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Muscular System
Muscle
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Makes up about 40-50 % of body weight
Myo – muscle
Myology – study of muscles
Sarco – “flesh”
Types of muscle:
• Skeletal muscle
– Attached primarily to bones
– Striated
– Voluntary
• Cardiac muscle
– Wall of the heart
– Striated
– Involuntary
– Autorhythmicity – the ability to contract by itself
– Influenced by neurotransmitters and hormones
• Smooth muscle
– Located in viscera – blood vessels, skin,
abdominal organs, etc.
– Nonstriated
– Involuntary
– May have autorhythmicity
– Influenced by neurotransmitters and hormones
Functions of muscle tissue
• Motion
• Movement of substances within the body
• Stabilizing body position and regulating
organ volume
• Thermogenesis (heat production)
– Heat is a “by-product” of muscle activity
Characteristics of Muscle Tissue
• Excitability (irritability) – the ability of muscles
and nerves to respond to a stimulus by
producing electrical signals called impulses or
action potentials
• Conductivity – the ability of a cell to conduct
action potentials (electrical current) along the
plasma membrane
• Contractility
• Extensibility
• Elasticity
Anatomy and innervation of
skeletal muscle tissue
• Connective tissue components:
– Fascia (“bandage”) –sheet or band of fibrous
C.T. under the skin or around organs
– Superficial fascia (subcutaneous fascia):
• Areolar C.T. and adipose tissue
• Stores water and fat
• Reduces heat loss (insulates)
• Protects against trauma
• Framework for nerves and blood vessels
• Deep fascia:
– Dense irregular C.T. – holds muscles together
and separates them into groups
– 3 layers:
• Epimysium – surrounds the whole muscle
• Perimysium – separates muscle into
bundles of muscle fibers – fascicles
• Endomysium – covers individual fibers
• These three layers come together to form
cords of dense, regular connective tissue
called tendons. Tendons attach muscle to
the periosteum of bones.
• When the connective tissues form a broad,
flat layer, the tendon is called an
aponeurosis.
Microscopic Anatomy
• Muscle cells are called muscle fibers or
myofibers
• Plasma membrane – sarcolemma
• Cytoplasm – sarcoplasm
• Myoblasts fuse to form one myofiber –
several nuclei
• Myofibrils run lengthwise
Myofibrils are made of filaments
• Thin filaments – primarily actin
• Thick filament – myosin
• Elastic filaments
• Sarcomeres are the basic, functional units
of striated muscle fibers.
• Each thick filament is surrounded by
interacts with 6 thin filaments
Thick filaments
• Made of about 200 molecules of myosin
• Each myosin molecule has two “heads”
with peptide chains (“light chains”)
• Each head has an actin binding site and
an ATP binding site
• The ATP site splits ATP and transfers
energy to myosin head; which remains
charged (“cocked”) until contraction.
Thin Filaments
• Actin molecules form a helix
– Each actin molecule has a myosin binding site
• Other proteins:
• Tropomyosin – long, filamentous protein,
it wraps around the actin and covers the
myosin binding sites
• Troponin – a smaller molecule bound to
tropomyosin, it has calcium binding sites.
Other proteins:
• Titin –suspends thick filaments
• Nebulin – stabilizes thin filaments during
contraction
• Α – actinin – anchor thin filaments to Z
lines
• Dystrophin – supports sarcolemma during
contraction
• Integrins – membrane-spanning proteins
• Laminin – link between integrins and
extracellular matrix
Sarcoplasmic reticulum
• Specialized smooth E. R.
• Tubes fuse to form cisternae
• In a relaxed muscle, S.R. stores Ca++
(Ca++ active transport pumps)
• When stimulated, Ca++ leaves through
Ca++ release channels.
Transverse tubules (T-tubules)
• Infoldings of sarcolemma that penetrate
into muscle fiber at right angles to
filaments. They are filled with extracellular
fluid.
• T-tubules and the cisternae on either side
form a triad.
Blood and nerve supply
• Muscle contraction uses a lot of ATP
• To generate ATP, muscles need oxygen
• Each muscle fiber is in close contact with
one or more capillaries
• Motor neurons – originate in brain and
spinal cord; cause muscle contraction
Motor unit
• A Motor Unit is made of one motor neuron
and all the muscle fibers it innervates.
• These cells all contract together.
• A single motor unit can have 2 – 2,000
muscle fibers.
• Precise movements are controlled by
small motor units, and large movements
by large motor units.
Neuromuscular Junction (NMJ)
• Nerves communicate with muscles and other
organs at structures called synapses.
• Synaptic cleft – gap between neuron and
sarcolemma
• Axon releases a chemical called a
neurotransmitter – Acetylcholine (Ach)
• Axon branches into axon terminals.
• At the end of each axon terminal is a swelling
called the synaptic end bulb.
• The region across the synaptic cleft from
the synaptic end bulb is called the motor
end plate.
• The sarcolemma of the motor end plate is
folded and contains many receptors for
ACh .
• When a nerve impulse reaches the
synaptic end bulbs, it causes synaptic
vesicles to fuse with the membrane and
release ACh by exocytosis.
• Acetylcholine diffuses across the synaptic cleft,
and binds with receptors on the motor end
plate.
• This binding causes the receptor to change
shape, and opens Na+ channels in the
membrane.
• When enough Na+ channels are opened, an
electrical current is generated and is carried
along the sarcolemma. This is called a muscle
impulse or muscle action potential. This
electrical activity can be recorded in an
electromyogram.
Have you played mousetrap ?
Sliding Filament Mechanism
• When a nerve impulse reaches an axon
terminal, the synaptic vesicles release
acetylcholine (ACh)
• ACh crosses the synaptic cleft and binds with
receptors on the motor end plate.
• This binding opens channels that allow
sodium to rush in, beginning a muscle action
potential in the sarcolemma.
• The action potential or impulse travels down the
sarcolemma and into the T-tubules, causing the
sarcoplasmic reticulum to release Ca++ into the
sarcoplasm.
• The Ca++ binds to the troponin, which changes
shape, pulling the tropomyosin away from the
myosin binding sites on the actin.
• The activated myosin attaches to the actin,
forming actin/myosin crossbridges.
• The myosin head moves toward the center of
the sarcomere, pulling the actin filaments past
the myosin. This is called a power stroke.
• When the myosin heads turn, they release
ADP, and ATP binds to the heads.
• When ATP binds, it causes the myosin to
release the actin.
• ATP is split, and the myosin heads again bind
to the actin, but further down the filament.
• The myosin again pulls the actin.
• This action is repeated many times.
• The Z lines (discs) get closer together as the
actin and myosin filaments slide past each
other, and the muscle fiber shortens.
Relaxation
• ACh is broken down by an enzyme called
acetylcholinesterase.
• Action potentials are no longer generated,
so the Ca++ release channels in the S.R.
close.
• Ca++ active transport pumps take Ca++ out
of the sarcoplasm and into the S.R. where
it binds to a protein called calsequestrin.
• As the Ca++ levels in the sarcoplasm fall,
troponin releases tropomyosin, which falls
back and covers the myosin binding sites
on the actin.
• The thin filaments slip back into their
relaxed positions.
Rigor mortis
• After death, muscle cells begin autolysis, and
Ca++ leaks out of the S.R.
• This causes muscles to begin to contract.
• Since the body is dead, no more ATP is
produced.
• Without the ATP to recharge the myosin heads,
they remain linked to the actin, and neither
relax nor contract any further.
• After about 24 - 72 hours it disappears as the
tissues begin to disintegrate.
Muscle contraction review:
• The neurotransmitter ______________
is released from the end bulb of the
axon of a motor nerve.
• The neurotransmitter crosses the
_________________and binds with
receptors on the _____________of the
muscle fiber.
• This binding opens _________________
channels in the ________________.
• The inflow of ions causes
depolarization of the membrane and the
propagation of a ___________________
along the membrane.
• This flow travels down the ___________
and causes the ____________________
to release __________________into the
sarcoplasm.
• This binds with the protein __________
which changes shape and pulls on the
protein ____________ and exposes the
myosin binding sites on the_________.
• Myosin heads, which are charged with
_____, grab onto the actin and perform
a___________, bringing the__________
closer together, ______________the
muscle.
• Myosin releases the actin to grab
another molecule of______.
Electrochemical gradient
Chemical agent
or disease
Mechanism
Black widow spider
Venom
Clostridium Botulinum
Toxin
Curare
Myesthenia Gravis
Organophosphates
Neostigmine
Alters release of
ACh
_______________
Blocks ACh
receptor sites____
Prevents ACh
inactivation
Muscle Metabolism
• Creatine phosphate can transfer a
phosphate group to ADP forming ATP and
creatine.
• Creatine phosphate CANNOT directly
supply energy to the cell.
• Together, ATP and creatine phosphate
make up the Phosphagen System.
• This system can provide energy for 10 -15
seconds of maximal contraction.
• For longer contractions, glucose must be used
to make ATP.
• Glycogen stored in muscle can be easily
broken down into glucose.
• Muscle cells can take in glucose from blood.
• Oxygen is stored in myoglobin – important
because contraction puts pressure on blood
vessels and compresses them.
• If not enough oxygen is present, we can
run glycolysis anaerobically, breaking
down glucose and making lactic acid.
• This can provide energy for 30-40 seconds
of maximal contraction.
• Prolonged activity must be fueled by
cellular respiration.
Maximal oxygen uptake
• You can only take in so much oxygen at a
time. This will vary with gender, size,
heredity and training.
Muscle fatigue
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Depletion of ATP, CP and glycogen stores
Insufficient O2 delivery
Lactic acid build up
Insufficient release of ACH at NMJ
Ion imbalances – K+, Na + and Ca++
Psychological responses (“I’m tired”)
Types of muscle fibers
• Slow oxidative (Type I) fibers
• Also called slow-twitch or fatigue-resistant
fibers
• Contain large amounts of myoglobin, many
mitochondria and blood capillaries. They look
red; generate ATP aerobically.
• Split ATP at a slow rate: contract slowly
• Resistant to fatigue because they generate a lot
of ATP
• Found in large #’s in postural muscles
Fast-twitch (Type II) fibers
• Fast oxidative (intermediate) fibers
– Intermediate in diameter and contraction speed
– Also fatigue- resistant fibers
– Large amounts of myoglobin, many mitochondria
and blood capillaries. Look red, and generate ATP
aerobically.
– Split ATP rapidly, so contraction is fast.
– Not quite as resistant to fatigue as Type I fibers
– In large proportions in leg muscles of sprinters
• Fast glycolytic fibers
– Largest in diameter
– Fast-twitch or fatigable fibers
– Low myoglobin, few mitochondria, few capillaries.
Fibers appear white
– Contain large amounts of glycogen and generate
ATP anaerobically (glycolysis)
– Fatigue easily
– Split ATP rapidly, contractions strong and rapid
– Found in arm muscles - used intensively for short
periods - throwing
Oxygen Debt
• Lactic acid builds up, decreases pH, increases
respiration. Extra oxygen needed to convert
lactic acid to pyruvic acid.
• Also need increased O2 :
– Increased body temp. speeds up chemical
reactions
– Heart rate and intercostal muscle activity are still
high, using more O2
– Tissue repair is occurring at increased rate
– Better term : Recovery Oxygen Consumption