Muscles of the upper and lower extremities

1. MUSCULAR SYSTEM
Introduction to Anatomy
Human Anatomy I • Describe the characteristics of muscle tissues
• Describe the process of muscle contraction
and related clinical correlate
• Describe particular body muscles
Learning objectives
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American International
University

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Smooth muscle
Non-straited;
mononucleated;
Spindle-shaped (fusiform)
cells; Innervated by the
ANS; involuntary, weak,
slow and sustained
contraction
Skeletal muscle
Straited; multinucleated;
cylindrical cells; innervated
by the motor nerve;
voluntary, quick, and strong
contraction; 40% 0f body
weight
Cardiac muscle
Straited; mononucleated; short
cylindrical cells; branched
fibers; cardiac conducting
system causes its contraction;
ANS, hormones regulate the
heartrate; involuntary, quick,
strong and continuous
contraction

3. Arrangement of skeletal muscle
Endomysium wraps muscle fiber
Perimysium wraps muscle
bundle/fasciculus
Epimysium wraps whole muscle
Tendon – unity of these
connective tissues
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4. Histology of a skeletal muscle
fiber
Organelles: multinucleated;
sarcolemma; sarcoplasm; numerous
myofibrils (contractile proteins);
numerous mitochondria; sarcoplasmic
reticulum (Ca2+
storage; wraps round
myofibril); glycogen; myoglobin,
transverse (T) tubules;.
Myofibrils
Contains numerous myofilaments
(protein microfilaments).
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5. Histology cont.
Thick filaments - made of numerous
myosin molecules
Thin filaments – actin (2 twisted strands
of G-actin monomers), tropomyosin (2
polypeptide chains in the groove of actin
helix) and troponin (3 polypeptides- TnT,
TnC, Tni).
Thick and thin filaments overlap to form
Dark (A, anisotropic) band, H zone, Light
(I, isotropic) band.
Z line to another Z line – sarcomere
(smallest unit of myofibril)
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6. Transverse (T) tubule
system
The system is the invagination of the
sarcolemma that surrounds the myofibril.
It is in close relationship with the terminal
cisterna of sarcoplasmic reticulum
The T tubules runs between 2 terminal
cisternae, forming a triad (T tubule and 2
terminal cisternae) at the A-I junction
Function: it conducts each impulse to the
deepest regions of the muscle fiber, this
ensures deeper myofibrils contract at the
same time as the superficial ones. As the
impulse travels, Ca2+
are released for
contraction. 17-Jun-22
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7. Neuromuscular Junction The point an axon terminal of a motor neuron
communicates with a muscle fiber.
Action potential gets to presynaptic terminal
Voltage-gated calcium channels
Ca2+
influx
Synaptic vesicles at the synaptic knob move
distally to eject neurotransmitter into the
synaptic cleft.
Acetylcholine (Ach), excitatory in action, binds
to nicotinic acetylcholine receptors, nAchRs
on the sarcolemma.
nAChRs are ionotropic receptors and they
function as ligand-gated channels.
Na+
influx → depolarize muscle fiber
NMJ is enclosed by basal lamina to prevent
excess leakage
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8. Myasthenia gravis
Autoimmune disorder caused by autoantibodies against the postsynaptic Ach
receptors
Most common NMJ disorder and it is characterized by weakness and easy fatigue of
muscles that worsens with muscle use, ptosis, diplopia. It tends to become fatal if
respiratory muscles are affected.
Ach receptors works for like 10 days and then they degraded by lysosomes and
replaced with new ones produced by golgi apparatus. The attack of autoantibodies
on the receptors reduces their half-life to about 2 days, leaving very few receptors
available to propagate and sustain muscle contraction.
Administration of AChE inhibitors (edrophonium, pyridostigmine) is used for
diagnosis and treatment. AChE inhibitors ↓rate of ACh degradation thereby ↑ the
binding time of Ach with the little available receptors. This improves muscle strength.
Myasthenia gravis is associated with thymoma and thymic hyperplasia
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9. Lambert-Eaton myasthenic syndrome
Autoimmune disorder caused by
autoantibodies against the presynaptic
Ca2+
channels leading to low Ach release
Uncommon NMJ disorder; characterized
by proximal muscle weakness and
autonomic symptoms (dry mouth and
impotence)
The features improves with the use of
the muscles and it is associated with
small cell lung cancer
Administration of AChE inhibitors has
little effect on reversing the symptoms
17-Jun-22
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pesticides that contain
cholinesterase inhibitors that
prevent degradation of ACh
thereby increasing the
binding-time of ACh making the
muscle contract excessively.
Flaccid paralysis: caused by
venom or poison (curare)that
competes with Ach on the nACh
receptors, causing inhibited
contraction of muscle

10. Muscle excitation, contraction and relaxation
Muscle excitation:
Na+
pumps open allowing Na+
influx into the muscle fiber (depolarization of the muscle
fibre).
Immediately, Na+
gates close and K+
gates open.
K+
rush out so the inside becomes negative again (repolarization).
Depolarization and repolarization create an action potential that excites the muscle
fiber (outside in).
Muscle contraction: threshold; Ca2+
exits to bind to troponin → tropomyosin changing
position exposing myosin-binding sites on the actin; myosin binds to this site →
filaments slide over themselves → shortens sarcomere (sliding filament theory).
Myosin–actin cross-bridge.
Muscle relaxation: nerve stimulation
stops; Ach release stops; Ca2+
withdraw;
breaking of cross-bridge → sarcomere
elongates.
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11. Muscles of facial expression and mastication
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12. BELL’S PALSY
Paralysis of upper and lower facial muscles due to lesion of
ipsilateral facial nucleus or facial n. along its course
Sudden symptoms that peak within 2 days, but pain in or
behind the ear can precede by a day or two
Mostly idiopathic or may be due to Herpes simplex virus
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Evident distorted face on the affected size (sagging corner of the mouth; drooping of the
eyebrow; sagging of the lower eyelid; inability to close or blink the eye; deviation of the
lower jaw [lesion of n. to digastric]); inability to smile, whistle, or blow; tingling around the
lips; decreased lacrimation, loss of taste in ant. 2/3 of tongue [lesion of chorda tympani
branch], hyperacusis [due to paralyzed stapedius].
Treatment: corticosteroids (prednisone [anti-inflammatory]) and/or anti-viral (acyclovir)
drugs. Most patients gradually recover function if they also avoid cold, wind, and eyes
drying out.

13. Muscles of the tongue and pharynx
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Muscles of the neck

14. Muscles of anterior abdominal wall
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Muscles of the back

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Muscles of the perineum

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Muscles that control the arm Muscles of the thorax

17. Muscles of the arm
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Muscles of the thigh

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Muscles of the leg

20. Duchenne muscular dystrophy (DMD),
X-linked recessive disorder caused by frameshift or
nonsense mutation causing dystrophin to be missing or
truncated.
Dystrophin connects the cytoskeleton (actin) to the
transmembrane proteins α- and β-dystroglycan
(cytoskeleton-transmembrane association), which are
connected to the extracellular matrix (ECM).
Contractions of muscles thus pull at the weakened
connections of the sarcolemma to create a leaky-hole
through which extracellular Ca2+
flood the muscle fiber
causing cell damage and eventual cell death.
DMD causes muscle weakness from the pelvis upward
(respiratory and cardiac muscles)
It evident at age 2-5 years and victims rarely live past 30
years. 3/29/2023
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