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Three Types of Muscle Tissue
1. Skeletal muscle tissue:
– Attached to bones and
skin
– Striated
– Voluntary (i.e., conscious
control)
– Powerful
– Fibers = cells
Three Types of Muscle Tissue
2. Cardiac muscle tissue:
–
–
–
–
–
Only in the heart
Striated
Involuntary
Branched cells
Intercalated disks
Three Types of Muscle Tissue
3. Smooth muscle tissue:
– In the walls of hollow
organs (e.g., stomach,
urinary bladder, and
airways)
– Not striated
– Involuntary
– Fibers = cells
Special Characteristics of Muscle Tissue
1. Excitability (responsiveness or irritability): ability to
receive and respond to stimuli
2. Contractility: ability to shorten when stimulated
3. Extensibility: ability to be stretched
4. Elasticity: ability to recoil to resting length
Muscle Functions
1.
2.
3.
4.
Movement of bones or fluids (e.g., blood)
Maintaining posture and body position
Stabilizing joints
Heat generation (especially skeletal muscle)
Skeletal Muscle
• Each muscle is served by one artery, one
nerve, and one or more veins
– Enter near center, branch extensively through
connective tissue sheaths
– Each muscle fiber has a nerve ending
• Connective Tissue sheaths
– Epimysium
– Perimysium
– Endomysium
Epimysium
Bone Epimysium
Perimysium
Endomysium
Tendon
(b)
Perimysium Fascicle
(a)
Muscle fiber
in middle of
a fascicle
Blood vessel
Fascicle
(wrapped by perimysium)
Endomysium
(between individual
muscle fibers)
Muscle fiber
Figure 9.1
Skeletal Muscle: Attachments
• Muscles attach:
– Directly—epimysium of muscle is fused to the
periosteum of bone or perichondrium of cartilage
– Indirectly—connective tissue wrappings extend
beyond the muscle as a ropelike tendon or
sheetlike aponeurosis
Table 9.1
Microscopic Anatomy of a Skeletal
Muscle Fiber
• Cylindrical cell 10 to 100 m in diameter, up to
30 cm long
• Multiple peripheral nuclei
• Many mitochondria
• Glycosomes for glycogen storage, myoglobin
for O2 storage
• Also contain myofibrils, sarcoplasmic
reticulum, and T tubules
Myofibrils
• Densely packed, rodlike elements
• ~80% of cell volume
• Exhibit striations: perfectly aligned repeating
series of dark A bands and light I bands
Sarcolemma
Mitochondrion
Myofibril
Dark A band Light I band Nucleus
(b) Diagram of part of a muscle fiber showing the myofibrils. One
myofibril is extended afrom the cut end of the fiber.
Sarcomere
• Smallest contractile unit (functional unit) of a
muscle fiber
• The region of a myofibril between two
successive Z discs
• Composed of thick and thin myofilaments
made of contractile proteins
Features of a Sarcomere
•
•
•
•
•
Thick filaments
Thin filaments
Z disc
H zone
M line
Ultrastructure of Thick Filament
• Composed of the protein myosin
– Myosin tails contain:
• 2 interwoven, heavy polypeptide chains
– Myosin heads contain:
• 2 smaller, light polypeptide chains that
act as cross bridges during contraction
• Binding sites for actin of thin filaments
• Binding sites for ATP
• ATPase enzymes
Ultrastructure of Thin Filament
• Twisted double strand of fibrous protein F
actin
• F actin consists of G (globular) actin subunits
• G actin bears active sites for myosin head
attachment during contraction
• Tropomyosin and troponin: regulatory
proteins bound to actin
Sarcoplasmic Reticulum (SR)
• Network of smooth endoplasmic reticulum
surrounding each myofibril
• Pairs of terminal cisternae form perpendicular
cross channels
• Functions in the regulation of intracellular
Ca2+ levels
T Tubules
• Continuous with the sarcolemma
• Penetrate the cell’s interior at each A band–I
band junction
• Associate with the paired terminal cisternae to
form triads that encircle each sarcomere
Part of a skeletal
muscle fiber (cell)
Myofibril
I band
A band
I band
Z disc
H zone
Z disc
M line
Sarcolemma
Sarcolemma
Triad:
• T tubule
• Terminal
cisternae
of the SR (2)
Tubules of
the SR
Myofibrils
Mitochondria
Figure 9.5
Triad Relationships
• T tubules conduct impulses deep into muscle
fiber
• Integral proteins protrude into the
intermembrane space from T tubule and SR
cisternae membranes
• T tubule proteins: voltage sensors
• SR foot proteins: gated channels that regulate
Ca2+ release from the SR cisternae
Contraction
• The generation of force
• Does not necessarily cause shortening of the
fiber
• Shortening occurs when tension generated by
cross bridges on the thin filaments exceeds
forces opposing shortening
Sliding Filament Model of Contraction
• In the relaxed state, thin and thick filaments
overlap only slightly
• During contraction, myosin heads bind to
actin, detach, and bind again, to propel the
thin filaments toward the M line
• As H zones shorten and disappear, sarcomeres
shorten, muscle cells shorten, and the whole
muscle shortens
Z
Z
H
A
I
I
Fully relaxed sarcomere of a muscle fiber
Z
Z
I
A
I
Fully contracted sarcomere of a muscle fiber
Figure 9.6
Requirements for Skeletal Muscle
Contraction
1. Activation: neural stimulation at a
neuromuscular junction
2. Excitation-contraction coupling:
– Generation and propagation of an action
potential along the sarcolemma
– Final trigger: a brief rise in intracellular Ca2+
levels
Events at the Neuromuscular Junction
Events at the Neuromuscular Junction
Myelinated axon
of motor neuron
Axon terminal of
neuromuscular
junction
Sarcolemma of
the muscle fiber
Action
potential (AP)
Nucleus
1 Action potential arrives at
axon terminal of motor neuron.
2 Voltage-gated
Ca2+
channels
open and Ca2+ enters the axon
terminal.
Ca2+
Ca2+
Axon terminal
of motor neuron
3 Ca2+ entry causes some
Fusing synaptic
vesicles
synaptic vesicles to release
their contents (acetylcholine)
by exocytosis.
ACh
4 Acetylcholine, a
neurotransmitter, diffuses across
the synaptic cleft and binds to
receptors in the sarcolemma.
Na+
K+
channels that allow simultaneous
passage of Na+ into the muscle
fiber and K+ out of the muscle
fiber.
by its enzymatic breakdown in
the synaptic cleft by
acetylcholinesterase.
Junctional
folds of
sarcolemma
Sarcoplasm of
muscle fiber
5 ACh binding opens ion
6 ACh effects are terminated
Synaptic vesicle
containing ACh
Mitochondrion
Synaptic
cleft
Ach–
Degraded ACh
Na+
Acetylcholinesterase
Postsynaptic membrane
ion channel opens;
ions pass.
Postsynaptic membrane
ion channel closed;
ions cannot pass.
K+
Figure 9.8
Events in Generation of an Action
Potential
1. Local depolarization (end plate potential):
– ACh binding opens chemically (ligand) gated ion
channels
– Simultaneous diffusion of Na+ (inward) and K+
(outward)
– More Na+ diffuses, so the interior of the
sarcolemma becomes less negative
Axon terminal
Open Na+
Channel
Na+
Synaptic
cleft
Closed K+
Channel
ACh
ACh
Na+ K+
Na+
K+
K+
++
++ +
+
Action potential
+
+ +++
+
1 Local depolarization: generation of the
end plate potential on the sarcolemma
Sarcoplasm of muscle fiber
Figure 9.9, step 1
Events in Generation of an Action
Potential
2. Generation and propagation of an action
potential:
– End plate potential spreads to adjacent
membrane areas
– Voltage-gated Na+ channels open
– Na+ influx decreases the membrane voltage
toward a critical threshold
– If threshold is reached, an action potential is
generated
Axon terminal
Open Na+
Channel
Na+
Synaptic
cleft
Closed K+
Channel
ACh
ACh
Na+ K+
Na+
K+
K+
++
++ +
+
Action potential
+
+ +++
+
2 Generation and propagation of the
action potential (AP)
1 Local depolarization: generation of the
end plate potential on the sarcolemma
Sarcoplasm of muscle fiber
Figure 9.9, step 2
Events in Generation of an Action
Potential
• Local depolarization wave continues to
spread, changing the permeability of the
sarcolemma
• Voltage-regulated Na+ channels open in the
adjacent patch, causing it to depolarize to
threshold
Events in Generation of an Action
Potential
3. Repolarization:
• Na+ channels close and voltage-gated K+
channels open
• K+ efflux rapidly restores the resting polarity
• Fiber cannot be stimulated and is in a
refractory period until repolarization is
complete
• Ionic conditions of the resting state are
restored by the Na+-K+ pump
Axon terminal
Open Na+
Channel
Na+
Synaptic
cleft
Closed K+
Channel
ACh
ACh
Na+ K+
Na+ K+
++
++ +
+
K+
Action potential
+
+ +++
+
2 Generation and propagation of
the action potential (AP)
1 Local depolarization:
generation of the end
plate potential on the
sarcolemma
Sarcoplasm of muscle fiber
Closed Na+ Open K+
Channel
Channel
Na+
K+
3 Repolarization
Figure 9.9
Depolarization
due to Na+ entry
Na+ channels
close, K+ channels
open
Repolarization
due to K+ exit
Na+
channels
open
Threshold
K+ channels
close
Figure 9.10
Excitation-Contraction (E-C) Coupling
• Sequence of events by which transmission of
an AP along the sarcolemma leads to sliding of
the myofilaments
• Latent period:
– Time when E-C coupling events occur
– Time between AP initiation and the beginning of
contraction
Events of Excitation-Contraction (E-C)
Coupling
• AP is propagated along sarcomere to T tubules
• Voltage-sensitive proteins stimulate Ca2+
release from SR
– Ca2+ is necessary for contraction
1 Action potential is
Steps in
E-C Coupling:
propagated along the
sarcolemma and down
the T tubules.
Voltage-sensitive
tubule protein
Sarcolemma
T tubule
Ca2+
release
channel
Terminal
cisterna
of SR
Ca2+
Figure 9.11, step 3
1 Action potential is
Steps in
E-C Coupling:
propagated along the
sarcolemma and down
the T tubules.
Voltage-sensitive
tubule protein
Sarcolemma
T tubule
Ca2+
release
channel
Terminal
cisterna
of SR
2 Calcium
ions are
released.
Ca2+
Figure 9.11, step 4
Actin
Ca2+
Troponin
Tropomyosin
blocking active sites
Myosin
The aftermath
Figure 9.11, step 5
Actin
Ca2+
Troponin
Tropomyosin
blocking active sites
Myosin
3 Calcium binds to
troponin and removes
the blocking action of
tropomyosin.
Active sites exposed and
ready for myosin binding
The aftermath
Figure 9.11, step 6
Actin
Ca2+
Troponin
Tropomyosin
blocking active sites
Myosin
3 Calcium binds to
troponin and removes
the blocking action of
tropomyosin.
Active sites exposed and
ready for myosin binding
4 Contraction begins
Myosin
cross
bridge
The aftermath
Figure 9.11, step 7
Role of Calcium (Ca2+) in Contraction
• At low intracellular Ca2+ concentration:
– Tropomyosin blocks the active sites on actin
– Myosin heads cannot attach to actin
– Muscle fiber relaxes
Role of Calcium (Ca2+) in Contraction
• At higher intracellular Ca2+ concentrations:
– Ca2+ binds to troponin
– Troponin changes shape and moves tropomyosin
away from active sites
– Events of the cross bridge cycle occur
– When nervous stimulation ceases, Ca2+ is pumped
back into the SR and contraction ends
Cross Bridge Cycle
• Continues as long as the Ca2+ signal and
adequate ATP are present
• Cross bridge formation—high-energy myosin
head attaches to thin filament
• Working (power) stroke—myosin head pivots
and pulls thin filament toward M line
Cross Bridge Cycle
• Cross bridge detachment—ATP attaches to
myosin head and the cross bridge detaches
• “Cocking” of the myosin head—energy from
hydrolysis of ATP cocks the myosin head into
the high-energy state
Figure 9.12
Principles of Muscle Mechanics
1. Same principles apply to contraction of a
single fiber and a whole muscle
2. Contraction produces tension, the force
exerted on the load or object to be moved
3. Contraction does not always shorten a
muscle:
– Isometric contraction: no shortening; muscle
tension increases but does not exceed the load
– Isotonic contraction: muscle shortens because
muscle tension exceeds the load
Principles of Muscle Mechanics
4. Force and duration of contraction vary in
response to stimuli of different frequencies
and intensities
Motor Unit
• Motor unit = a motor neuron and all muscle
fibers it supplies
– Small motor units in muscles that control fine
movements (fingers, eyes)
– Large motor units in large weight-bearing muscles
(thighs, hips)
• Muscle fibers from a motor unit are spread
throughout the muscle
• Motor units in a muscle usually contract
asynchronously
Spinal cord
Motor Motor
unit 1 unit 2
Axon terminals at
neuromuscular junctions
Nerve
Motor neuron
cell body
Motor
Muscle
neuron
axon
Muscle
fibers
Axons of motor neurons extend from the spinal cord to the
muscle. There each axon divides into a number of axon
terminals that form neuromuscular junctions with muscle
fibers scattered throughout the muscle.
Figure 9.13a
Muscle Twitch
• Response of a muscle to a single, brief
threshold stimulus
• Three phases of a twitch:
– Latent period: events of excitation-contraction
coupling
– Period of contraction: cross bridge formation;
tension increases
– Period of relaxation: Ca2+ re-entry into the SR;
tension declines to zero
Latent Period of
period contraction
Period of
relaxation
Single
stimulus
(a) Myogram showing the three phases of an isometric twitch
Figure 9.14a
Muscle Twitch Comparisons
Different strength
and duration of
twitches are due to
variations in
metabolic
properties and
enzymes between
muscles
Graded Muscle Responses
• Variations in the degree of muscle contraction
• Required for proper control of skeletal
movement
Responses are graded by:
1. Changing the frequency of stimulation
2. Changing the strength of the stimulus
Response to Change in Stimulus
Frequency
• A single stimulus results in a single contractile
response—a muscle twitch
Response to Change in Stimulus
Frequency
• Increase frequency of stimulus (muscle does
not have time to completely relax between
stimuli)
• Ca2+ release stimulates further contraction 
temporal (wave) summation
• Further increase in stimulus frequency 
unfused (incomplete) tetanus
Low stimulation frequency
unfused (incomplete) tetanus
Partial relaxation
Stimuli
(b) If another stimulus is applied before the muscle
relaxes completely, then more tension results.
This is temporal (or wave) summation and results
in unfused (or incomplete) tetanus.
Figure 9.15b
Response to Change in Stimulus
Frequency
• If stimuli are given quickly enough, fused
(complete) tetany results
Response to Change in Stimulus
Strength
• Threshold stimulus: stimulus strength at
which the first observable muscle contraction
occurs
• Muscle contracts more vigorously as stimulus
strength is increased above threshold
• Contraction force is precisely controlled by
recruitment (multiple motor unit summation)
– Increase in the number of active motor units
Stimulus strength
Maximal
stimulus
Threshold
stimulus
Proportion of motor units excited
Strength of muscle contraction
Maximal contraction
Figure 9.16
Response to Change in Stimulus
Strength
• Size principle: motor units with larger and
larger fibers are recruited as stimulus intensity
increases
Muscle Tone
• Constant, slightly contracted state of all
muscles
• Due to spinal reflexes that activate groups of
motor units alternately in response to input
from stretch receptors in muscles
• Keeps muscles firm, healthy, and ready to
respond
Isotonic Contractions
• Muscle changes in length and moves the load
• Isotonic contractions are either concentric or
eccentric:
– Concentric contractions—the muscle shortens and
does work
– Eccentric contractions—the muscle contracts as it
lengthens
Figure 9.18a
Isometric Contractions
• The load is greater than the
tension the muscle is able
to develop
• Tension increases to the
muscle’s capacity, but the
muscle neither shortens nor
lengthens
Muscle Metabolism: Energy for
Contraction
• ATP is the only source used directly for
contractile activities
• Available stores of ATP are depleted in 4–6
seconds
Muscle Metabolism: Energy for
Contraction
• ATP is regenerated by:
– Direct phosphorylation of ADP by creatine
phosphate (CP)
– Anaerobic pathway (glycolysis)
– Aerobic respiration
(a)
Direct phosphorylation
Coupled reaction of creatine
phosphate (CP) and ADP
Energy source: CP
CP
ADP
Creatine
kinase
Creatine
ATP
Oxygen use: None
Products: 1 ATP per CP, creatine
Duration of energy provision:
15 seconds
Figure 9.19a
Anaerobic Pathway
• At 70% of maximum contractile activity:
– Bulging muscles compress blood vessels
– Oxygen delivery is impaired
– Pyruvic acid is converted into lactic acid
Anaerobic Pathway
• Lactic acid:
– Diffuses into the
bloodstream
– Used as fuel by the liver,
kidneys, and heart
– Converted back into
pyruvic acid by the liver
Aerobic Pathway
• Produces 95% of ATP
during rest and light to
moderate exercise
• Fuels: stored glycogen,
then bloodborne
glucose, pyruvic acid
from glycolysis, and
free fatty acids
Muscle Fatigue
• Physiological inability to contract
• Occurs when:
– Ionic imbalances (K+, Ca2+, Pi) interfere with E-C
coupling
– Prolonged exercise damages the SR and interferes
with Ca2+ regulation and release
• Total lack of ATP occurs rarely, during states of
continuous contraction, and causes
contractures (continuous contractions)
Oxygen Deficit
Extra O2 needed after exercise for:
• Replenishment of
– Oxygen reserves
– Glycogen stores
– ATP and CP reserves
• Conversion of lactic acid to pyruvic acid,
glucose, and glycogen
Heat Production During Muscle
Activity
• ~ 40% of the energy released in muscle
activity is useful as work
• Remaining energy (60%) given off as heat
• Dangerous heat levels are prevented by
radiation of heat from the skin and sweating
Force of Muscle Contraction
• The force of contraction is affected by:
– Number of muscle fibers stimulated (recruitment)
– Relative size of the fibers—hypertrophy of cells
increases strength
– Frequency of stimulation— frequency allows
time for more effective transfer of tension to
noncontractile components
– Length-tension relationship—muscles contract
most strongly when muscle fibers are 80–120% of
their normal resting length
Sarcomeres
greatly
shortened
Sarcomeres at
resting length
Sarcomeres excessively
stretched
75%
100%
170%
Optimal sarcomere
operating length
(80%–120% of
resting length)
Figure 9.22
Velocity and Duration of Contraction
Influenced by:
1. Muscle fiber type
2. Load
3. Recruitment
Muscle Fiber Type
Classified according to two characteristics:
1. Speed of contraction: slow or fast, according
to:
– Speed at which myosin ATPases split ATP
– Pattern of electrical activity of the motor neurons
2. Metabolic pathways for ATP synthesis:
– Oxidative fibers—use aerobic pathways
– Glycolytic fibers—use anaerobic glycolysis
Muscle Fiber Type
Three types:
– Slow oxidative fibers
– Fast oxidative fibers
– Fast glycolytic fibers
Table 9.2
FO
SO
FG
Figure 9.24
Influence of Load
 load   latent period,  contraction, and 
duration of contraction
Influence of Recruitment
Recruitment  faster contraction and 
duration of contraction
Effects of Exercise
Aerobic (endurance) exercise:
• Leads to increased:
– Muscle capillaries
– Number of mitochondria
– Myoglobin synthesis
• Results in greater endurance, strength, and resistance to
fatigue
• May convert fast glycolytic fibers into fast oxidative
fibers
Effects of Resistance Exercise
• Resistance exercise (typically anaerobic)
results in:
– Muscle hypertrophy (due to increase in fiber size)
– Increased mitochondria, myofilaments, glycogen
stores, and connective tissue
Smooth Muscle
• Found in walls of most hollow organs
(except heart)
• Usually in two layers (longitudinal and
circular)
Peristalsis
• Alternating contractions and relaxations of
smooth muscle layers that mix and squeeze
substances through the lumen of hollow
organs
– Longitudinal layer contracts; organ dilates and
shortens
– Circular layer contracts; organ constricts and
elongates
Microscopic Structure
• Spindle-shaped fibers: thin and short
compared with skeletal muscle fibers
• Connective tissue: endomysium only
• SR: less developed than in skeletal muscle
• Pouchlike infoldings (caveolae) of sarcolemma
sequester Ca2+
• No sarcomeres, myofibrils, or T tubules
Innervation of Smooth Muscle
• Autonomic nerve
fibers innervate
smooth muscle at
diffuse junctions
• Varicosities (bulbous
swellings) of nerve
fibers store and release
neurotransmitters
Myofilaments in Smooth Muscle
• Ratio of thick to thin filaments (1:13) is much lower
than in skeletal muscle (1:2)
• Thick filaments have heads along their entire length
• No troponin complex; protein calmodulin binds Ca2+
• Myofilaments are spirally arranged, causing smooth
muscle to contract in a corkscrew manner
• Dense bodies: proteins that anchor noncontractile
intermediate filaments to sarcolemma at regular
intervals
Figure 9.28
Contraction of Smooth Muscle
• Slow, synchronized contractions
• Cells are electrically coupled by gap junctions
• Some cells are self-excitatory (depolarize
without external stimuli); act as pacemakers
for sheets of muscle
– Rate and intensity of contraction may be modified
by neural and chemical stimuli
Contraction of Smooth Muscle
•
•
•
•
•
Sliding filament mechanism
Final trigger is  intracellular Ca2+
Ca2+ is obtained from the SR and extracellular space
Ca2+ binds to and activates calmodulin
Activated calmodulin activates myosin (light chain)
kinase
• Activated kinase phosphorylates and activates
myosin
• Cross bridges interact with actin
Extracellular fluid (ECF)
Ca2+
Plasma membrane
Cytoplasm
1 Calcium ions (Ca2+)
enter the cytosol from
the ECF via voltagedependent or voltageindependent Ca2+
channels, or from
the scant SR.
Ca2+
Sarcoplasmic
reticulum
Figure 9.29, step 1
Contraction of Smooth Muscle
• Very energy efficient (slow ATPases)
• Myofilaments may maintain a latch state for
prolonged contractions
Relaxation requires:
• Ca2+ detachment from calmodulin
• Active transport of Ca2+ into SR and ECF
• Dephosphorylation of myosin to reduce
myosin ATPase activity
Regulation of Contraction
Neural regulation:
• Neurotransmitter binding   [Ca2+] in
sarcoplasm; either graded (local) potential or
action potential
• Response depends on neurotransmitter released
and type of receptor molecules
Hormones and local chemicals:
– May bind to G protein–linked receptors
– May either enhance or inhibit Ca2+ entry
Special Features of Smooth Muscle
Contraction
Stress-relaxation response:
– Responds to stretch only briefly, then adapts to
new length
– Retains ability to contract on demand
– Enables organs such as the stomach and bladder
to temporarily store contents
Length and tension changes:
– Can contract when between half and twice its
resting length
Special Features of Smooth Muscle
Contraction
Hyperplasia:
– Smooth muscle cells can divide and increase their
numbers
– Example:
• estrogen effects on uterus at puberty and during
pregnancy
Types of Smooth Muscle
Single-unit (visceral) smooth muscle:
– Sheets contract rhythmically as a unit (gap junctions)
– Often exhibit spontaneous action potentials
– Arranged in opposing sheets and exhibit stress-relaxation
response
Multiunit smooth muscle:
– Located in large airways, large arteries, arrector pili
muscles, and iris of eye
– Gap junctions are rare
– Arranged in motor units
– Graded contractions occur in response to neural stimuli
Other interesting points..
• Athletics and training can improve neuromuscular
control
• Female skeletal muscle makes up 36% of body
mass, male 42% (testosterone!)
– Body strength per unit muscle mass is the same in
both sexes
• With age, connective tissue increases and muscle
fibers decrease
• By age 30, loss of muscle mass (sarcopenia)
begins
– Regular exercise reverses sarcopenia
Muscular Dystrophy
Duchenne muscular dystrophy (DMD):
– Most common and severe type
– Inherited, sex-linked, carried by females and expressed in
males (1/3500) as lack of dystrophin
– Victims become clumsy and fall frequently; usually die of
respiratory failure in their 20s
– No cure, but viral gene therapy or infusion of stem cells
with correct dystrophin genes show promise