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The Muscular
System
A. Function of Muscles
 Muscles are responsible for four functions
1. Produce movement
 Contraction!
 Skeletal: Run away from danger, smile in
flirtation
 Smooth: peristalsis of digestion
 Cardiac: beat of heart
2. Maintain posture
 Upright/seated – fight downward pull of gravity
3. Stabilize joints
 Tendons attaching muscles to bones of joints
for stabilization
4. Generate heat
 By-product of muscle activity produces
heat
 As ATP (adenosine triphosphate) is used to
power contraction, ¾ energy released as
heat
 Maintains normal body temperature
(homeostasis!)
 Skeletal muscle (40% body mass) most
responsible
B. Types of Muscles
Three basic muscle types are found in
the body
Skeletal muscle - attached to bones
ii. Smooth muscle - hollow visceral
(internal) organs
iii. Cardiac muscle – heart
i.
i.
Skeletal Muscles
 Most are attached by tendons to bones
 Cells are multinucleate (many nuclei in one cell)
 Striated – have visible banding
 Voluntary – subject to conscious control
 Cells are surrounded and bundled by connective
tissue
“Packaging” of Skeletal Muscles
 Muscle fiber = muscle cell
 Endomysium – around single
muscle fiber
 Fascicle = bundle of fibers
 Perimysium – around a fascicle
 Typical skeletal muscle =
bundle of fascicles
 Epimysium – covers the entire
skeletal muscle
 Fascia – on the outside of the
epimysium
Figure 6.1
 Epimysium blends into a connective tissue
attachment
Tendon – cord-like structure
Aponeuroses – sheet-like structure
 Sites of muscle attachment
Bones
Cartilages
Connective tissue coverings
ii. Smooth Muscle
 Has no striations
 Spindle-shaped cells
 Single nucleus
 Involuntary – no
conscious control
 Found mainly in the
walls of hollow organs
Figure 6.2a
iii. Cardiac Muscle
 Has striations
 Usually has a single
nucleus
 Joined to another
muscle cell at an
intercalated disc
 Involuntary
 Found only in the
heart
Figure 6.2b
C. Anatomy of Skeletal Muscle
 Cells are multinucleate (many nuclei per cell)
 Nuclei (oval-shaped) are just beneath the
sarcolemma (specialized plasma membrane)
 Contain sarcoplasmic reticulum (specialized
smooth endoplasmic reticulum [ER]) for Ca2+
storage
Figure 6.3a
 One muscle fiber (muscle cell) is made of a bundle
of myofibrils (organelles) that nearly fill
cytoplasm
Figure 6.3a
 One myofibril (organelle) is made of chains
of tiny contractile units called sarcomeres (Z
disc to Z disc)
SARCOMERE
 one sarcomere is made of two myofilaments
(protein filaments):
 actin (thin) and myosin (thick)
 Thick filaments
 Composed of the protein myosin
 Has ATPase enzymes which break ATP bonds to make
energy for muscle contraction!
 Thin filaments
 Composed of the protein actin
Figure 6.3c
 Myosin filaments have heads (extensions, or cross
bridges which look like golf club heads) that move
 Myosin and actin overlap somewhat
Figure 6.3d
RECAP
Muscle fiber
Myofibrils
Sarcomere
oMyofilaments
• Actin
Site of muscle contraction
• Myosin
 Alignment of myofibrils in sarcomere
creates banding pattern
I band (light band) = absence of myosin
A band (dark band) = concentration of
myosin
Figure 6.3b
 Z disc =Area where actin joins other actin molecules,
forms Z-shaped pattern
 H zone (bare zone) = area that lacks thin filaments
 M line = center of H zone that contains tiny protein
rods that hold adjacent myosin proteins together
 Banding pattern changes shape during
contraction when each sarcomere segment gets
shortened (H zone gets smaller)
D. Muscle Activity: Contraction
Muscle has two functional properties
that are necessary for contraction:
1. Irritability – ability to receive and
respond to a stimulus (nerve to muscle)
2. Contractility – ability to shorten
when an adequate stimulus is received via
sliding filament theory (inside muscle)
1. Irritation: Nerve Stimulus to Muscles
 Skeletal muscles must be stimulated by a nerve
 Motor units are responsible for stimulating a few
to hundreds of muscle cells. Consist of
 One neuron
 All muscle cells stimulated by that one neuron
Figure 6.4a
 Neuron (nerve cell) relays message through electrical
and chemical signals. Consists of
 Cell body (with dendrite fingers)
 Axon or nerve fiber (with axon terminal projections)
 Axon terminals approach (never physically touch)
muscle’s sarcolemma via neuromuscular
junctions
 Gap between axon terminals and muscle cells
called synaptic cleft
 Filled with interstitial (“between tissues”) fluid
Figure 6.5b
Steps of Nerve Stimulation
1. Electrical nerve impulse reaches dendrites
2. Signal moves down cell body, to axon
terminals, signals vesicles with chemical
neurotransmitter called acetylcholine
(ACh) to move to nerve membrane
3. ACh is released via exocytosis into synaptic
cleft (space between nerve and muscle)
4. ACh attaches to receptors on the
sarcolemma membrane
5. Triggers Na+/K+ (sodium/potassium)
pumps to open, making sarcolemma
permeable to Na+ (Na+ rushes in, K+ rushes
out)
6. Rapid change in ion movement (sodium in,
potassium out of the cell) is called
depolarization which generates an electrical
current called action potential
7. Action potential will start, muscle
contraction which cannot be stopped travels
over entire surface of sarcolemma
 In the meantime, ACh is now broken down by
enzyme (AChase) to acetic acid and choline
 This is why one nerve impulse produces one
contraction
Steps of Nerve Stimulation
1. Nerve cell receives electrical stimulus through
dendrites
2. Stimulus send down cell body, out through axon
terminals as chemical signal
3. ACh neurotransmitter released from vesicles into
synaptic cleft
4. Receptors on sarcolemma receive ACh
5. Sarcolemma now permeable to Na+ ions = Na+
rushes in, K+ rushes out
6. Depolarization of muscle cells creates action
potential
2. Contraction: The Sliding Filament Theory
 Activation by nerve causes
myosin heads (cross bridges) to
attach to binding sites on the
thin (actin) filament
 Myosin heads then bind to the
next site of the thin filament
due to Ca2+ and ATP
Figure 6.7
 Ca2+ from sarcoplasmic
reticulum which was
triggered to release Ca2+
as a result of action
potential
 This continued action
causes a sliding of the
myosin along the actin
 The result is that the
muscle is shortened
(contracted)
Figure 6.7
Figure 6.8
 Muscle cell relaxes again when:
 1. diffusion of K+ ions out of cell
 2. Na+/K+ pump brings ions back to original
state (Na+ back out, K+ back in)
Sliding Filament Contraction Recap
1. Action potential triggers sarcoplasmic
reticulum to release Ca2+
2. Action potential causes myosin heads to
attach to binding sites on actin filament
3. Ca2+ with ATP triggers myosin heads to
attach to neighbor binding sites on same
actin filament, causing actin to move
toward each other = contraction!
Contraction Responses
 Muscle fiber contraction is “all or none”
 Within a skeletal muscle, not all fibers may be stimulated
during the same interval
 Different combinations of muscle fiber contractions may give
differing responses
 Graded responses – different degrees of skeletal muscle
shortening
Types of Graded Responses
1. Twitch
Single, brief contraction
Not a normal muscle function
Figure 6.9a–b
2. Tetanus (summing of
contractions)
One contraction is
immediately followed by
another
The muscle does not
completely return to a
resting state
The effects are added
(summed)
Figure 6.9a–b
3.
Fused (complete) tetanus
No evidence of relaxation before the
following contractions
The result is a sustained muscle contraction
Figure 6.9c–d
 Muscle force depends upon the number of fibers
stimulated
 More fibers contracting results in greater muscle
tension
 Muscles can continue to contract unless they run out of
energy
Muscle Fatigue and Oxygen Debt
 When a muscle is fatigued, it is unable to contract
 The common reason for muscle fatigue is oxygen
debt
 Oxygen must be “repaid” to tissue to remove
oxygen debt
 Oxygen is required to get rid of accumulated
lactic acid
 Breathing heavy!
 Increasing acidity (from lactic acid) and lack of
ATP causes the muscle to contract less
Types of Muscle Contractions
 Isotonic contractions
 Myofilaments are able to slide past each other
during contractions
 The muscle shortens (movement)
 Ex: bending knee, smiling
 Isometric contractions
 Tension in the muscles increases
 The muscle is unable to shorten (no movement)
 Ex: lifting 400-lb table alone, push against wall
Muscle Tone
 Some fibers are contracted even in a relaxed muscle
 Different fibers contract at different times to provide
muscle tone
 The process of stimulating various fibers is under
involuntary control
E. Body Movements
 Movement is attained due
to a muscle moving an
attached bone
 Muscles are attached to at
least two points
 Insertion – attachment
to a moveable bone
 Origin– attachment to
an immovable bone
Figure 6.12
opposites
opposites
Ordinary Body Movements
 Flexion – decreases angle of joint & brings two
bones closer together
 Extension – opposite of flexion (increases angle,
bones farther apart)
 Rotation – movement of bone around longitudinal
axis
 Abduction – move AWAY from midline
 Adduction – move TOWARD midline
 Circumduction – proximal end of bone stationary,
distal end moves in circle
Figure 6.13a–c
Figure 6.13d
opposites
opposites
Special Movements
 Dorsiflexion – lifting foot so its superior surface
approaches shin (decrease angle)
 Plantar flexion – pointing toes away from shin
(increase angle)
 Retraction – moving bone slightly backward
 Protraction – moving bone slightly forward
opposites
 Inversion – move sole of foot up and inward
 Eversion – move sole of foot up and outward
opposites
 Supination – radius and ulna are parallel (palm up)
 Pronation – radius rotates over ulna (palm down)
 Opposition –thumb touching tip of other fingers
F. Types of Muscles
 Prime mover (agonist) – muscle with the
major responsibility for contracting
 Antagonist – muscle that opposes or reverses
a prime mover (relaxes)
 Synergist – muscle that aids a prime mover in
a movement and helps prevent rotation
 Fixator – stabilizes the origin of a prime
mover
Agonist vs. Antagonist Muscle
Naming of Skeletal Muscles
 Direction of muscle fibers
Example: rectus (straight)
 Relative size of the muscle
Example: maximus (largest)
 Location of the muscle
Example: many muscles are named for
bones (e.g., temporalis)
 Number of origins
Example: triceps
(three heads)
 Location of the muscle’s origin and insertion
Example: sterno (on the sternum)
 Shape of the muscle
Example: deltoid (triangular)
Action of the muscle
Example: flexor and
extensor (flexes or
extends a bone)
Head and Neck Muscles
Figure 6.15
Trunk Muscles
Figure 6.16
Deep Trunk and Arm Muscles
Figure 6.17
Muscles of the Pelvis & Hip
Figure 6.19c
Muscles of the Thigh
Muscles of the Lower Leg
Figure 6.20
Muscles of the Arm
Muscles For Injections
Superficial Muscles: Anterior
Figure 6.21
Superficial Muscles: Posterior
Figure 6.22
G. Muscular Development
 In embryo, muscular system develops quickly
 Muscles have to cover and move bones of limbs
 Nervous system invades muscles to allow
conscious control
 Skeletal movements occur by 16th week of
development
 Fetus will start moving around 14th week
 Sucking thumb, tugging, kicking
Fetus at 16 weeks
 Development occurs in:
 cephalic/caudal direction (head to toe)
 Can raise its head before it can sit up
 Can sit up before it can walk
 Proximal/distal direction
 Can wave “bye-bye” before it can hold a pencil
 Due to rich blood supply, skeletal muscles are
 resistant to infection
 able to repair/regenerate selves very efficiently
 Aging will alter muscle ability and can lead to atrophy
 Amount of connective tissue increases, muscle tissue
decreases
 Leads to stringy/sinewy muscles
 Leads to decreased body weight/mass
 Muscle strength decreases by about 50% by age 80
 Continued or new dedication to weight-bearing
exercise (pumping iron) will offset or reverse effects
Jack LaLanne, at age 83 (left), and 93 (right)
 Often referred to as the Godfather of Fitness, Jack Lalane was a
pioneer in American fitness. He advocated healthy eating and
daily weight training exercises starting in the 1930s.
H. Diseases/Homeostatic Imbalances
 Two major diseases affect muscles:
 Muscular dystrophy: genetic disease group
in which muscles degenerate due to fat and
connective tissue deposits
 Myasthenia gravis: autoimmune disease in
adults of general weakness and fatigability as a
result of shortage of ACh receptors
Muscular Dystrophy (MD)
 Nine different types of muscular
dystrophy in which all are
genetic and result in
degeneration of voluntary and
sometimes involuntary muscles
 Most common (and most
serious) type is Duchenne’s MD
 X-linked (affects males almost
always)
 Diagnosed between ages 2 – 6
Active, normal-appearing children
become clumsy and begin to fall as
muscles start to weaken
First muscles stricken are around hips,
pelvis, thighs, and shoulders
By early teens, attacks involuntary
muscles like heart and respiratory
muscles
A group of interdependent
proteins along the
membrane surrounding
each fiber helps to keep
muscle cells working
properly. When one of
these proteins, dystrophin,
is absent, the result is
Duchenne muscular
dystrophy; poor or
inadequate dystrophin
results in Becker
muscular dystrophy.
Myasthenia Gravis (MG)
 Chronic autoimmune neuromuscular disease
characterized by varying degrees of weakness of the
skeletal (voluntary) muscles of the body.
 First signs are weakness in head and neck muscles
 droopy eyelids (orbicularis oculi), difficulty chewing
(masseter), swallowing & talking
 May eventually lead to difficulty breathing
 Result of shortage of ACh
receptors available to receive
ACh
 Antibodies bind to ACh
receptors which prevent
them from binding Ach
 Body thinks receptors are
foreign body so produces
antibodies to fight it off
 Receptors not triggered lead
to weakened contractions
The End
Test Wednesday, November 23