Chapter 9
Muscles and Muscle Tissue
J.F. Thompson, Ph.D. & J.R. Schiller, Ph.D. & G. Pitts, Ph.D.
Muscles and Muscle Tissues
Use the extra PPTs and audio PPTs to
review muscle anatomy:
CH 9 Skeletal Muscle Histology
CH 9 Skeletal Muscle Development
CH 9 Cardiac Muscle Histology
CH 9 Smooth Muscle Tissue
At Dr. Thompson’s website
Some Muscle Terminology
Myology: the scientific study of muscle
muscle fibers = muscle cells
myo, mys & sarco: word roots referring to muscle
Three Types of Muscle
Skeletal, cardiac, and smooth muscle differ in:
 Microscopic anatomy
 Location
 Regulation by the endocrine system and the
nervous system
Functions of Muscle Tissue
• Motion: external (walking, running, talking, looking)
and internal (heartbeat, blood pressure, digestion,
elimination) body part movements
• Posture: maintain body posture
• Stabilization: stabilize joints – muscles have tone even
at rest
• Thermogenesis: generating heat by normal contractions
and by shivering
Functional Characteristics
• Excitability (irritability)
– the ability to receive and respond to a stimulus (chemical
signal molecules)
• Contractility
– ability of muscle tissue to shorten
• Extensibility
– the ability to be stretched without damage
– most muscles are arranged in functionally opposing pairs – as
one contracts, the other relaxes, which permits the relaxing
muscle to be stretched back
• Elasticity
– the ability to return to its original shape
• Conductivity (impulse transmission)
– the ability to conduct excitation over length of muscle
Myofibrils –
Sarcomeres Myofilaments
• Thin filaments: actin (plus
some tropomyosin &
troponin)
• Thick filaments: myosin
• Elastic filaments: titin
(connectin) attaches myosin
to the Z discs (very high
mol. wt.)
Sarcomere
• The foundation of the muscle cell’s contractile organelle,
myofibril
• The functional unit of striated muscle contraction
• The myofilaments between two adjacent Z discs
• The regular geometric arrangement of the actin and myosin
produces the visible banding pattern (striations)
Myosin Protein
• Rod-like tail with two heads
• Each head contains ATPase and an actin-binding site; point to the Z
line
• Tails point to the M line
• Splitting ATP releases energy which causes the head to “ratchet” and
pull on actin fibers
Thick (Myosin) Myofilaments
• Each thick filament contains many myosin
units woven together
Thin (Actin) Myofilaments
Two G actin strands are arranged into helical strands
• Each G actin has a binding site for myosin
• Two tropomyosin filaments spiral around the actin
strands
• Troponin regulatory proteins (“switch molecules”) may
bind to actin and tropomyosin & have Ca2+ binding sites
Muscle Fiber Triads
• Triads: 2 terminal cisternae + 1 T tubule
• Sarcoplasmic reticulum (SER): modified smooth ER, stores
Ca2+ ions
• Terminal cisternae: large flattened sacs of the SER
• Transverse (T) tubules: inward folding of the sarcolemma
Regulation of Contraction &
The Neuromuscular Junction
The Neuromuscular Junction:
• where motor neurons
communicate with the muscle
fibers
• composed of an axon terminal, a
synapse and a motor end plate
• axon terminal: the end of the
motor neuron’s branches (axon)
• motor end plate: the specialized
region of the muscle cell plasma
membrane adjacent to the axon
terminal
The Neuromuscular Junction:
• Synapse: point of
communication is a small
gap
• Synaptic cleft: the space
between axon terminal &
motor end plate
• Synaptic vesicles:
membrane-enclosed sacs
in the axon terminals
containing the
neurotransmitter
The Neuromuscular Junction:
• Neurotransmitter: the chemical signal molecule that diffuses across the
synapse, i.e., acetylcholine, ACh)
• Acetylcholine (ACh) receptors: integral membrane proteins which bind ACh
Generation of an Action Potential
(Excitation)
• Binding of the
neurotransmitter
(ACh) causes the
ligand-gated Na+
channels to open
axonal terminal
• Opening of the Na+
channels depolarizes
the sarcolemma (cell
membrane)
motor end plate
Generation of an Action Potential
• Initial depolarization
causes adjacent voltagegated Na+ channels to
open; Na+ ions flow in,
beginning an action
potential
• Action potential: a
large transient
depolarization of the
membrane potential
– transmitted over the
entire sarcolemma (and
down the T tubules)
Generation of an Action Potential
Generation of an Action Potential
Generation of an Action Potential
• Repolarization: the return to polarization due to the
closing voltage-gated Na+ channels and the opening of
voltage gated K+ channels
• Refractory period: the time during membrane
repolarization when the muscle fiber cannot respond
to a new stimulus (a few milliseconds)
• All-or-none response: once an action potential is
initiated it results in a complete contraction of the
muscle cell
Excitation-Contraction Coupling
• The action potential
(excitation) travels over the
sarcolemma, including Ttubules
• Voltage sensors on the Ttubules cause corresponding
SR receptors to open gated
channels and release Ca2+ ions
• And now, for the interactions
between calcium and the
sarcomere…
The Sliding Filament Model of
Muscle Contraction
• Thin and thick
filaments slide past
each other to
shorten each
sarcomere and,
thus, each
myofibril
• The cumulative
effect is to shorten
the muscle
• This simulation of the sliding filament model can also be
viewed on line at the web site below along with additional
information on muscle tissue
http://www.lab.anhb.uwa.edu.au/mb140/CorePages/Muscle/Muscle.htm#SKELETAL
Calcium
2+
(Ca )
The “on-off switch”: allows myosin to bind to actin
off
on
Calcium Movements Inside
Muscle Fibers
An action potential causes the release of Ca2+ ions
(from the cisternae of the SR)
Ca2+ combines with troponin, causing a change in
the position of tropomyosin, allowing actin to
bind to myosin and be pulled (“slide”)
Ca2+ pumps on the SR remove calcium ions from the
sarcoplasm when the stimulus ends
The Power Stroke & ATP
1. Cross bridge
attachment. Myosin
heads bind to actin
2. The working stroke.
myosin changes shape
(pulls actins toward M
line); releases ADP + Pi
3. Cross bridge
detachment. Myosin
heads bind to a new ATP;
releases actin
The Power Stroke & ATP
4. "Cocking" of the
myosin head. ATP is
hydrolyzed (split) to
ADP + Pi; this provides
potential energy for the
next stroke
The “Ratchet Effect”
Repeat steps 1-4:
The “ratchet
action” repeats the
process,
shortening all the
sarcomeres and the
myofibrils, until
Ca2+ ions are
removed from the
sarcoplasm or the
ATP supply is
exhausted
Attach
Repeat
Power
Stroke
Release
RATCHET EFFECT ANIMATION
http://www.sci.sdsu.edu/movies/actin_myosin_gif.html
Excitation-Contraction Coupling
1.
The action potential
(excitation) travels over the
sarcolemma, including Ttubules
2.
Voltage sensors on the Ttubules cause corresponding
SR receptors to open gated
channels and release Ca2+
ions
3.
Ca2+ binds to troponin,
causing tropomyosin to move
out of its blocking position
4.
Myosin forms cross bridges to
actin, the power stroke
occurs, filaments slide,
muscle shortens
5.
Calsequestrin and
calmodulin help regulate
Ca2+ levels inside muscle
cells
Destruction of Acetylcholine
• Acetylcholinesterase: an enzyme that rapidly
breaks down acetylcholine is located in the
neuromuscular junction
– Prevents continuous excitation (generation of more
action potentials)
• Many drugs and diseases interfere with events in the
neuromuscular junction
– Myasthenia gravis: loss of function at ACh receptors
(autoimmune disease?)
– Curare (poison arrow toxin): binds irreversibly to and
blocks the ACh receptors
MUSCLE CONTRACTION
• One power stroke shortens a muscle about 1%
• Normal muscle contraction shortens a muscle by about 35%
– cross bridge (ratchet effect) cycle repeats
• continue repeating power strokes, continue pulling
• increasing overlap of fibers; Z lines come together
– about half the myosin molecules are attached at any time
• Cross bridges are maintained until Ca2+ levels decrease
– Ca2+ is released in response to the action potential delivered by the
motor neuron
– Ca2+ ATPase pumps Ca2+ ions back into the SR, using more ATP
RIGOR MORTIS IN DEATH
•
Ca2+ ions leak from SR causing binding of actin and
myosin and some contraction of the muscles
•
Lasts ~24 hours, then enzymatic tissue disintegration
eliminates it in another 12 hours
This suicide victim used a
shotgun to kill himself;
when it was removed, his
arms retained this posture.
Skeletal Muscle Motor Units
• The Motor Unit = Motor Neuron + Muscle Fibers to
which it connects (Synapses)
Skeletal Muscle Motor Units
• The size of Motor Units
varies:
– Small - two muscle
fibers/unit (larynx, eyes)
– Large – hundreds to
thousands/unit (biceps,
gastrocnemius, lower back
muscles)
• The individual muscle
cells/fibers of each unit are
spread throughout the
muscle for smooth efficient
operation of the muscle as a
whole
The Myogram
• Myogram: a recording of
muscle contraction
• Stimulus: nerve impulse
or electrical charge
• Twitch: a single
contraction of all the
muscle fibers in a motor
unit (one nerve signal)
Myogram
• 1. latent period: delay
between stimulus and
response
• 2. contraction phase:
tension or shortening occurs
• 3. relaxation phase:
relaxation or lengthening
• refractory period: time
interval after excitation
when muscle will not
respond to a new stimulus
Muscle Twitchs
• All or None
Rule: all the
muscle fibers
of a motor unit
contract all the
way when
stimulated
Graded Muscle Responses
• Force of muscle contraction varies
depending on need. How much tension is
needed?
• Twitch does not provide much force
• Contraction force can be altered in 3 ways:
1. changing the frequency of stimulation (temporal
summation)
2. changing the stimulus strength (recruitment)
3. changing the muscle’s length
Temporal Summation
• Temporal (wave) summation: contractions repeated before
complete relaxation, leads to progressively stronger contractions
– unfused (incomplete) tetanus: frequency of stimulation allows only
incomplete relaxation
– fused (complete) tetanus: frequency of stimulation allows no relaxation
Treppe: the staircase effect
“warming up” of a muscle fiber
Multiple Motor Unit Recruitment
(Summation)
The stimulation of
more motor units
leads to a more
forceful muscle
contraction
The Size Principle
As greater force is required, the
nervous system will stimulate more
motor units, and motor units with
larger fibers and larger numbers
of fibers to achieve the desired
strength of contraction.
Stretch: Length-Tension Relationship
• Stretch (sarcomere length)
determines the number of
cross bridges
– extensive overlap of actin
with myosin: less tension
– optimal overlap of actin with
myosin: most tension
– reduced overlap of actin with
myosin: less tension
• Optimal overlap: most cross
bridges available for the
power stroke and least
structural interference
more resistance
most cross bridges/least resistance
fewest cross bridges
Stretch: Length-Tension Relationship
Optimal length - Lo
• maximum number of cross bridges
• no overlap of actin fibers from opposite ends of the sarcomere
• normal working muscle range from 70 - 130% of Lo
Contraction of a Skeletal Muscle
• Isometric Contraction: Muscle does not shorten
• Tension increases
Contraction of a Skeletal Muscle
• Isotonic Contraction: tension does not change
• Muscle (length) shortens
Muscle Tone
Regular small contractions caused by spinal
reflexes
Respond to tendon stretch receptor sensory input
Activate different motor units over time
Provide constant tension development
muscles are firm
but do not shorten
e.g., neck, back and leg muscles
maintain posture
Muscle Metabolism
• Energy availability
–
–
–
–
Not much ATP is available at any given moment
ATP is needed for cross bridges and Ca++ removal
Maintaining ATP levels is vital for continued activity
Three ways to replenish ATP:
1. Creatine Phosphate energy storage system
2. Anaerobic Glycolysis -- Lactic Acid system
3. Aerobic Respiration
Direct Phosphorylation –
Creatine Phosphate System
• CrP stored in cell
• Allows for rapid
ATP replenishment
• Only a small amount
available (10-30
seconds worth)
Anaerobic Glycolysis –
Lactic Acid System
• Anaerobic system - no
O2 required
• Very inefficient, does
not create much ATP
• Only useful in short
term situations (30 sec
- 1 min)
• Produces lactic acid
as a by-product
Aerobic System
- Uses oxygen for ATP
production
- Oxygen comes from the
RBCs in the blood and the
myoglobin storage depot
- Uses many substrates:
carbohydrates, lipids, proteins
- Good for long term exercise
- May provide 90-100% of the
needed ATP during these
periods
Summary of Muscle Metabolism
Oxygen Debt
• The amount of oxygen needed to
restore muscle tissue (and the body)
to the pre-exercise state
• Muscle O2, ATP, creatine phosphate, and
glycogen levels, and a normal pH must be
restored after any vigorous exercise
• Circulating lactic acid is converted/recycled
back to glucose by the liver
Factors Affecting the
Force of Contraction
1. Number of muscle fibers contracting (recruitment)
2. Size of the muscle
3. Frequency of stimulation
4. Degree of muscle stretch when the contraction begins
5. Series elastic elements
Series Elastic Elements
• All of the noncontractile structures of a
muscle:
– Connective tissue coverings and tendons
– Elastic elements of sarcomeres
Internal load: force generated by myofibrils on the
series elastic elements
External load: force generated by series elastic
elements on load
Muscle Fiber Type: Speed of
Contraction
• Slow oxidative fibers contract slowly, have slow
acting myosin ATPases, and are fatigue resistant
(red)
• Fast oxidative fibers contract quickly, have fast
myosin ATPases, and have moderate resistance to
fatigue
• Fast glycolytic fibers contract quickly, have fast
myosin ATPases, and are easily fatigued (white)
Force, Velocity, and Duration of
Muscle Contraction
Homeostatic Imbalances
• The muscular dystrophies (MD) are a group of more
than 30 genetic diseases characterized by progressive
weakness and degeneration of the skeletal muscles
that control movement.
• Some forms of MD are seen in infancy or childhood,
while others may not appear until middle age or later.
• The disorders differ in terms of
–
–
–
–
–
the distribution and extent of muscle weakness
(some forms of MD also affect cardiac muscle)
age of onset
rate of progression
pattern of inheritance
Homeostatic Imbalances
Duchenne Muscular Dystrophy:
• Inherited lack of functional gene
for formation of a protein,
dystrophin, that helps maintain the
integrity of the sarcolemma
• Onset in early childhood, victims
rarely live to adulthood
End Chapter 9
Some extra slides for your review
follow this slide.
Smooth Muscle Contractions
• Peristalsis – alternating contractions and
relaxations of smooth muscles that squeeze
substances through the lumen of hollow organs
• Segmentation – contractions and relaxations of
smooth muscles that mix substances in the lumen
of hollow organs
Peristalsis Animation
Developmental Aspects of the Muscular
System
• Muscle tissue develops from embryonic mesoderm called myoblasts
(except the muscles of the iris of the eye and the arrector pili muscles
in the skin)
• Multinucleated skeletal muscles form by fusion of myoblasts
• The growth factor agrin stimulates the clustering of ACh receptors at
newly forming motor end plates
• As muscles are brought under the control of the somatic nervous
system, the numbers of fast and slow fibers are also determined
• Cardiac and smooth muscle myoblasts do not fuse but develop gap
junctions at an early embryonic stage
Regeneration of Muscle Tissue
• Cardiac and skeletal muscle become amitotic, but
can lengthen and thicken
• Myoblast-like satellite cells show very limited
regenerative ability
• Satellite (stem) cells can fuse to form new skeletal
muscle fibers
• Cardiac cells lack satellite cells
• Smooth muscle has good regenerative ability
Developmental Aspects: After Birth
• Muscular development reflects neuromuscular
coordination
• Development occurs head-to-toe, and proximal-to-distal
• Peak natural neural control of muscles is achieved by
midadolescence
• Athletics and training can improve neuromuscular control
Developmental Aspects: Male and Female
• There is a biological basis for greater
strength in men than in women
• Women’s skeletal muscle makes up 36% of
their body mass
• Men’s skeletal muscle makes up 42% of
their body mass
Developmental Aspects: Male and Female
• These differences are due primarily to the
male sex hormone testosterone
• With more muscle mass, men are generally
stronger than women
• Body strength per unit muscle mass,
however, is the same in both sexes
Developmental Aspects: Age Related
• With age, connective tissue increases and muscle
fibers decrease
• Muscles become stringier and more sinewy
• By age 80, 50% of muscle mass is lost (sarcopenia)
• Regular exercise reverses sarcopenia
• Aging of the cardiovascular system affects every
organ in the body
• Atherosclerosis may block distal arteries, leading to
intermittent claudication and causing severe pain in
leg muscles
End Chapter 9
End of review slides.