9 The Muscular System: Skeletal Muscle Tissue and
Organization
Slide 2
There are three types of muscle tissue: Skeletal muscle Pulls
on skeletal bones Voluntary contraction Cardiac muscle Pushes blood
through arteries and veins Rhythmic contractions Smooth muscle
Pushes fluids and solids along the digestive tract, for example
Involuntary contraction
Slide 3
Muscle tissues share four basic properties : Excitability The
ability to respond to stimuli Contractility The ability to shorten
and exert a pull or tension Extensibility The ability to continue
to contract over a range of resting lengths Elasticity The ability
to recoil to its original length
Slide 4
Skeletal muscles perform the following functions Produce
skeletal movement Pull on tendons to move the bones Maintain
posture and body position Stabilize the joints to aid in posture
Support soft tissue Support the weight of the visceral organs
Regulate entering and exiting of material Voluntary control over
swallowing, defecation, and urination Maintain body temperature
Some of the energy used for contraction is converted to heat
Slide 5
Gross anatomy Connective tissue of muscle Epimysium: dense
collagen fiber tissue that surrounds the entire muscle Perimysium:
dense tissue that divides the muscle into parallel compartments of
fascicles of ms. fibers Endomysium: dense tissue that surrounds
individual muscle fibers to connect them together. Capillary
network nerve fibers satellite cells (stem cells that repair
damage)
Anatomy of Skeletal Muscles Connective Tissue of Muscle
Epimysium, perimysium, and endomysium converge to form tendons
Tendons and Aponeuroses Tendons connect a muscle to a bone
Aponeuroses connect a muscle to a muscle
Slide 9
Anatomy of Skeletal Muscles Nerves Nerves innervate the muscle
There is a chemical communication between a nerve and a muscle The
nerve is connected to the muscle via the motor end plate This is
the neuromuscular junction
Slide 10
Anatomy of Skeletal Muscles blood vessels Blood vessels
innervate the endomysium of the muscle They then branch to form
coiled networks to accommodate flexion and extension of the
muscle
Slide 11
Figure 9.2a Skeletal Muscle Innervation Axons Neuromuscular
synapse Skeletal muscle fibers LM 230 A neuromuscular synapse as
seen on a muscle fiber of this fascicle
Slide 12
Anatomy of Skeletal Muscles Microanatomy of skeletal muscle
fibers Sarcolemma Membrane that surrounds the muscle cell
Sarcoplasm The cytosol of the muscle cell Muscle fiber (same thing
as a muscle cell) Can be 3040 cm in length Multinucleated (each
muscle cell has hundreds of nuclei) Nuclei are located just deep to
the sarcolemma
Slide 13
Figure 9.3ab The Formation and Structure of a Skeletal Muscle
Fiber Development of a skeletal muscle fiber External appearance
and histological view Myoblasts Muscle fibers develop through the
fusion of mesodermal cells called myoblasts. Myosatellite cell
Nuclei Immature muscle fiber
Slide 14
Levels of Organization Skeletal muscles consist of - fascicles
Muscle fascicles consist of - fibers Muscle fibers consist of-
myofibrils Myofibrils consist of - sarcomeres Sarcomeres consist
of- myofilaments Myofilaments are- actin and myosin
Slide 15
Myofibrils and Myofilaments The sarcoplasm contains myofibrils
Myofibrils are responsible for the contraction of muscles
Myofibrils are attached to the sarcolemma at each end of the muscle
cell Surrounding each myofibril is the sarcoplasmic reticulum
Myofibrils are segmented into sarcomeres Sarcomeres are made of
myofilaments Actin Myosin
Slide 16
Figure 9.3bd The Formation and Structure of a Skeletal Muscle
Fiber External appearance and histological view The external
organization of a muscle fiber Internal organization of a muscle
fiber. Note the relationships among myofibrils, sarcoplasmic
reticulum, mitochondria, triads, and thick and thin filaments.
Myofibril Sarcolemma Sarcoplasm Nuclei MUSCLE FIBER Mitochondria
Sarcolemma Myofibril Thin filament Thick filament Triad T tubules
Sarcoplasmic reticulum Terminal cisterna Sarcolemma Sarcoplasm
Myofibrils
Slide 17
Sarcomere Organization Myosin (thick filament) Anisotropic
-dark Actin (thin filament) isotropic-light Both are arranged in
repeating units called sarcomeres All the myofilaments are arranged
parallel to the long axis of the cell
Slide 18
Anatomy of Skeletal Muscles Sarcomere Organization Sarcomere
Main functioning unit of muscle fibers Approximately 10,000 per
myofibril Consists of overlapping actin and myosin This overlapping
creates the striations that give the skeletal muscle its
identifiable characteristic
Slide 19
Muscle Contraction A contracting muscle shortens in length
Contraction is caused by interactions between thick and thin
filaments within the sarcomere Muscle contraction requires the
presence of ATP When a muscle contracts, actin filaments slide
toward each other This sliding action is called the sliding
filament theory
Slide 20
Sarcomere Organization Each sarcomere consists of: Z line (Z
disc) I band A band (overlapping A bands create striations) H band
M line
Slide 21
Figure 9.4b Sarcomere Structure A corresponding view of a
sarcomere in a myofibril in the gastrocnemius muscle of the calf
and a diagram showing the various components of this sarcomere Z
lineTitin H band A band I band M line Zone of overlap Thin filament
Thick filament Sarcomere H band Z line I band Z line Zone of
overlap M line Sarcomere TEM 64,000 A band
Slide 22
The sliding filament theory A relaxed sarcomere showing
location of the A band, Z lines, and I band During a contraction,
the A band stays the same width, but the Z lines move closer
together and the I band gets smaller. When the ends of a myofibril
are free to move, the sarcomeres shorten simultaneously and the
ends of the myofibril are pulled toward its center. I band A band Z
line H band Upon contraction : The H band and I band get smaller
The zone of overlap gets larger The Z lines move closer together
The width of the A band remains constant throughout the
contraction
Slide 23
Slide 24
The neuromuscular junction is formed by an enlarged nerve
terminal that rests in the invaginations of the sarcolemma.
Slide 25
Neuromuscular Junction Motor neurons are specialized nerve
cells that propagate action potentials to skeletal muscle fibers.
each axon branch projects to one muscle fiber and forms a
neuromuscular junction (synapse), each muscle fiber receives a
branch of an axon each axon innervates more than one muscle
fiber.
Slide 26
Motor unit- a motor neuron and all the muscle fibers it
activates. motor neurons reside in the spinal cord - their axons
extend to the muscle. axons divide into multiple axonal terminals
& attach to multiple muscle fibers
Slide 27
presynaptic terminal -An enlarged nerve terminal synaptic cleft
-the space between pre and post synaptic terminals Postsynaptic
terminal accepts the neurotransmitter motor endplate -the muscle
cell membrane in the area of the junction or the postsynaptic
terminal synaptic vesicles -spherical sacs in the presynaptic
terminal containing acetylcholine a neurotransmitter
neurotransmitter - substance released from a presynaptic terminal
that diffuses across the synaptic cleft and stimulates (or
inhibits) the production of an action potential in the postsynaptic
terminal.
Slide 28
The attachment of thin filaments to the Z line The detailed
structure of a thin filament showing the organization of G actin,
troponin, and tropomyosin Myofibril Z line M line H band Sarcomere
ActininZ line Titin TroponinNebulin Tropomyosin Active site G actin
molecules F actin strand Actin-- Twisted filament consisting of G
actin molecules Each G actin molecule has an active site (binding
site) Myosin heads binds to active sites & forms cross-bridges
Tropomyosin: A protein that covers the binding sites (when the
muscle is relaxed) Troponin: Holds tropomyosin in position
Slide 29
Myofibril Z line M line H band Sarcomere The structure of thick
filaments Titin M line Myosin tail Myosin head Hinge Myosin
filaments consist of an elongated tail and a globular head ( forms
cross-bridges) Myosin is a stationary molecule. It is held in place
by: Protein forming the M line A core of titin connecting to the Z
lines
Slide 30
Slide 31
1.A nerve impulse is sent from the central nervous system 2.The
action potential reaches the presynaptic terminal 3.causes calcium
(Ca2*) channels in the axon's cell membrane to open 4.Ca ions
diffuse into the cell 5.Ca ions cause synaptic vesicles to secrete
ACh by exocytosis from the presynaptic terminal into the synaptic
cleft. 6. The acetylcholine molecules then diffuse across the
cleft
Slide 32
7. ACh binds to receptor molecules on the membrane of the
postsynaptic terminal. 8. Receptors cause the sarcolemma to become
temporarily permeable to sodium ions which rush into the muscle
cell. 9. This gives the cell interior an excess of positive ions,
which upsets and changes the electrical conditions of the
sarcolemma and causes an action potential. 10. the action potential
travels over the entire surface of the sarcolemma, conducting the
electrical impulse from one end of the cell to the other
Slide 33
excitation contraction coupling =The mechanism by which action
potential production causes contraction of a muscle fiber 11.
action potential Na is propagated along sarcolemma & penetrates
T- tubules. 12. T tubules carry the action potentials into the
muscle fiber's interior. 13. when action potentials reach the area
of the sarcoplasmic reticulum membranes increase their permeability
to Ca+ ions. 14. Ca+ ions rapidly diffuse out from the sarcoplasmic
reticulum
Slide 34
18. exposed active sites bind to the heads of the myosin
molecules to form cross bridges 19. hinged areas of the myosin move
causing the actin to slide past the myosin. 20. Thus causing the
sarcomere to shorten (contraction) 15. Ca2+ ions bind to troponin
of the actin myofilaments 16. Ca+ causes the tropomyosin to move
deeper into the groove between the two F-actin molecules 17. this
exposes the active sites on the actin
Slide 35
When the heads of the myosin molecules bind to actin, a series
of events resulting in contraction which proceeds very rapidly. The
myosin heads bend at their hinged area, forcing the actin to slide
over the surface of the myosin After movement, each myosin head
releases from the actin and returns to its original position. It
can then form another cross bridge.
Slide 36
Energy Requirements for Contraction one ATP energy molecule is
required for each cycle of cross- bridge formation, cross-bridge
movement, and cross-bridge release. After a cross bridge has formed
and movement has occurred, ATP binds to the head of the myosin
molecule allowing its release from the actin The ATP is broken down
by ATPase in the head of the myosin and energy is stored in the
head of the myosin molecule. The cross bridge is then released and
the myosin head is restored to its original position (Figure 10-13,
A). When the myosin molecule binds to actin to form another cross
bridge, much of the stored energy is used for cross bridge
formation and movement (Figure 10-13, B and C). Before the cross
bridge can be released for another cycle, once again, an ATP
molecule must bind to the head of the myosin molecule. Movement of
the myosin molecule while the cross bridge is attached is a power
stroke, whereas return of the myosin head to its original position
after cross-bridge release is a recovery stroke. Many cycles of
power and recovery strokes occur during each muscle contraction.
While muscle is relaxed, energy stored in the heads of the myosin
molecules is held in reserve until the next contraction. When
calcium is released from the sarcoplasmic reticulum in response to
an action potential, the cycle of cross-bridge formation and
release, which results in contraction, begins (Table 10-2).
Slide 37
Other events of skeletal muscle contraction Before contraction
ATP energy is stored in the head of the myosin ATP binds to the
head of the myosin and is broken down to ADP energy is needed to
release actin from myosin energy causes the hinged area of myosin
to return to its original position. The remainder of the energy is
stored in the head of the myosin As long as actin-active sites are
available, the process continues resulting in further contraction.
If no additional action potentials are produced in the skeletal
muscle fibers Ca ions are taken up by the sarcoplasmic reticulum,
Ca ions unbind from troponin & the troponin- tropomyosin
complex covers the actin-active sites Then relaxation occurs.
Slide 38
ACh is rapidly broken down to acetic acid and choline by
acetylcholinesterase Acetylcholines rapid degradation in the
neuromuscular junction ensures that one presynaptic action
potential yields only one postsynaptic action potential. Choline
molecules are actively reabsorbed by the presynaptic terminal and
then combined with the acetic acid produced within the cell to form
acetylcholine. Recycling choline molecules requires less energy and
is more rapid than completely synthesizing new acetylcholine
molecules each time they are released from the presynaptic
terminal.
Slide 39
Figure 9.10bc The Neuromuscular Synapse One portion of a
neuromuscular synapse Myofibril Mitochondrion Sarcolemma Glial cell
Synaptic terminal Detailed view of a terminal, synaptic cleft, and
motor end plate. See also Figure 9.2. Synaptic vesicles ACh ACh
receptor site AChE molecules Junctional fold Sarcolemma of motor
end plate Arriving action potential Synaptic cleft
Slide 40
Anything that affects the production, release, and degradation
of acetylcholine or its ability to bind to its receptor molecule
will also affect the transmission of action potentials across the
neuromuscular junction. For example, some insecticides contain
organophosphates that bind to and inhibit the function of
acetylcholinesterase. As a result, acetylcholine is not degraded
and accumulates in the synaptic cleft where it acts as a constant
stimulus to the muscle fiber. Insects exposed to the insecticide
die. partly because their muscles contract and cannot relaxa
condition called spastic paralysis. Other organic poisons such as
curare bind to the acetylcholine receptors, preventing
acetylcholine from binding to them. Curare does not allow
activation of the receptors; therefore the muscle is not capable of
contracting in response to nervous stimulationa condition called
flaccid paralysis. Myasthenia graVIs {mi'as-the'ne-ah grS'vis)
results from the production of antibodies that bind to
acetylcholine receptors, eventually causing the destruction of the
receptor and thus reducing the number of receptors. As a
consequence, muscles exhibit a degree of flaccid paralysis or are
extremely weak. A class of drugs that' includes neostigmine
partially blocks the action of acetylcholinesterase and sometimes
is used to treat myasthenia gravis. The drugs cause acetylcholine
levels to increase in the synaptic cleft and combine more
effectively with the remaining acetylcholine receptor sites.
Slide 41
Slide 42
MUSCLE TWITCH
Slide 43
Muscle Twitch A muscle twitch is contraction of a whole muscle
in response to a stimulus that causes an action potential in one or
more muscle fibers. lag, or latent phase =The time period between
application of the stimulus to the motor neuron and the beginning
of contraction contraction phase =the time during which contraction
occurs relaxation phase =the time during which relaxation occurs
The action potential is an electrochemical event, but contraction
is a mechanical event. =
Slide 44
all-or-none law of skeletal muscle contraction = an isolated
skeletal muscle fiber either contracts maximally or does not
contract at all. subthreshold stimulus does not produce an action
potential, and no muscle contraction threshold stimulus = an action
potential that results in contraction of the muscle cell;
submaximal stimuli = activates additional motor units until all of
the motor units are activated by maximal stimulus = contracts all
motor units supramaximal stimulus = an action potential of the same
magnitude as the threshold stimulus and therefore produces an
identical contraction. =
Slide 45
multiple motor unit summation = As the stimulus strength
increases between threshold and maximum values, motor units are
recruited, and the force of contraction produced by the muscle
increases in a graded fashion. A whole muscle contracts with either
a small force or a large force, depending on the number of motor
units recruited, but each motor unit responds to an action
potential either maximally or not at all. =
Slide 46
Stimulus Frequency and Muscle Contraction incomplete tetanus =
muscle fibers partially relax between contractions complete tetanus
= action potentials occur so rapidly there is no muscle relaxation
between the action potentials. multiple wave summation = tension
produced by a muscle increases as the stimulus frequency increases.
Treppe - a second contraction produces a greater tension than the
first, and the third produces greater tension than the second.
After only few stimuli, the tension produced by all the
contractions is equal. =
Slide 47
isometric contractions = the length of the muscle does not
change, but the amount of tension does increase isotonic
contractions = the amount of tension is constant during
contraction, but the length of the muscle changes Concentric
contractions an isotonic contraction that is big enough to overcome
the opposing resistance and the muscle shortens Eccentric
contractions an isotonic contraction that maintains tension while
the muscle increases in length.(lowering a weight) Most muscle
contractions are a combination of isometric and isotonic
contractions =
Slide 48
Muscle tone = constant tension by muscles of the body for long
periods of time. Muscle tone is responsible for keeping the back
and legs straight, the head held in an upright position, and the
abdomen from bulging.
Slide 49
Length versus Tension Active tension force applied to an object
when a muscle contracts Passive tension the tension applied to a
load when a muscle is stretched but not stimulated
Slide 50
Fatigue The decreased capacity to do work following a period of
activity Psychologic fatigue person perceives that more muscle work
is not possible.(most common type) Muscular fatigue depletion of
ATP Synaptic fatigue acetylcholine synthesis cant keep up with ms.
use
Slide 51
Muscle disorders are caused by disruption of normal
innervation, degeneration and replacement of muscle cells, injury,
lack of use, or disease. Exercise causes muscular hypertrophy.
disuse of muscle results in muscular atrophy. Extreme disuse of
muscle results in muscular atrophy in which there is a permanent
loss of skeletal muscle fibers and the replacement of those fibers
by connective tissue. Immobility caused by damage to the nervous
system or by old age may lead to permanent and severe muscular
atrophy. Denervation When motor neurons innervating skeletal muscle
fibers are severed, the result is flaccid paralysis. If the muscle
is reinnervated, muscle function is restored, and atrophy is
stopped. However, if skeletal muscle is permanently denervated, it
atrophies and exhibits permanent flaccid paralysis. Muscles that
have been denervated sometimes are stimulated electrically to
prevent severe atrophy. The strategy is to slow the process of
atrophy while motor neurons slowly grow toward the muscles and
eventually reinnervate them. Neither cardiac muscle nor smooth
muscle atrophies in response to denervation.
Slide 52
Muscular Dystrophy Muscular dystrophy refers to a group of
diseases called myopa-thies that destroy skeletal muscle tissue.
Usually the diseases are inherited and are characterized by
degeneration of muscle cells, leading to atrophy and eventual
replacement by fatty tissue. Duch-enne muscular dystrophy affects
only males, and by early adolescence the individual is confined to
a wheelchair. As the muscles atrophy, they shorten, causing
conditions such as immobility of the joints and postural
abnormalities such a scoliosis. Facioscapulohu-moral
(fa'sT-o-skap'u-Io- hu'mor-al) muscular dystrophy is generally less
severe, and it affects both sexes later in life. The muscles of the
face and shoulder girdle are primarily involved. Both types of
muscular dystrophy are inherited and progressive, and no drugs
prevent the progression of the disease. Therapy primarily involves
exercises. Braces and corrective surgery sometimes help correct
abnormal posture caused by the advanced disease.
Slide 53
Fibrosis Fibrosis is the replacement of damaged cardiac muscle
or skeletal muscle by connective tissue. Fibrosis, or scarring, is
associated with severe trauma to skeletal muscle and with heart
attack (myocardial infarction) in cardiac muscle. Fibrositis
Fibrositis is an inflammation of fibrous connective tissue,
resulting in stiffness, pain, or soreness. It is not progressive,
nor does it lead to tissue destruction. Fibrositis may be caused by
repeated muscular strain or prolonged muscular tension. Cramps
Painful, spastic contractions of muscles (cramps) are usually due
to an irritation within a muscle that causes a reflex contraction
(see Chapter 13). Local inflammation resulting from a buildup of
lactic acid and fibrositis causes reflex contraction of muscle
fibers surrounding the irritated region.
Slide 54
Slide 55
Slide 56
Motor Units and Muscle Control Motor Units (motor neurons
controlling muscle fibers) Precise control A motor neuron
controlling two or three muscle fibers Example: the control over
the eye muscles Less precise control A motor neuron controlling
perhaps 2000 muscle fibers Example: the control over the leg
muscles
Slide 57
Figure 9.12 The Arrangement of Motor Units in a Skeletal Muscle
Motor unit 1 Motor unit 2 Motor unit 3 KEY SPINAL CORD Muscle
fibers Axons of motor neurons Motor nerve
Slide 58
Motor Units and Muscle Control Muscle Tension Muscle tension
depends on: The frequency of stimulation The number of motor units
involved
Slide 59
Motor Units and Muscle Control Muscle Tone The tension of a
muscle when it is relaxed Stabilizes the position of bones and
joints Muscle Spindles These are specialized muscle cells that are
monitored by sensory nerves
Slide 60
Motor Units and Muscle Control Muscle Hypertrophy Exercise
causes: An increase in the number of mitochondria An increase in
the activity of muscle spindles An increase in the concentration of
glycolytic enzymes An increase in the glycogen reserves An increase
in the number of myofibrils The net effect is an enlargement of the
muscle (hypertrophy)
Slide 61
Motor Units and Muscle Control Muscle Atrophy Discontinued use
of a muscle Disuse causes: A decrease in muscle size A decrease in
muscle tone Physical therapy helps to reduce the effects of
atrophy
Slide 62
Types of Skeletal Muscle Fibers Three major types of skeletal
muscle fibers : Fast fibers (white fibers) Associated with eye
muscles Intermediate fibers (pink fibers) Slow fibers (red fibers)
Associated with leg muscles
Slide 63
Figure 9.13a Types of Skeletal Muscle Fibers Note the
difference in the size of slow muscle fibers (above) and fast
muscle fibers (below). LM 170 Slow fibers Smaller diameter, darker
color due to myoglobin; fatigue resistant Fast fibers Larger
diameter, paler color; easily fatigued
Slide 64
Figure 9.13b Types of Skeletal Muscle Fibers Slow fibers
Smaller diameter, darker color due to myoglobin; fatigue resistant
Fast fibers Larger diameter, paler color; easily fatigued The
relatively slender slow muscle fiber (R) has more mitochondria (M)
and a more extensive capillary supply (cap) than the fast muscle
fiber (W). LM 783 W cap M R
Slide 65
Fast-twitch muscle fibers TYPE II break down ATP more rapidly
than slow-twitch muscle fibers cross bridges that form, release,
and reform more rapidly than those in slow-twitch muscles less
well-developed blood supply than slow-twitch muscles very little
myoglobin fewer and smaller mitochondria. large deposits of
glycogen and are well adapted to perform anaerobic metabolism
contract rapidly for a shorter time and fatigue relatively quickly.
Training causes fast-twitch muscles to improve their ability to
carry out aerobic metabolism. Trained fast-twitch muscles are
called fatigue- resistant fast-twitch muscles. =
Slide 66
Types of Skeletal Muscle Fibers Features of fast fibers: Large
in diameter Large glycogen reserves Relatively few mitochondria
Muscles contract using anaerobic metabolism Fatigue easily Can
contract in 0.01 second or less after stimulation Produce powerful
contractions
Slide 67
Slow Twitch muscle Type 1 oxidative Slow-twitch muscle fibers
contract more slowly smaller in diameter, have a better developed
blood supply, have more mitochondria, and are more fatigue
resistant than fast-twitch muscle fibers. Aerobic metabolism is the
primary source large amounts of myoglobin =
Slide 68
Types of Skeletal Muscle Fibers Features of slow fibers: Half
the diameter of fast fibers Take three times longer to contract
after stimulation Can contract for extended periods of time Contain
abundant myoglobin (creates the red color) Muscles contract using
aerobic metabolism Have a large network of capillaries
Slide 69
Types of Skeletal Muscle Fibers Features of intermediate
fibers: Similar to fast fibers Have low myoglobin content Have high
glycolytic enzyme concentration Contract using anaerobic metabolism
Similar to slow fibers Have lots of mitochondria Have a greater
capillary supply Resist fatigue
Slide 70
Table 9.1 Properties of Skeletal Muscle Fiber Types
Slide 71
Types of Skeletal Muscle Fibers Distribution of fast, slow, and
intermediate fibers Fast fibers High density associated with eye
and hand muscles Sprinters have a high concentration of fast fibers
Repeated intense workouts increase the fast fibers
Slide 72
Types of Skeletal Muscle Fibers Distribution of fast, slow, and
intermediate fibers Slow and intermediate fibers None are
associated with the eyes or hands Found in high density in the back
and leg muscles Marathon runners have a high amount Training for
long distance running increases the proportion of intermediate
fibers
Slide 73
Slide 74
Aging and the Muscular System Changes occur in muscles as we
age Skeletal muscle fibers become smaller in diameter There is a
decrease in the number of myofibrils Contain less glycogen reserves
Contain less myoglobin All of the above results in a decrease in
strength and endurance Muscles fatigue rapidly
Slide 75
Aging and the Muscular System Changes occur in muscles as we
age (continued) There is a decrease in myosatellite cells There is
an increase in fibrous connective tissue Results in fibrosis The
ability to recover from muscular injuries decreases
