Muscles & Muscle Tissue
Part A
Human Anatomy & Physiology, Sixth Edition
Elaine N. Marieb
9
Pocket Guide to Muscle Tissues
 Skeletal (Striated)
 Multinucleate, syncytial cells
 Has obvious striations (aligned myofilaments)
 Predominantly under voluntary neural control
 Contracts rapidly but tires quickly
 Wide range in contractile force
 Smooth
 Mononucleate, unfused cells
 Not striated
 Under involuntary neural control
 Cardiac
 Comprises majority of heart walls
 Large, mononucleate with extensive myofilament bundles
 Striated
 Autonomously contractile & under involuntary neural control
Muscle Terminology
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Excitability – the ability to receive & respond to stimuli
Contractility – the ability to shorten forcibly
Extensibility – the ability to be stretched or extended
Elasticity – the ability to recoil & resume the original resting
length
Muscle Terminology
 Myo-, mys-, & sarco- all refer to muscle
 Muscle Cells
 Sarcolemma – muscle plasma membrane
 Sarcoplasm – cytoplasm of a muscle cell
 Muscle subunits
 Myofiber (myotube)
 Myofibril
 Sarcomere
 Myofilament
 actin (thin myofilaments)
 myosin (thick myofilaments)
Organizational Levels of Muscle
Organizational Levels of Muscle
Skeletal Muscle
 Each muscle is a discrete organ composed of muscle tissue,
blood vessels, nerve fibers, & connective tissue
 3 connective tissue sheaths
 Endomysium – reticular fibers
surrounding each myotube
 Perimysium – fibrous CT
surrounding each fascicle
 Epimysium – layer of dense,
regular CT surrounding entire
muscle
Skeletal Muscle: Nerve & Blood Supply
 Each muscle is served by one nerve, an artery, & one or
more veins
 Each skeletal muscle fiber is supplied with a nerve ending
that controls contraction
 Contracting fibers require continuous delivery of oxygen &
nutrients via arteries
 Wastes must be removed via veins
Skeletal Muscle: Attachments
 Skeletal muscles span joints & attach to bones in at least two
places
 Muscle contraction moves one bone toward another
 moveable bone - muscle’s insertion
 immovable bone - muscle’s origin
 Muscles attach:
 Directly – epimysium fused to periosteum
 Indirectly – connective tissue extends as a tendon
Microscopic Anatomy of a Skeletal Muscle Fiber
 Each fiber (myotube) is a long, cylindrical multinucleated
syncytium produced by fusion of embryonic cells
 Fiber size
 diameter - 10 to 100 m
 Length - 1 - 3000 mm
 Unique sarcoplasm features & organelles
 glycosomes
 myoglobin
 sarcoplasmic reticulum
 T tubules
Myofibrils
 Densely packed, rodlike contractile elements
 The aligned arrangement of myofibrils creates a repeating series of dark
A bands & light I bands
Myofilament Banding Elements
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Thick filaments – extend the length of an A band
Thin filaments – extend across the I band into the A band
Z-disc – disc of proteins that anchor thin filaments
H zone – Where thin filaments don’t overlap thick filaments
M lines - band of desmin anchoring myosin
Sarcomeres
 Smallest contractile unit
 The region of a myofibril between two successive Z discs
 Composed of myofilaments made up of contractile proteins
 Myofilaments are of two types – thick & thin
Myofilaments: Banding Pattern
Figure 9.3 (c, d)
Ultrastructure of Myofilaments: Thick Filaments
 Each myosin molecule is a dimer with a rodlike tail & two
globular heads
 Tails – two interwoven, large polypeptide chains (MHC)
 Heads – two smaller, polypeptide chains (MLC)
Ultrastructure of Myofilaments: Thin Filaments
 Composed of the proteins actin, tropomyosin, & troponin
 Actin myofilament (F-actin) is a helical polymer of globular
subunits (G-actin)
 Myosin heads attach to specific sites on each actin molecule
 Tropomyosin & troponin regulate the binding of myosin to
actin
 Tropomyosin covers myosin binding sites
 Troponin moves tropomyosin
Arrangement of the Myofilaments in a Sarcomere
Figure 9.4 (d)
Sarcoplasmic Reticulum (SR)
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An elaboratenet of smooth ER surrounding each myofibril
Is a Ca2+ reservoir & regulates intracellular calcium levels
Paired terminal cisternae form perpendicular cross channels
T tubules penetrate into the cell’s interior at each A band–I band
junction
 T tubules associate with the terminal SR cisternae to form triads
T Tubules
 T tubules are continuous with the sarcolemma
 Conduct impulses to interior myofibrils of myofiber
 These impulses trigger release of Ca2+ from the terminal
cisternae of SR
Triad Relationships
 T tubules & SR provide tightly linked signals for muscle
contraction
 Integral membrane proteins in T tubules sense voltage
changes
 These proteins interact with SR proteins that allow Ca2+ to
be released from the SR cisternae
Excitation-Contraction Coupling
Role Calcium (Ca2+) in the Contraction Mechanism
 At low intracellular Ca2+
concentration:
 Tropomyosin blocks the
binding sites on actin
 Myosin cross bridges cannot
attach to binding sites on actin
 The relaxed state of the muscle
is enforced
Figure 9.10 (a)
Role of Ca2+ in the Contraction Mechanism
 At higher intracellular Ca2+
concentrations:
 Additional calcium binds to
troponin (inactive troponin
binds two Ca2+)
 Calcium-activated troponin
binds an additional two Ca2+
at a separate regulatory site
Figure 9.10 (b)
Role of Ca2+ in the Contraction Mechanism
 Calcium-activated troponin
undergoes a conformational
change
 This change moves
tropomyosin away from
actin’s binding sites
Figure 9.10 (c)
Role of Ca2+ in the Contraction Mechanism
 Myosin head can now
bind & cycle
 This permits
contraction (sliding of
the thin filaments by
the myosin cross
bridges) to begin
Figure 9.10 (d)
Sequential Events of Contraction
 Cross bridge formation – myosin attaches to actin filament
 Power stroke – myosin head pivots & pulls actin filament
toward M line
 Cross bridge detachment –myosin head binds ATP & the
cross bridge detaches
 “Cocking” of the myosin head –ATP hydrolysis energy
returns the myosin head to its original position
Sequential Events of Contraction
Myosin head
(high-energy
configuration)
1 Myosin cross bridge attaches to
the actin myofilament
Thin filament
ADP & Pi (inorganic
phosphate) released
Thick
filament
2 Working stroke—the myosin head pivots &
4 As ATP is split into ADP & Pi,
cocking of the myosin head occurs
bends as it pulls on the actin filament, sliding it
toward the M line
Myosin head
(low-energy
configuration)
3 As new ATP attaches to the myosin
head, the cross bridge detaches
Cessation of Contraction
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Ca2+ is pumped back into the SR,
Tropomyosin blockage is restored
Myosin can not attach to actin
Thin myofilaments spring back to original position
The muscle fiber relaxes
Sliding Filament Model of Muscle Contraction
Skeletal Muscle Contraction
 contraction requires:
 chemical stimulation by nerve ending
 propagation of action potential (voltage change) along
sarcolemma
 intracellular [Ca2+] ↑ triggers myosin-actin interaction
 Excitation-contraction coupling
 Linking electrical signal to contraction of myofilaments
Nerve Stimulus of Skeletal Muscle
Skeletal muscles stimulated by
motor neurons of somatic nervous
system
 Axons travel in nerves to muscle cells
 Motor neuron axons branch within muscles
 Each branch forms a neuromuscular junction with a
single myofiber (cell)
Neuromuscular Junction
 Axonal endings
 synaptic vesicles containing acetylcholine (ACh)
 Motor end plate
 region of sarcolemma containing ACh receptors
 axon & sarcolemma separated by synaptic cleft
Neuromuscular
Junction
Role of Acetylcholine (Ach)
 ACh receptors
 ligand gated Na+ channels
 ACh binding opens channels
 Na+ goes into cell
 inside of sarcolemma depolarizes
 becomes less negative
Depolarization And Action Potentials
 end plate potential
 initial, local depolarization
 If strong enough, action triggered
 transient, self-propagating depolarization that spreads over
sarcolemma
 action potential passes over sarcolemma & into T tubules
 sarcolemma repolarizes in wake of action potential
Action Potential: Electrical Conditions of a
Polarized Sarcolemma
 The extracellular face
is positive,
 the intracellular face is
negative
 The difference in
charge is the resting
membrane potential
Figure 9.8 (a)
Action Potential: Depolarization & Generation of
the Action Potential
 Axon terminus of a motor
neuron releases ACh
 A patch of the sarcolemma
becomes permeable to Na+
(Na channels open)
Figure 9.8 (b)
Action Potential: Depolarization & Generation of
the Action Potential
 Depolarization
 Resting potential
increases as Na+
enters
 A strong enough
stimulus causes an
action potential
Figure 9.8 (b)
Action Potential: Propagation of the Action
Potential
 Polarity reversal of the
initial patch of
sarcolemma changes
the permeability of the
adjacent patch
 Voltage-regulated Na+
channels open in the
adjacent patch causing
it to depolarize
Figure 9.8 (c)
Action Potential: Propagation of the Action
Potential
 Thus, the action
potential travels
rapidly along the
sarcolemma
 Once initiated, the
action potential is
unstoppable, &
ultimately results in the
contraction of a muscle
Figure 9.8 (c)
Action Potential: Repolarization
 Immediately after the
depolarization wave
passes, the sarcolemma
permeability changes
 Na+ channels close & K+
channels open
 K+ diffuses from the cell,
restoring the electrical
polarity of the
sarcolemma
Figure 9.8 (d)
Action Potential: Repolarization
 Repolarization occurs in
the same direction as
depolarization, & must
occur before the muscle
can be stimulated again
(refractory period)
 The ionic concentration
of the resting state is
restored by the
Na+-K+ pump
Figure 9.8 (d)
Excitation-Contraction Coupling
 The action potential propagates along the sarcolemma &
travels down the T tubules
 Triggers Ca2+ release from SR
 Ca2+ binds to troponin & causes shape change
 Troponin move tropomyosin off myosin binding sites
 Myosin heads bind to exposed sites on actin
 Myosin heads alternately attach & detach pulling thin
filaments to the M line
 Hydrolysis of ATP powers this process (the release step)
Contraction of Skeletal Muscle (Organ Level)
 The two types of muscle contractions are:
 Isometric contraction – increasing muscle tension (muscle
does not shorten during contraction)
 Isotonic contraction – decreasing muscle length (muscle
shortens during contraction)
Motor Unit: The Nerve-Muscle Functional Unit
 Motor neuron & the muscle
fibers it controls
 Muscle fibers/motor unit varies
 The smaller the motor units, the
more precise motor control
 Fingers & eyes – small units
 Thighs & hips – large units
 Motor unit fibers are spread
throughout the muscle;
 stimulation of a single motor unit
causes weak contraction of the
entire muscle
Muscle Twitch
 A muscle twitch is the response of a muscle to a single, brief
threshold stimulus
 The three phases of a muscle twitch are:
 Latent period –
first few milliseconds after
stimulation
when excitationcontraction
coupling is
taking place
Figure 9.13 (a)
Muscle Twitch
 Period of contraction – cross bridges actively form & the
muscle shortens
 Period of relaxation –
Ca2+ is reabsorbed
into the SR, &
muscle tension
goes to zero
Figure 9.13 (a)
Graded Muscle Responses
 Graded muscle responses are:
 Variations in the degree of muscle contraction
 Required for proper control of skeletal movement
 Responses are graded by:
 Changing the frequency of stimulation
 Changing the strength of the stimulus
Muscle Response to Varying Stimuli
 single stimulus  single contractile response
 twitch
 Frequent stimuli increase contractile force (muscle doesn’t completely
relax)
 wave summation
 Increase stimulus frequency
 incomplete tetanus
 then complete tetanus
Figure 9.14
Muscle Response: Stimulation Strength
 Threshold stimulus
 stimulus strength where muscle contraction first occurs
 muscle contracts more vigorously as stimulus strength is
increased above threshold
 Force of contraction controlled by multiple motor unit
summation
 recruitment
 using more & more muscle fibers as stimulus strength
increases
 Each motor unit has its own threshold
Stimulus Intensity & Muscle Tension
Figure 9.15 (a, b)
Treppe: The Staircase Effect
 Increased contraction in response to multiple stimuli of the same strength
 increasing availability of Ca2+ in the sarcoplasm
 Muscle enzyme system efficiency increases as muscle contraction warms
cells.
Muscle Tone
 Muscle tone:
 Constant, slightly contracted state of all muscles
 Does not produce movement
 Keeps the muscles firm & ready to respond to stimulus
 Spinal reflexes account for muscle tone by:
 Alternatively activating motor units
 Responding to activation of stretch receptors in muscles &
tendons
Isotonic Contractions
 Muscle changes in length (decreasing the angle of the joint)
& moves a load
 2 types
 Concentric
 muscle shortens & does work
 Eccentric
 muscle contracts while being lengthened
Isotonic Contractions
Figure 9.17 (a)
Isometric Contractions
 Muscle remains same length
 Tension (tone) increases up to muscle’s capacity with out
decrease in length
 Occurs when the load is greater than the tension the muscle
is able to develop
Isometric Contractions
Figure 9.17 (b)
Factors Affecting the Force of Muscle Contraction
 number of muscle fibers (motor units) contracting
 more fibers = stronger contraction
 size of muscle fibers excited
 rapidity of neural stimuli
 degree of muscle stretch
 strongest when 80-120% of resting length
Muscle Fiber Type: Functional Characteristics
 contraction speed
 determined by ATP hydrolysis rate
 2 fiber types - fast & slow
 fast myosin v. slow myosin
 ATP-forming pathways
 Oxidative fibers – use aerobic pathways
 Glycolytic fibers – use anaerobic glycolysis
 These criteria define 3 fiber types
 slow oxidative
 fast oxidative
 fast glycolytic
Muscle Fiber Type: Speed of Contraction
 Slow oxidative
 contract slowly,
 slow myosin ATPases
 fatigue resistant
 Fast oxidative
 contract quickly
 fast myosin ATPases
 moderate fatigue resistance
 Fast glycolytic fibers
 contract quickly
 fast myosin ATPases,
 easily fatigued
Muscle Metabolism: Energy for Contraction
 ATP is only energy source used directly for contraction
 myosin binding cycling
 Muscle cells store ~ 6 sec worth of ATP
 ATP regeneration:
 Substrate level
 creatine phosphate (CP)
 anaerobic glycolysis
 Oxidative phosphorylation
 Aerobic respiration
Muscle Metabolism: Energy for Contraction
Figure 9.18
Muscle Metabolism: Aerobic Respiration
 Pyruvic acid produced by glycolysis enters the mitochondria
& is converted to acetyl Co-A
 Produces NADH & releases CO2
 Acetyl Co-A enters the Kreb’s Cycle which converts it to
more NADH & CO2
 The NADH is used in the process of oxidative
phosphorylation to produce H2O (from O2) & ATP
 These steps require O2 to be available to form H2O
 If O2 is limiting, oxidative phosphorylation stops, Kreb’s
cycle stops & pyruvic acid accumulates
 Metabolism switches form aerobic to anaerobic
Muscle Metabolism: Anaerobic Gycolysis
 When muscle contractile activity reaches 70% of maximum:
 Blood vessels become compressed
 Oxygen delivery is impaired
 Pyruvic acid is converted into lactic acid
 lactic acid is slowly converted back into pyruvic acid by an
enzyme called lactate dehydrogenase (LDH)
Muscle Fatigue
 Muscle fatigue – when the muscle is physiological unable to
contract
 Occurs when:
 ATP production fails to keep pace with ATP use
 A deficit of ATP results in contractures (rigor)
 Lactic acid accumulates in the muscle
 Ionic imbalances occur (no ATP to drive Na/K pumps)
Oxygen Debt
 The amount of O2 needed to restore normal muscle
physiology
 Conversion of lactic acid to pyruvic acid
 Replenishment of ATP & CP reserves
 Replenishment of glycogen stores
 12sec 100m sprint requires 6L O2 for aerobic conditions to
be met
 1.2L of O2 can be delivered to muscles in 12 sec (VO2 max)
 O2 debt is 6-1.2=4.8L