Professional Documents
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Muscle Tissue
Lecture Presentation by
Lee Ann Frederick
University of Texas at Arlington
• Learning Outcomes
• 10-1 Specify the functions of skeletal muscle
tissue.
• 10-2 Describe the organization of muscle at the
tissue level.
• 10-3 Describe the characteristics of skeletal
muscle fibers, and identify the structural
components of a sarcomere.
• 10-4 Identify the components of the
neuromuscular junction, and summarize the
events involved in the neural control of
skeletal muscle contraction and relaxation.
© 2015 Pearson Education, Inc.
10-1 An Introduction to Muscle Tissue
• Learning Outcomes
• 10-5 Describe the mechanism responsible for
tension production in a muscle fiber, and
compare the different types of muscle
contraction.
• 10-6 Describe the mechanisms by which muscle
fibers obtain the energy to power
contractions.
• 10-7 Relate the types of muscle fibers to muscle
performance, and distinguish between
aerobic and anaerobic endurance.
• Learning Outcomes
• 10-8 Identify the structural and functional
differences between skeletal muscle fibers
and cardiac muscle cells.
• 10-9 Identify the structural and functional
differences between skeletal muscle fibers
and smooth muscle cells, and discuss the
roles of smooth muscle tissue in systems
throughout the body.
• Muscle Tissue
• A primary tissue type, divided into:
• Skeletal muscle tissue
• Cardiac muscle tissue
• Smooth muscle tissue
• Skeletal Muscles
• Are attached to the skeletal system
• Allow us to move
• The muscular system
• Includes only skeletal muscles
• Skeletal Muscle
• Muscle tissue (muscle cells or fibers)
• Connective tissues
• Nerves
• Blood vessels
• Epimysium
• Exterior collagen layer
• Connected to deep fascia
• Separates muscle from surrounding tissues
• Perimysium
• Surrounds muscle fiber bundles (fascicles)
• Contains blood vessel and nerve supply to
fascicles
• Endomysium
• Surrounds individual muscle cells (muscle fibers)
• Contains capillaries and nerve fibers contacting
muscle cells
• Contains myosatellite cells (stem cells) that repair
damage
Epimysium
Blood vessels
and nerves
Tendon
Endomysium
Perimysium
Perimysium
Muscle fiber
Epimysium
Blood vessels
and nerves
Endomysium
Tendon
Endomysium
Perimysium
Sarcoplasm
Epimysium
Endomysium
Perimysium
Myoblasts
a A muscle
Muscle fiber LM × 612
fiber forms by
the fusion of
myoblasts. Sarcolemma Striations Nuclei
Myofibrils
Myosatellite cell
Nuclei
Mitochondria
Immature
muscle fiber
Up to 30 cm
in length
Myoblasts
a A muscle
fiber forms by
the fusion of
myoblasts.
Myosatellite cell
Nuclei
Immature
muscle fiber
Myosatellite cell
Up to 30 cm
in length
Myofibrils
Mitochondria
Myofibril
Muscle fiber
Sarcolemma Nuclei
Sarcoplasm
Mitochondria
Terminal cisterna
Sarcolemma
Sarcolemma
Sarcoplasm
Myofibril
Myofibrils
Thin filament
Thick filament
Triad Sarcoplasmic T tubules
reticulum
Myofibril
Muscle fiber
Sarcolemma Nuclei
Sarcoplasm
Mitochondria
Terminal cisterna
Sarcolemma
Sarcolemma
Sarcoplasm
Myofibril
Myofibrils
Thin filament
Thick filament
Triad Sarcoplasmic T tubules
reticulum
Mitochondria
Sarcolemma
Myofibril
Thin filament
Thick filament
Terminal cisterna
Sarcolemma
Sarcoplasm
Myofibrils
• Sarcomeres
• The contractile units of muscle
• Structural units of myofibrils
• Form visible patterns within myofibrils
• A striped or striated pattern within myofibrils
• Alternating dark, thick filaments (A bands) and
light, thin filaments (I bands)
• Sarcomeres
• The A Band
• M line
• The center of the A band
• At midline of sarcomere
• The H Band
• The area around the M line
• Has thick filaments but no thin filaments
• Zone of overlap
• The densest, darkest area on a light micrograph
• Where thick and thin filaments overlap
• Sarcomeres
• The I Band
• Z lines
• The centers of the I bands
• At two ends of sarcomere
• Titin
• Are strands of protein
• Reach from tips of thick filaments to the Z line
• Stabilize the filaments
I band A band
a A longitudinal view of a
sarcomere, showing bands
of thick and thin filaments
I band A band
H band Z line
b A corresponding
longitudinal section of a
sarcomere in a myofibril
from a muscle fiber in
the gastrocnemius (calf) Myofibril TEM × 64,000
muscle of the leg
Sarcomere
Sarcomere
Myofibril
a A superficial view
of a sarcomere
Thin Thick
filament filament
Attachment
of titin
Sarcomere
I band A band
Muscle Fascicle
Contains:
Thick filaments
Surrounded by:
Perimysium Thin filaments
Perimysium
Contains:
Muscle fibers
Z line M line Titin Z line
H band
Muscle Fiber
Surrounded by:
Endomysium
Endomysium
Contains:
Myofibrils
Skeletal Muscle
Surrounded by:
Epimysium
Epimysium
Contains:
Muscle fascicles
Muscle Fascicle
Surrounded by:
Perimysium
Perimysium
Contains:
Muscle fibers
Muscle Fiber
Surrounded by:
Endomysium
Endomysium
Contains:
Myofibrils
Myofibril
Surrounded by:
Sarcoplasmic
reticulum
Consists of:
Sarcomeres
(Z line to Z line)
Sarcomere
I band A band
Contains:
Thick filaments
Thin filaments
• Thin Filaments
• F-actin (filamentous actin)
• Is two twisted rows of globular G-actin
• The active sites on G-actin strands bind to myosin
• Nebulin
• Holds F-actin strands together
• Thin Filaments
• Tropomyosin
• Is a double strand
• Prevents actin–myosin interaction
• Troponin
• A globular protein
• Binds tropomyosin to G-actin
• Controlled by Ca2+
Sarcomere
F-actin
strand
• Initiating Contraction
• Ca2+ binds to receptor on troponin molecule
• Troponin–tropomyosin complex changes
• Exposes active site of F-actin
• Thick Filaments
• Contain about 300 twisted myosin subunits
• Contain titin strands that recoil after stretching
• The mysosin molecule
• Tail
• Binds to other myosin molecules
• Head
• Made of two globular protein subunits
• Reaches the nearest thin filament
Titin
• Myosin Action
• During contraction, myosin heads:
• Interact with actin filaments, forming cross-bridges
• Pivot, producing motion
Myofibril at rest
I band A band
Contracted myofibril
I band A band
Neuromuscular
junction
Axon
terminal
SEE BELOW
Sarcoplasmic Motor
reticulum end plate
Myofibril
Motor end plate
1
The cytoplasm of the axon
terminal contains vesicles filled
with molecules of acetylcholine,
or ACh. Acetylcholine is a
neurotransmitter, a chemical
released by a neuron to change
the permeability or other
properties of another cell’s plasma
membrane. The synaptic cleft and
the motor end plate contain
molecules of the enzyme
acetylcholinesterase (AChE),
which breaks down ACh.
Vesicles ACh
2
The stimulus for ACh release
is the arrival of an electrical
impulse, or action potential,
at the axon terminal. An action
potential is a sudden change in
the membrane potential that
travels along the length of the
axon.
Arriving action
potential
3
When the action potential
reaches the neuron’s axon
terminal, permeability
changes in its membrane
trigger the exocytosis of ACh
into the synaptic cleft.
Exocytosis occurs as vesicles
fuse with the neuron’s plasma
membrane.
Motor
end plate
4
ACh molecules diffuse across the
synaptic cleft and blind to ACh
receptors on the surface of the
motor end plate. ACh binding
alters the membrane’s permeabil-
ity to sodium ions. Because the
extracellular fluid contains a high
concentration of sodium ions,
and sodium ion concentration
inside the cell is very low, sodium
ions rush into the cytosol.
Na+
Na+
Na+
ACh
receptor site
© 2015 Pearson Education, Inc.
Figure 10-9 Events at the Neuromuscular Junction (Part 9 of 9).
5
The sudden inrush of sodium ions
results in the generation of an
action potential in the sarcolemma.
ACh is removed from the
synaptic cleft in two ways. ACh
either diffuses away from the
synapse, or it is broken down by
AChE into acetic acid and choline.
This removal inactivates the ACh
receptor sites. The muscle fiber
pictured above indicates the
propagation of the action
potential along the sarcolemma.
Action
potential
1
Contraction Cycle Begins
The contraction cycle involves a
series of interrelated steps. It begins
with the arrival of calcium ions
(Ca2+) within the zone of overlap in
a sarcomere.
ADP
+ Ca2+ Myosin head
P
Troponin
Tropomyosin Actin
ADP Ca2+
P+
2
Active-Site Exposure
Calcium ions bind to troponin,
weakening the bond between
actin and the troponin–tropomyosin
complex. The troponin molecule
then changes position, rolling the
tropomyosin molecule away from
the active sites on actin and
allowing interaction with the
energized myosin heads.
ADP
+ P
Cytosol
Ca2+
Ca2+
Active
site ADP
P+
3
Cross-Bridge Formation
Once the active sites are
exposed, the energized myosin
heads bind to them, forming
cross-bridges.
ADP
+ Ca2+
P
Ca2+
ADP
P+
4
Myosin Head Pivoting
After cross-bridge formation,
the energy that was stored in the
resting state is released as the
myosin head pivots toward the M
line. This action is called the power
stroke; when it occurs,
the bound ADP and phosphate
group are released.
ADP + P
Ca2+
Ca2+
ADP + P
5
Cross-Bridge Detachment
When another ATP binds to the
myosin head, the link between the
myosin head and the active site on
the actin molecule is broken. The
active site is now exposed and able
to form another cross-bridge.
ATP
Ca2+
Ca2+
ATP
6
Myosin Reactivation
Myosin reactivation occurs
when the free myosin head
splits ATP into ADP and P.
The energy released is used
to recock the myosin head.
ADP
+ P
Ca2+
Ca2+
ADP
P+
• Fiber Shortening
• As sarcomeres shorten, muscle pulls together,
producing tension
• Muscle shortening can occur at both ends of the
muscle, or at only one end of the muscle
• This depends on the way the muscle is attached at
the ends
• Relaxation
• Contraction duration
• Depends on:
• Duration of neural stimulus
• Number of free calcium ions in sarcoplasm
• Availability of ATP
• Relaxation
• Ca2+ concentrations fall
• Ca2+ detaches from troponin
• Active sites are re-covered by tropomyosin
• Rigor Mortis
• A fixed muscular contraction after death
• Caused when:
• Ion pumps cease to function; ran out of ATP
• Calcium builds up in the sarcoplasm
Axon
6 ACh is broken down terminal Sarcolemma
9 Contraction ends
Without cross-bridge formation, contraction ends.
100
Tension (percent of maximum)
80
60
Eye muscle
Gastrocnemius
Soleus
Tension
0 10 20 30 40 50 60 70 80 90 100
Time (msec)
Stimulus
a A myogram showing differences in tension over
time for a twitch in different skeletal muscles.
© 2015 Pearson Education, Inc.
Figure 10-15b The Development of Tension in a Twitch.
Maximum tension
development
Tension
Stimulus
Time (msec) 0 5 10 20 30 40
= Stimulus
Maximum tension (in tetanus)
Tension
Time Time
a Treppe. Treppe is an increase in b Wave summation. Wave summation
peak tension with each successive occurs when successive stimuli
stimulus delivered shortly after the arrive before the relaxation phase
completion of the relaxation phase of has been completed.
the preceding twitch.
Time Time
c Incomplete tetanus. Incomplete d Complete tetanus. During
tetanus occurs if the stimulus complete tetanus, the stimulus
frequency increases further. Tension frequency is so high that the
production rises to a peak, and the relaxation phase is eliminated.
periods of relaxation are very brief. Tension plateaus at maximum levels.
Axons of
motor neurons
SPINAL CORD
Motor
nerve
KEY
Muscle fibers
Motor unit 1
Motor unit 2
Motor unit 3
Tension in tendon
Time
b The tension applied to the tendon
remains relatively constant, even
though individual motor units cycle
between contraction and relaxation.
80
6 kg
70
b In this eccentric contraction, the muscle elongates as it generates tension. Time
Amount of load
6
Muscle
Muscle relaxes
4
tension
(kg) Peak tension
Muscle 2
contracts production
(isometric
0
contraction)
Contraction
begins Length unchanged
100
Muscle
90 length
6 kg 6 kg (percent
80 of resting
length)
70
c The same muscle is attached to a weight that exceeds its peak Time
tension capabilities. On stimulation, tension will rise to a peak,
but the muscle as a whole cannot shorten. This is an isometric
contraction.
Distance shortened
Small load
Intermediate load
Large load
• ATP Generation
• Cells produce ATP in two ways
1. Aerobic metabolism of fatty acids in the
mitochondria
2. Anaerobic glycolysis in the cytoplasm
• Aerobic Metabolism
• Is the primary energy source of resting muscles
• Breaks down fatty acids
• Produces 34 ATP molecules per glucose molecule
• Glycolysis
• Is the primary energy source for peak muscular
activity
• Produces two ATP molecules per molecule of
glucose
• Breaks down glucose from glycogen stored in
skeletal muscles
© 2015 Pearson Education, Inc.
Table 10-1 Sources of Energy in a Typical Muscle Fiber.
• In a resting skeletal muscle, the demand for ATP is low, Fatty acids O2 G Blood vessels
and there is more than enough oxygen available for
mitochondria to meet that demand.
• During moderate levels of activity, the demand for ATP Fatty acids
O2
increases.
• There is still enough oxygen for the mitochondria to meet
that demand, but no excess ATP is produced.
Glucose Glycogen
• The muscle fiber now relies primarily on the aerobic
2 ADP
metabolism of glucose from stored glycogen to
generate ATP. 2 ATP
• If the glycogen reserves are low, the muscle fiber can also Pyruvate
break down other substrates, such as fatty acids.
34 ADP
• All of the ATP now produced is used to power muscle 34 ATP
contraction.
CO2 To myofibrils to support
muscle contraction
• Muscle Fatigue
• When muscles can no longer perform a required
activity, they are fatigued
• Results of Muscle Fatigue
• Depletion of metabolic reserves
• Damage to sarcolemma and sarcoplasmic
reticulum
• Low pH (lactic acid)
• Muscle exhaustion and pain
• Muscle Performance
• Force
• The maximum amount of tension produced
• Endurance
• The amount of time an activity can be sustained
• Force and endurance depend on:
• The types of muscle fibers
• Physical conditioning
• Fast Fibers
• Contract very quickly
• Have large diameter, large glycogen reserves, few
mitochondria
• Have strong contractions, fatigue quickly
• Slow Fibers
• Are slow to contract, slow to fatigue
• Have small diameter, more mitochondria
• Have high oxygen supply
• Contain myoglobin (red pigment, binds oxygen)
• Intermediate Fibers
• Are mid-sized
• Have low myoglobin
• Have more capillaries than fast fibers, slower to
fatigue
Capillary
Slow fibers
Smaller diameter,
darker color due to
myoglobin; fatigue
resistant
LM × 170
Fast fibers
Larger diameter,
paler color;
easily fatigued
LM × 170 LM × 783
• Muscle Hypertrophy
• Muscle growth from heavy training
• Increases diameter of muscle fibers
• Increases number of myofibrils
• Increases mitochondria, glycogen reserves
• Muscle Atrophy
• Lack of muscle activity
• Reduces muscle size, tone, and power
• Physical Conditioning
• Improves both power and endurance
• Anaerobic activities (e.g., 50-meter dash,
weightlifting)
• Use fast fibers
• Fatigue quickly with strenuous activity
• Improved by:
• Frequent, brief, intensive workouts
• Causes hypertrophy
• Physical Conditioning
• Improves both power and endurance
• Aerobic activities (prolonged activity)
• Supported by mitochondria
• Require oxygen and nutrients
• Improves:
• Endurance by training fast fibers to be more like
intermediate fibers
• Cardiovascular performance
• Importance of Exercise
• What you don’t use, you lose
• Muscle tone indicates base activity in motor units
of skeletal muscles
• Muscles become flaccid when inactive for days or
weeks
• Muscle fibers break down proteins, become
smaller and weaker
• With prolonged inactivity, fibrous tissue may
replace muscle fibers
• Intercalated Discs
• Are specialized contact points between
cardiocytes
• Join cell membranes of adjacent cardiocytes (gap
junctions, desmosomes)
• Functions of intercalated discs
• Maintain structure
• Enhance molecular and electrical connections
• Conduct action potentials
• Intercalated Discs
• Coordination of cardiocytes
• Because intercalated discs link heart cells
mechanically, chemically, and electrically, the heart
functions like a single, fused mass of cells
Cardiac
muscle cell
Intercalated
discs
Nucleus
Cardiac muscle
cell (intact)
Intercalated disc
(sectioned)
b A diagrammatic view of
cardiac muscle. Note
the striations and
intercalated discs.
Mitochondria
Nucleus
Myofibrils
Entrance to T tubule
Sarcolemma
Mitochondrion
Contact of sarcoplasmic
reticulum with
T tubule
Sarcoplasmic
Myofibrils reticulum
T
Circular
muscle layer
Longitudinal
muscle layer
Actin Myosin
Contracted
(superficial
view)
• Excitation–Contraction Coupling
• Free Ca2+ in cytoplasm triggers contraction
• Ca2+ binds with calmodulin
• In the sarcoplasm
• Activates myosin light chain kinase
• Enzyme breaks down ATP, initiates contraction
• Length–Tension Relationships
• Thick and thin filaments are scattered
• Resting length not related to tension development
• Functions over a wide range of lengths
(plasticity)
• Control of Contractions
• Multiunit smooth muscle cells
• Connected to motor neurons
• Visceral smooth muscle cells
• Not connected to motor neurons
• Rhythmic cycles of activity controlled by pacesetter
cells