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Chapter 10
Muscle Tissue
Principles of Human Anatomy and Physiology, 11e
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Chapter 10
Muscle Tissue
• Alternating contraction
and relaxation of cells
• Chemical energy
changed into
mechanical energy
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OVERVIEW OF MUSCLE TISSUE
• Types of Muscle Tissue
• Skeletal muscle tissue is primarily attached to bones. It is
striated and voluntary.
• Cardiac muscle tissue forms the wall of the heart. It is
striated and involuntary.
• Smooth (visceral) muscle tissue is located in viscera. It is
nonstraited (smooth) and involuntary.
• Table 4.4 compares the different types of muscle.
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3 Types of Muscle Tissue
• Skeletal muscle
– attaches to bone, skin or fascia
– striated with light & dark bands visible with scope
– voluntary control of contraction & relaxation
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3 Types of Muscle Tissue
• Cardiac muscle
– striated in appearance
– involuntary control
– autorhythmic because of built in pacemaker
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3 Types of Muscle Tissue
• Smooth muscle
– attached to hair follicles in skin
– in walls of hollow organs -- blood vessels & GI
– nonstriated in appearance
– involuntary
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Properties of Muscle Tissue
• Excitability
– respond to chemicals released from nerve cells
• Conductivity
– ability to propagate electrical signals over membrane
• Contractility
– ability to shorten and generate force
• Extensibility
– ability to be stretched without damaging the tissue
• Elasticity
– ability to return to original shape after being stretched
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Skeletal Muscle -- Connective Tissue
• Connective tissue components of the muscle include
– epimysium = surrounds the whole muscle
– perimysium = surrounds bundles (fascicles) of 10-100
muscle cells
– endomysium = separates individual muscle cells
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Connective Tissue
Components
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Sarcolemma, T Tubules, and Sarcoplasm
• Skeletal muscle consists of fibers (cells) covered by a
sarcolemma (Figure 10.3b).
– The fibers contain T tubules and sarcoplasm
– T tubules are tiny invaginations of the sarcolemma that
quickly spread the muscle action potential to all parts of
the muscle fiber.
• Sarcoplasm is the muscle cell cytoplasm and contains a
large amount of glycogen for energy production and
myoglobin for oxygen storage.
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Transverse Tubules
• T (transverse) tubules are invaginations of the sarcolemma
into the center of the cell
– filled with extracellular fluid
– carry muscle action potentials down into cell
• Mitochondria lie in rows throughout the cell
– near the muscle proteins that use ATP during contraction
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Sarcoplasmic Reticulum (SR)
• System of tubular sacs similar to smooth ER in
nonmuscle cells
• Stores Ca+2 in a relaxed muscle
• Release of Ca+2 triggers muscle contraction
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Filaments and the Sarcomere
• Thick and thin filaments overlap each other in a pattern
that creates striations (light I bands and dark A bands)
• The I band region contains only thin filaments.
• They are arranged in compartments called sarcomeres,
separated by Z discs.
• In the overlap region, six thin filaments surround each
thick filament
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Thick & Thin Myofilaments Overlap
Dark(A) & light(I) bands (electron microscope)
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The Proteins of Muscle -- Myosin
• Thick filaments are composed of myosin
– each molecule resembles two golf clubs twisted together
– myosin heads (cross bridges) extend toward the thin
filaments
• Held in place by the M line proteins.
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The Proteins of Muscle -- Actin
• Thin filaments are made of actin, troponin, & tropomyosin
• The myosin-binding site on each actin molecule is covered by
tropomyosin in relaxed muscle
• The thin filaments are held in place by Z lines. From one Z
line to the next is a sarcomere.
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Sliding Filament Mechanism Of Contraction
• Myosin cross bridges
pull on thin filaments
• Thin filaments slide
inward
• Z Discs come toward
each other
• Sarcomeres
shorten.The muscle
fiber shortens. The
muscle shortens
• Notice :Thick & thin
filaments do not change
in length
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Overview: From Start to Finish
Basic Structures
• Nerve ending
• Neurotransmitter
• Muscle membrane
• Stored Ca+2
• ATP
• Muscle proteins
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How Does Contraction Begin?
1. Nerve impulse reaches an axon terminal & synaptic vesicles
release acetylcholine (ACh)
2. ACh diffuses to receptors on the sarcolemma & Na+
channels open and Na+ rushes into the cell
3. A muscle action potential spreads over sarcolemma and
down into the transverse tubules
4. SR releases Ca+2 into the sarcoplasm
5. Ca+2 binds to troponin & causes troponin-tropomyosin
complex to move & reveal myosin binding sites on actin--the
contraction cycle begins
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Contraction Cycle
• Repeating sequence of events that cause the thick & thin
filaments to move past each other.
• 4 steps to contraction cycle
– ATP hydrolysis
– attachment of myosin to actin to form crossbridges
– power stroke
– detachment of myosin from actin
• Cycle keeps repeating as long as there is ATP available
& there is a high Ca+2 level near the filaments.
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Steps in the Contraction Cycle
• Notice how the myosin head attaches and pulls on the thin
filament with the energy released from ATP
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ATP and Myosin
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•
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•
•
•
Myosin heads are activated by ATP
Activated heads attach to actin & pull (power stroke)
ADP is released. (ATP released P & ADP & energy)
Thin filaments slide past the thick filaments
ATP binds to myosin head & detaches it from actin
All of these steps repeat over and over
– if ATP is available &
– Ca+ level near the troponin-tropomyosin complex is
high
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Rigor Mortis
• Rigor mortis is a state of muscular rigidity that begins
3-4 hours after death and lasts about 24 hours
• After death, Ca+2 ions leak out of the SR and allow
myosin heads to bind to actin
• Since ATP synthesis has ceased, crossbridges
cannot detach from actin until proteolytic enzymes
begin to digest the decomposing cells.
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Excitation - Contraction Coupling
• All the steps that occur from the muscle action potential
reaching the T tubule to contraction of the muscle fiber.
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Structures of NMJ Region
• Synaptic end bulbs are
swellings of axon
terminals
• End bulbs contain
synaptic vesicles filled
with acetylcholine (ACh)
• Motor end plate
membrane contains 30
million ACh receptors.
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Neuromuscular Junction (NMJ) or Synapse
• NMJ = myoneural junction
– end of axon nears the surface of a muscle fiber at its motor end
plate region (remain separated by synaptic cleft or gap)
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Relaxation
• Acetylcholinesterase (AChE) breaks down ACh within the
synaptic cleft
• Muscle action potential ceases
• Ca+2 release channels close
• Active transport pumps Ca2+ back into storage in the
sarcoplasmic reticulum
• Calcium-binding protein (calsequestrin) helps hold Ca+2 in
SR (Ca+2 concentration 10,000 times higher than in cytosol)
• Tropomyosin-troponin complex recovers binding site on the
actin
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Overview: From Start to Finish
•
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Nerve ending
Neurotransmittor
Muscle membrane
Stored Ca+2
ATP
Muscle proteins
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Length-Tension Relationship
• The forcefulness of muscle contraction depends on the
length of the sarcomeres within a muscle before contraction
begins.
• Figure 10.10 plots the length-tension relationships for
skeletal muscle.
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Length Tension Curve
• Graph of Force of contraction
(Tension) versus Length of
sarcomere
• Optimal overlap at the top
of the graph
• When the cell is too stretched
and little force is produced
• When the cell is too short, again
little force is produced
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Pharmacology of the NMJ
• Botulinum toxin blocks release of neurotransmitter at the
NMJ so muscle contraction can not occur
– bacteria found in improperly canned food
– death occurs from paralysis of the diaphragm
• Curare (plant poison from poison arrows)
– causes muscle paralysis by blocking the ACh receptors
– used to relax muscle during surgery
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Muscle Metabolism
Production of ATP in Muscle Fibers
• Muscle uses ATP at a great rate when active
• Sarcoplasmic ATP only lasts for few seconds
• 3 sources of ATP production within muscle
– creatine phosphate
– anaerobic cellular respiration
– aerobic cellular respiration
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MUSCLE METABOLISM
• Creatine phosphate and ATP can power maximal muscle
contraction for about 15 seconds and is used for maximal
short bursts of energy (e.g., 100-meter dash) (Figure
10.13a).
– Creatine phosphate is unique to muscle fibers.
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Creatine Phosphate: Details
• Excess ATP within resting muscle used to form creatine
phosphate
• Creatine phosphate 3-6
times more plentiful
than ATP within muscle
• Its quick breakdown
provides energy for
creation of ATP
• Sustains maximal contraction for 15 sec (used for 100 meter
dash).
• Athletes tried creatine supplementation
– gain muscle mass but shut down bodies own synthesis
(safety?)
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MUSCLE METABOLISM
• The partial catabolism of glucose to generate ATP occurs in
anaerobic cellular respiration (Figure 10.13b). This system
can provide enough energy for about 30-40 seconds of
maximal muscle activity (e.g., 300-meter race).
• Muscular activity lasting more than 30 seconds depends
increasingly on aerobic cellular respiration (reactions
requiring oxygen). This system of ATP production involves
the complete oxidation of glucose via cellular respiration
(biological oxidation) (Figure 10.13c).
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Muscle Fatigue
• Inability to contract after prolonged activity
• Factors that contribute to fatigue
– central fatigue is feeling of tiredness and a desire
to stop (protective mechanism)
– insufficient release of acetylcholine from motor
neurons
– depletion of creatine phosphate
– decline of Ca+2 within the sarcoplasm
– insufficient oxygen or glycogen
– buildup of lactic acid and ADP
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The Motor Unit
• Motor unit = one somatic motor neuron & all the skeletal muscle cells
(fibers) it stimulates (10 cells to 2,000 cells)
– muscle fibers normally scattered throughout belly of muscle
• Total strength of a contraction depends on how many motor units are
activated & how large the motor units are
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Parts of a Twitch Contraction
• Latent Period--2msec
– Ca+2 is being released from SR
– slack is being removed from elastic components
• Contraction Period
– 10 to 100 msec
– filaments slide past each other
• Relaxation Period
– 10 to 100 msec
– active transport of Ca+2 into SR
• Refractory Period
– muscle can not respond and has lost its excitability
– 5 msec for skeletal & 300 msec for cardiac muscle
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Wave Summation
• If second stimulation applied after the refractory period but
before complete muscle relaxation---second contraction is
stronger than first
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Complete and Incomplete Tetanus
• Unfused tetanus
– if stimulate at 20-30 times/second, there will be only partial relaxation
between stimuli
• Fused tetanus
– if stimulate at 80-100 times/second, a sustained contraction with no
relaxation between stimuli will result
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Muscle Tone
• Involuntary contraction of a small number of motor units
(alternately active and inactive in a constantly shifting
pattern)
– keeps muscles firm even though relaxed
– does not produce movement
• Essential for maintaining posture (head upright)
• Important in maintaining blood pressure
– tone of smooth muscles in walls of blood vessels
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Isotonic and Isometric Contraction
• Isotonic contractions = a load is moved
– concentric contraction = a muscle shortens to produce force and
movement
– eccentric contractions = a muscle lengthens while maintaining force and
movement
• Isometric contraction = no movement occurs
– tension is generated without muscle shortening
– maintaining posture & supports objects in a fixed position
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Classification of Muscle Fibers
• Slow oxidative (slow-twitch)
– red in color (lots of mitochondria, myoglobin & blood vessels)
– prolonged, sustained contractions for maintaining posture
• Oxidative-glycolytic (fast-twitch A)
– red in color (lots of mitochondria, myoglobin & blood vessels)
– split ATP at very fast rate; used for walking and sprinting
• Fast glycolytic (fast-twitch B)
– white in color (few mitochondria & BV, low myoglobin)
– anaerobic movements for short duration; used for weight-lifting
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Fiber Types within a Whole Muscle
• Most muscles contain a mixture of all three fiber types
• Proportions vary with the usual action of the muscle
– neck, back and leg muscles have a higher proportion of
postural, slow oxidative fibers
– shoulder and arm muscles have a higher proportion of
fast glycolytic fibers
• All fibers of any one motor unit are same.
• Different fibers are recruited as needed.
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Regeneration of Muscle
• Skeletal muscle fibers cannot divide after 1st year
– growth is enlargement of existing cells
– repair
• bone marrow produce some new cells
• if not enough numbers---fibrosis occurs most often
• Cardiac muscle fibers cannot divide or regenerate
– all healing is done by fibrosis (scar formation)
• Smooth muscle fibers (regeneration is possible)
– cells can grow in size (hypertrophy)
– some cells (uterus) can divide (hyperplasia)
– new fibers can form from stem cells in BV walls
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Aging and Muscle Tissue
• Skeletal muscle starts to be replaced by fat beginning at 30
– “use it or lose it”
• Slowing of reflexes & decrease in maximal strength
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Myasthenia Gravis
• Progressive autoimmune disorder that blocks the ACh
receptors at the neuromuscular junction
• The more receptors are damaged the weaker the muscle.
• More common in women 20 to 40 with possible line to thymus
gland tumors
• Begins with double vision & swallowing difficulties & progresses
to paralysis of respiratory muscles
• Treatment includes steroids that reduce antibodies that bind to
ACh receptors and inhibitors of acetylcholinesterase
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Muscular Dystrophies
• Inherited, muscle-destroying diseases
• Sarcolemma tears during muscle contraction
• Mutated gene is on X chromosome so problem is with
males almost exclusively
• Appears by age 5 in males and by 12 may be unable to
walk
• Degeneration of individual muscle fibers produces
atrophy of the skeletal muscle
• Gene therapy is hoped for with the most common form =
Duchenne muscular dystrophy
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Abnormal Contractions
• Spasm = involuntary contraction of single muscle
• Cramp = a painful spasm
• Tic = involuntary twitching of muscles normally under
voluntary control--eyelid or facial muscles
• Tremor = rhythmic, involuntary contraction of
opposing muscle groups
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Atrophy and Hypertrophy
• Atrophy
– wasting away of muscles
– caused by disuse (disuse atrophy) or severing of the nerve
supply (denervation atrophy)
– the transition to connective tissue can not be reversed
• Hypertrophy
– increase in the diameter of muscle fibers
– resulting from very forceful, repetitive muscular activity and
an increase in myofibrils, SR & mitochondria
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