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A Few Skeletal Muscle Disorders
and Other Conditions
Note
Much of the text material is from, “Principles of Anatomy and
Physiology” by Gerald J. Tortora and Bryan Derrickson (2009,
2011, and 2014). I don’t claim authorship. Other sources are
noted when they are used.
The lecture slides are mapped to the three editions of the
textbook based on the color-coded key below.
14th edition
13th edition
12th edition
Same figure or table reference in all three editions
2
Muscular Atrophy
•
Muscular atrophy is a condition that involves wasting away of skeletal
muscle.
•
In this condition, the individual fibers decrease in size due to the loss
of myofibrils.
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Disuse Atrophy
•
Disuse atrophy can occur when skeletal muscles are not used, such
as in bedridden individuals or in the zero-gravity environment of longduration spaceflight.
•
The condition results from less stimulation of skeletal muscle fibers.
•
Disuse atrophy is often reversible.
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Denervation Atrophy
•
Denervation atrophy results if the nerve supply to a muscle is cut or
disrupted.
•
The muscle shrinks to about one-quarter of its original size in 6 to 24
months.
•
The muscle fibers are irreversibly replaced by fibrous connective tissues.
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Muscular Hypertrophy
•
Although not a disorder, muscle hypertrophy results from an increase
in the diameter of muscle fibers.
•
The increase is due to increased production of myofibrils, mitochondria, sarcoplasmic reticulum, and other organelles.
•
It can occur from forceful, repetitive muscular activity such as strength
training.
•
Hypertrophied muscles can produce more forceful contractions due to
an increased number of myofibrils.
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Exercise-Induced Muscle Damage
•
Skeletal muscles may become sore within 12 to 48 hours of intense
exercise.
•
Stiffness, tenderness, and swelling may result—recovery often occurs
quickly.
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Exercise-Induced Muscle Damage (continued)
•
Electron micrographs of muscle tissue from athletes after intense
exercise sometimes show muscle damage.
•
The damage includes torn sarcolemmas, damaged myofibrils, and
disrupted Z discs.
•
Increased concentrations of some types of proteins, including myoglobin and some enzymes usually found only muscle fibers, may be
detected in the blood.
•
Damaged skeletal muscle fibers can undergo repair, which involves
the replacement of torn sarcolemmas and synthesis of new muscle
proteins.
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Rigor Mortis
•
Rigor mortis is not a muscle disorder, but it is included in this lecture
module.
•
Cell membranes, including for skeletal muscle tissue, become leaky
soon after the death of an organism.
•
Ca2+ leaks from the sarcoplasmic reticulum and into the sarcoplasm,
enabling myosin heads to bind to the myosin binding sites on actin to
form crossbridges.
•
ATP synthesis stops soon after breathing stops, and therefore myosin
in the crossbridges cannot detach from actin.
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Rigor Mortis (continued)
•
The skeletal muscles become rigid since they can neither contract nor
stretch.
•
Rigor mortis begins about 3 to 4 hours after death, and lasts about 24
hours, when enzymes from the lysosomes in the muscle fibers breakdown the crossbridges between myosin and actin in the thick and thin
filaments.
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Botulinum Toxin
•
Botulinum toxin from the bacterium, Clostridium botulinum blocks the
release of ACh from the synaptic vesicles—therefore, muscle contraction cannot occur.
•
The bacterium, which can grow in improperly canned foods, is one of
the most lethal chemicals known.
•
Breathing stops due to paralysis of respiratory muscles of the external
intercostals and diaphragm.
•
The condition is known as botulism.
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Botulinum Toxin (continued)
•
Injections of the medicine, Botox® derived from the botulinum toxin
can help patients who have:
Crossed eyes (strabismus)
- Uncontrolled blinking (blepharospasm)
- Spasms of the vocal cords
-
•
Botox® is also used to relax the skeletal muscles that cause facial
wrinkles.
• It is also used to alleviate chronic back pain due to muscle spasms
in the lumbar region.
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Curare
•
Curare, a plant derivative, causes paralysis by binding to and blocking the ACh receptors in the motor end plates of the neuromuscular
junctions.
•
The result is a slowing of the removal of ACh from the postsynaptic
region.
•
Skeletal muscles remain in a prolonged stage of contraction (known
as tetanus).
•
The diaphragm and external intercostal muscles are no longer able to
control inhalation and breathing stops.
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Electromyography
•
Electromyography (EMG) is a technique for measuring electrical activity
(muscle action potentials) in skeletal muscles.
•
Electrodes are attached to the skin—the electrical potentials are amplified and displayed on an oscilloscope or computer screen.
•
The amount of electrical activity increases with increased forcefulness of
the muscle contractions.
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Electromyography (continued)
•
EMG can be used to help determine if muscle weakness or paralysis is
due to a malfunction of either the muscle or the nerve fibers that supply
the muscle.
•
The technique can be used in diagnosing some muscle disorders such
as muscular dystrophy.
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Myasthenia Gravis
•
Myasthenia gravis is an autoimmune disease that causes damage to
the neuromuscular junctions, which leads to progressive weakening of
the skeletal muscles.
•
The immune system produces antibodies that bind to and block many
ACh receptors in the motor end plates.
•
The number of available receptors to initiate a muscle action potential
is diminished.
Autoimmune disease = an illness that occurs when the body
tissues are attacked by its own immune system.
(http://www.medterms.com)
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Myasthenia Gravis (continued)
•
Myasthenia gravis condition occurs in about one in 10,000 people.
•
It is more common in women, with a typical onset between ages 20
and 40.
•
The onset in men is generally later, typically between ages 50 and
60.
•
Anticholinesterase drugs are the first-line treatment for inhibiting the
enzyme (AChE) that breaks-down ACh.
•
Steroid drugs may be used to reduce antibody levels responsible for
the autoimmune reaction.
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Muscular Dystrophy
•
Muscular dystrophy is a collection of inherited genetic diseases that
can cause progressive degeneration of skeletal muscle fibers.
•
A common type, Duchenne Muscular Dystrophy (DMD), is the result
of a recessive gene on the X chromosome of the 23rd chromosomal
pair (sex chromosomes).
•
DMD affects boys almost exclusively since males usually have only
one X chromosome.
•
Women would need to have the recessive gene on both X chromosomes, a much rarer event.
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Muscular Dystrophy (continued)
•
The incidence of DMD is about 1 in 3,500 newborn males.
•
The rate can be much higher in some tight-knit communities such as
in the Amish of southeastern Pennsylvania and other localities where
genetic exchange has been limited.
•
The disorder often becomes apparent between the ages of 2 and 5,
when parents notice their child has difficulty in performing physical
activities.
•
By age 12, most boys with DMD are unable to walk, and have great
difficulty in breathing.•
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Muscular Dystrophy (continued)
•
The proximal cause is that gene that codes for the structural protein
dystrophin is mutated in DMD so that little or none of this molecule is
present in the sarcolemma.
•
The sarcolemma can therefore tear easily during muscle contractions,
causing the muscle fibers to rupture and die.
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