Chapter 10
Muscle Tissue
Alternating contraction and relaxation of cells
Chemical energy changed into mechanical energy
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
3 Types of Muscle Tissue
Cardiac muscle
striated in appearance
involuntary control
autorhythmic because of built in
pacemaker
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
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)
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
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
Connective Tissue Components
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
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.
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)
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
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
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
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
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
Thick & Thin Myofilaments
Supporting proteins (M line, titin and Z disc help anchor
the thick and thin filaments in place)
Overlap of Thick & Thin Myofilaments within a Myofibril
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
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
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.
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.
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
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
troponin-tropomyosin complex to move & reveal myosin binding sites on
actin--the contraction cycle begins
Excitation - Contraction Coupling
All the steps that occur from the muscle
action potential reaching the T tubule to contraction of the muscle fiber.
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
Steps in the Contraction Cycle
Notice how the myosin head attaches and pulls on the thin
filament with the energy released from ATP
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
Overview: From Start to Finish
Nerve ending
Neurotransmittor
Muscle membrane
Stored Ca+2
ATP
Muscle proteins
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
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.
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.
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 potential will cease and
the muscle cell will relax.
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
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
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)
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
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
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
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
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)
anaerobic movements for short
duration; used for weight-lifting
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.
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
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
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
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
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
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
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
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
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
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
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
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