropomyosin
• The myosin-binding site on each actin molecule is
covered by tropomyosin in relaxed muscle
– The muscle fiber
shortens
– The muscle shortens
• Note: Thick & thin
filaments do not change
in length
21
Overview: From
Start to Finish
22
How Does Contraction Begin?
1. Nerve impulse reaches an axon terminal & synaptic
vesicles release acetylcholine (ACh)
2. ACh binds 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 troponintropomyosin complex to move & reveal myosin
binding sites on actin--the contraction cycle begins
Basic Structures
• Nerve ending
• Neurotransmitter
• Muscle
membrane
• Stored Ca+2
• ATP
• Muscle proteins
23
24
Steps in the Contraction Cycle
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.
• Notice how the myosin head attaches and pulls on
the thin filament with the energy released from ATP
25
26
Excitation - Contraction Coupling
ATP and Myosin
• Myosin heads are activated by ATP
• Activated heads attach to actin & pull (power
stroke)
• ADP is released
• 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+2 level near the troponin-tropomyosin complex is
high
• All the steps that occur from the muscle action potential
reaching the T tubule to contraction of the muscle fiber
27
28
Overview: From
Start to Finish
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
•
•
•
•
•
•
Nerve ending
Neurotransmittor
Muscle membrane
Stored Ca+2
ATP
Muscle proteins
29
30
Length Tension Curve
Length of Muscle Fibers
•The forcefulness of muscle contraction depends on
the length of the sarcomeres within a muscle before
contraction begins.
• Optimal overlap of thick & thin filaments
– produces greatest number of crossbridges and the
greatest amount of tension
• As stretch muscle (past optimal length)
• 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
– 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
31
32
Structures of NMJ Region
Neuromuscular Junction (NMJ) or Synapse
• 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.
33
1.
2.
3.
4.
5.
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
along the cell membrane 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 so the
muscle action potential will cease and the muscle
cell will relax
34
Pharmacology of the NMJ
• Botulinum toxin (Botox) 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 muscle
• 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
35
36
Muscle Metabolism
Creatine Phosphate
Production of ATP in Muscle Fibers
• Creatine phosphate and ATP can power maximal
muscle contraction for about 15 seconds and is
used for maximal short bursts of energy (e.g., 100meter dash)
• 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
– Creatine phosphate is unique to muscle fibers
37
38
Aerobic Cellular Respiration
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
• ATP for any activity lasting over 30 seconds
– if sufficient oxygen is available, pyruvic acid enters the
mitochondria to generate ATP
– fatty acids and amino acids can also be used by the
mitochondria
• Glycolysis can continue
anaerobically to provide
ATP for 30 to 40 seconds
of maximal activity (200
meter race)
• Provides 90% of ATP energy if activity lasts more
than 10 minutes
39
40
The Motor Unit
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
• 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
41
42
Twitch Contraction
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
• The refractory period is the time when a muscle
has temporarily lost excitability
• 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
43
– the action potential lasts 1-2 msec
– the twitch contraction lasts from 20 to 200 msec
44
Wave Summation
Frequency of Stimulation
• If second stimulation applied after the refractory period but
before complete muscle relaxation---second contraction is
stronger than first
• 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
• A sustained muscle contraction that permits partial
relaxation between stimuli is called incomplete
(unfused) tetanus
• a sustained contraction that lacks even partial
relaxation between stimuli is called complete
(fused) tetanus
45
46
Muscle Tone
Motor Unit Recruitment
• Involuntary contraction of a small number of motor
units (alternately active and inactive in a constantly
shifting pattern)
• Motor units in a whole muscle fire asynchronously
– some fibers are active others are relaxed
– delays muscle fatigue so contraction can be sustained
– keeps muscles firm even though relaxed
– does not produce movement
• Produces smooth muscular contraction
– not series of jerky movements
• Essential for maintaining posture (head upright)
• Important in maintaining blood pressure
• Precise movements require smaller contractions
– motor units must be smaller (less fibers/nerve)
– tone of smooth muscles in walls of blood vessels
• Large motor units are active when large tension is
needed
47
48
Classification of Muscle Fibers
Isotonic and Isometric Contraction
• Slow oxidative (slow-twitch)
– red in color (lots of mitochondria, myoglobin & blood vessels)
– prolonged, sustained contractions for maintaining posture
• Isotonic contractions = a load is moved
• Oxidative-glycolytic (intermediate)
– concentric contraction = a muscle shortens to produce force and
movement
– eccentric contractions = a muscle lengthens while maintaining force
and movement
– red in color (lots of mitochondria, myoglobin & blood vessels)
– split ATP at very fast rate; used for walking and sprinting
• Fast glycolytic (fast-twitch)
• Isometric contraction = no movement occurs
– tension is generated without muscle shortening
– maintaining posture & supports objects in a fixed position
– white in color (few mitochondria & BV, low myoglobin)
– anaerobic movements for short duration; used for weight-lifting
49
50
Fiber Types within a Whole Muscle
Anabolic Steroids
• Most muscles contain a mixture of all three fiber
types
• Proportions vary with the usual action of the
muscle
• Similar to testosterone
• Increases muscle size, strength, and endurance
• side effects:
–
–
–
–
–
–
– 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
51
liver cancer
kidney damage
heart disease
mood swings
facial hair & voice deepening in females
atrophy of testicles & baldness in males
52
Regeneration of Muscle
Aging and Muscle Tissue
• Skeletal muscle fibers cannot divide after 1st year
– growth is enlargement of existing cells
– repair
• satellite cells & bone marrow produce some new cells
• Skeletal muscle starts to be replaced by fat
beginning at 30
– “use it or lose it”
• Cardiac muscle fibers cannot divide or regenerate
• 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
– 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
53
Myasthenia Gravis
54
Muscular Dystrophies
• 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
• 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
• 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
55
56
Atrophy and Hypertrophy
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
• 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
57
58
Rigor Mortis
Exercise-Induced Muscle Damage
• 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
• 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
59
60