ANATOMY AND PHYSIOLOGY

CHAPTER 7: Muscular System control, while smooth and cardiac muscles contract
spontaneously or through involuntary signals.
7.1 FUNCTIONS OF THE MUSCULAR
SYSTEM 3. EXTENSIBILITY: Muscles can stretch beyond
their usual length and still contract. For example,
Movement in the body arises through cilia, gravity, you can stretch to reach something while
or muscle contractions, with muscles being the main maintaining the ability to retrieve it.
source.
4. ELASTICITY: Muscles can bounce back to their
There are three muscle types: original length after being stretched.
1. Skeletal
2. Cardiac
3. Smooth 7.3 SKELETAL MUSCLE ANATOMY

Whole Skeletal Muscle Anatomy

Key functions of the muscular system include
1. Body movement Skeletal muscle makes up about 40% of body
2. Posture maintenance weight, attached to skeleton or skin, showing
3. Respiration striations under a microscope. Individual muscles
4. Heat production like biceps are complete organs with muscle, nerve,
5. Communication connective, and adipose tissues. Discussion begins
6. Organ/vessel constriction at organ level, ends at cellular level (muscle fibers).
7. Cardiac contraction for blood circulation. Connective Tissue Coverings

Skeletal muscles have three connective tissue

layers:
 EPIMYSIUM - surrounds entire muscle
 PERIMYSIUM - divides into fascicles with
blood vessels and nerves
 ENDOMYSIUM - separates individual muscle
fibers.
These layers merge into tendons connecting muscle
to bone.

Connective Tissue Coverings

 Skeletal muscle fibers are large cells with many
nuclei, ranging from 1mm to 30cm in length.
 Muscle size varies, with striated appearance
from light and dark bands.
 Muscle growth is due to larger fibers, not more
fibers.
 Exercise-induced muscle enlargement comes
from larger fibers, not increased numbers.
7.2 GENERAL PROPERTIES OF MUSCLE
Histology of Muscle Fibers
TISSUE
Understanding muscle contraction involves muscle
Muscle tissue is specialized with four key traits:
fiber structure: electrical and mechanical
1. CONTRACTILITY: Muscles can forcefully components. Muscle fiber parts categorized by their
shorten (contract), causing movement in structures roles in contraction.
they're attached to. Skeletal muscles move bones,
smooth muscles affect organ pressure, and cardiac
muscles impact heart pressure. Muscles also
passively lengthen due to opposing forces like
gravity or fluid pressure.
2. EXCITABILITY: Muscles can respond to stimuli.
Skeletal muscles contract via conscious nerve
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Structure of a Muscle
(a) Skeletal muscle components organization:
Epimysium surrounds whole muscle, perimysium
encloses fascicles, endomysium covers individual
fibers. Muscle fibers contain myofibrils made of
myofilaments. (b) Muscle fiber enlargement with
myofibrils, sarcoplasmic reticulum with terminal
cisternae and T-tubules forming triads.
Electrical Component Structures
Excitability is vital in skeletal muscle
Components for electrical signal response:
1. Sarcolemma – muscle fiber membrane.
2. Transverse tubules (T tubules) – extensions
of sarcolemma.
3. Sarcoplasmic reticulum – Ca²⁺ store,
releasing it for contraction. Triad formed by
T tubules and terminal cisternae.
Mitochondria and glycogen in sarcoplasm.
Mechanical Component Structures
Muscle's contractility is due to two main structures
in muscle fibers:
1. Myofibrils are bundles of protein in muscle
fibers, extending lengthwise.
2. Myofilaments consist of actin (thin) and
myosin (thick), forming sarcomeres, the
units of muscle contraction. Sarcomeres'
myofilaments cause muscle shortening.
Skeletal Muscle Fiber
a. Electron micrograph of skeletal muscle showing
multiple sarcomeres in a muscle fiber.
b. Diagram of adjacent sarcomeres, composed of
actin and myosin myofilaments. Z disks anchor
actin, M line holds myosin.
c. Actin myofilaments: actin (purple spheres),
tropomyosin (blue strands), troponin (red
spheres).
d. Myosin myofilaments made of golf-club-shaped
myosin molecules with heads in opposite
directions.
Sarcomeres
 Sarcomeres are the smallest contractile units in
muscles, formed by joining myofibrils.
 They have Z disks that anchor actin
myofilaments, giving the striated appearance.
 Each sarcomere has I bands (lighter) containing
actin, and A bands (darker) containing
overlapping actin and myosin myofilaments,
with an H zone in the middle of A band
containing only myosin.
 The M line holds myosin in place.
 Myofibrils align to create the striated pattern.
Actin and Myosin Myofilament Structure
Actin Myofilaments
Actin myofilaments are made of three proteins:
1. Actin
2. Tropomyosin
3. Troponin
Actin has attachment sites for myosin during
contraction.
 TROPOMYOSIN covers actin's attachment
sites in relaxed muscle.
 ANATOMY AND PHYSIOLOGY
 TROPONIN has subunits: anchors to actin,
prevents tropomyosin block, binds Ca²⁺.
Troponin and tropomyosin control muscle
contraction timing.
Myosin Myofilaments
 Myosin myofilaments are made of elongated
myosin molecules resembling golf clubs.
 Each myosin molecule has a rod portion and
two heads.
 The heads:
1. bind to actin for muscle contraction
2. are hinged for bending during contraction,
3. break down ATP, releasing energy. Energy
bends the hinge during contraction.
Neuromuscular Junction Structure
 Neuromuscular Junction Structure:
o Muscle fiber contacts motor neuron axon
branch from brain/spinal cord.
o Motor neurons trigger muscle fiber action
potentials for contraction.
o Contact point = neuromuscular junction or
synapse.
o Junction consists of:
1. Axon terminals: Enlarged motor neuron
axon endings.
2. Muscle fiber sarcolemma: Innervated
muscle fiber area
o Axon terminal = presynaptic terminal.
o Space between terminal and fiber =
synaptic cleft.
o Muscle cell membrane at junction = motor
end-plate or postsynaptic membrane.
o Presynaptic terminal contains:
 Mitochondria.
 Synaptic vesicles: Hold
neurotransmitter acetylcholine
(ACh).
 Neurotransmitter:
o Enables neuron-target communication.
o Released from presynaptic membrane,
diffuses across synaptic cleft.
o Affects muscle fiber activity by
stimulating/inhibiting action potentials.
o Acts on ligand-gated ion channels:
 Specialized membrane proteins.
 Open/close due to specific molecules
(neurotransmitters)
 Ligands bind to channels.
o Opened channels allow ion movement
across cell membrane.
Sliding Filament Model
 Skeletal muscle cells' main function: Generate
force through contraction.
 Myofilaments in sarcomere's parallel
arrangement interact for contraction.
 Contraction explained by sliding filament
model.
 During contraction, actin and myosin
myofilaments slide past each other, shortening
sarcomere.
 Myofilaments retain length from resting state.
 Sarcomere and myofibril shortening causes
muscle fiber, fascicle, and muscle shortening.
 Muscle contraction countered by external
forces, like gravity or opposing muscles.
 Muscles lengthen during relaxation due to
external forces.
 Understanding muscle contraction involves
considering electrical properties of muscle
fibers.
7.3 SKELETAL MUSCLE FIBER
PHYSIOLOGY
Excitability of Muscle Fibers
 Muscle fibers have two key components:
1. electrical
2. mechanical.
 Muscle fibers are electrically excitable.
 Electrical properties of skeletal muscle fibers
described here.
 Action potentials from brain/spinal cord trigger
muscle fiber contraction.
 Electrically excitable cells exhibit polarization:
o inside negatively charged vs. outside.
 Resting membrane potential: Voltage difference
across unstimulated cell membrane
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Ion Channels
 To understand skeletal muscle fiber electrical
properties, review membrane permeability and
transport proteins' role.
 Cell membrane's hydrophobic interior impedes
ion movement.
 Skeletal muscle cell electrical properties rely on
ion movement.
 Ions cross cell membrane via ion channels.
 Two major ion channel types: leak and gated.
 Leak channels allow slow ion leak based on
concentration gradient.
 Gated channels vital in stimulated cells.
 Gated channels presence influences ion
movement during cell excitation.
The Resting Membrane
Electrically excitable cells, like neurons and muscle
fibers, have an electrical difference across their
outer walls. This difference is called the "resting
membrane potential," which is like a ready-to-go
state. Three things create this potential:
1. Different Ions Inside and Outside: There are
more positively charged potassium ions (K+)
inside the cell and more positively charged
sodium ions (Na+) outside. There are also
negatively charged molecules stuck inside.
2. Ion Movement: Potassium ions have an easier
time moving out of the cell than sodium ions
have getting in. This makes the inside of the cell
more negative compared to the outside.
3. Sodium-Potassium Pump: A special pump
works to keep this difference by moving
potassium ions in and sodium ions out. This
pump uses energy to maintain this setup.
In simple terms, the resting membrane potential is
like a charged balance that makes cells ready to
respond to signals. It's caused by the difference in
ion concentrations and how they move, helped by a
special pump that keeps the balance.
Action Potentials
When a cell gets a signal, it can have something like
an "electric flip." This is called an "action
potential." Imagine a battery turning upside down
for a moment.
1. Starting State: Normally, the inside of the cell
has a different charge than the outside. Think of
it like a battery that's not being used. Special
doors that allow sodium (Na+) and potassium
(K+) ions in and out are closed.
2. Getting Charged: When the cell gets a signal,
the doors for sodium open. Positive sodium ions
rush inside, making the cell more positive inside
than outside. This is called "depolarization." If
this charge becomes strong enough, it triggers
an action potential.
3. Flipping Back: To go back to the normal state,
the doors for potassium open, and the positive
potassium ions go out. This makes the inside
negative again. This is "repolarization."
4. Resetting: The action potential doesn't last long,
only a tiny moment. After it's done, the cell goes
back to its usual state, like a battery that's right
side up again. A special pump helps put things
back in place.
In simple terms, an action potential is like a quick
electrical switch that happens when a cell gets a
signal. It starts with positive ions rushing in and
ends with them rushing out, making everything go
back to normal.
 ANATOMY AND PHYSIOLOGY
The Function of the Neuromuscular Junction
The neuromuscular junction is where a motor
neuron connects with a muscle fiber, allowing
muscle contraction.
1. When the neuron's action potential reaches
its end, calcium ions enter, causing vesicles
to release acetylcholine.
2. Acetylcholine crosses the gap and binds to
the muscle fiber, opening sodium channels.
3. Sodium enters, causing depolarization and
muscle action potential.
4. Acetylcholine unbinds, sodium channels
close, and acetylcholinesterase breaks down
acetylcholine.
5. Choline is reabsorbed, combines with acetic
acid to make more acetylcholine.
6. This recycling conserves energy and
maintains muscle responsiveness.
In simple terms, the neuromuscular junction works
like a messenger sending notes to a light switch.
The notes make the switch let in positive stuff,
which makes the muscle light up. Then the
messenger cleans up the notes and gets ready to
send more.
Muscle Contraction Process:
1. Action potential travels along motor neuron.
2. Ca2+channels in neuron open due to action
potential.
3. Ca2+ influx triggers acetylcholine release.
4. Acetylcholine opens Na+,channels in
sarcolemma.
5. Action potential travels through sarcolemma.
6. Action potential moves through T tubules.
7. T tubules activate Ca2+ channels in
sarcoplasmic reticulum.
8. Ca2+released from sarcoplasmic reticulum into
sarcoplasm.
9. Ca2+binds to troponin on actin myofilaments.
10. Binding shifts tropomyosin, exposing actin
binding sites.
11. Myosin heads bind to actin, forming cross-
bridges.
12. ATP breaks into ADP and P, releasing energy for
myosin movement.
13. Myosin heads bend, sliding actin over myosin
(contraction).
14. Cycle continues as long as Ca2+ is present.
Cross-Bridge Movement
1. Myosin head stores energy from previous ATP
breakdown.
2. Ca2+ causes myosin heads to bind to actin.
3. Myosin heads move (power stroke), pulling
actin.
4. ATP binding detaches myosin from actin.
5. Myosin breaks ATP into ADP and P, staying
ready.
6. Myosin heads return to "high-energy" position
(recovery stroke).
 ANATOMY AND PHYSIOLOGY
7. Myosin binds farther down actin, shortening
sarcomere.
Muscle Relaxation
Muscle relaxation occurs when acetylcholine
release stops at the neuromuscular junction. This
halts action potentials, preventing Ca2+ release
from the sarcoplasmic reticulum. Ca2+ is pumped
back into the sarcoplasmic reticulum, decreasing its
concentration in the sarcoplasm. This causes Ca2+
to dissociate from troponin and tropomyosin,
blocking actin attachment sites. Without cross-
bridges, the muscle relaxes. Muscle relaxation
requires ATP:
1. The sodium-potassium pump transports
Na+ out and K+ into the muscle fiber to
maintain membrane potential.
2. ATP detaches myosin heads for the
recovery stroke.
3. ATP transports Ca2+ into the
sarcoplasmic reticulum. Muscle
relaxation is slower due to slower Ca2+
return, taking at least twice as long as
contraction.
7.5 WHOLE SKELETAL MUSCLE
PHYSIOLOGY
The Muscle Twitch
 The muscle twitch is a muscle fiber's response
to a single motor neuron action potential.
 It has three phases:
1. Lag
2. Contraction
3. Relaxation
 While typically observed in lab settings, it
represents a complete cycle of muscle
activation.
Phases of Muscle Twitch
A twitch has three phases
1. lag phase, starting from stimulus application
to motor neuron until contraction initiation,
involving action potential travel and Ca2+
release;
2. contraction phase, beginning with Ca2+-
induced cross-bridge formation; and
3. relaxation phase, lasting longer due to slow
Ca2+ return to the sarcoplasmic reticulum.
Types of Muscle Contractions
There are two main types
1. isometric contractions, where muscle tension
increases but length remains unchanged
(e.g., holding a heavy object); and
2. isotonic contractions, causing muscle
shortening, increasing tension (e.g., lifting
an object). Isotonic contractions can change
with varying force requirements.
Muscle contraction strength changes due to
1. summation, the force in an individual
muscle fiber, and
2. recruitment, the force in the entire muscle
based on the number of contracting fibers.
Increasing overall force in a muscle relies on
the total number of active muscle fibers.
Remember, a twitch can refer to the contraction
of a single muscle fiber, a motor unit, or the
whole muscle. Understanding motor units is
crucial before exploring individual fiber
responses.
Motor units
- Motor units composed of motor neurons and
innervated muscle fibers, cause muscle
contractions. Motor units vary in size and
 ANATOMY AND PHYSIOLOGY
sensitivity, enabling precise or powerful Types of Isotonic and Isometric Contractions
movements. Small motor units are precise
 Concentric Contractions: Muscle tension
(e.g., eye muscles), while large units are for
overcomes resistance, muscle shortens.
powerful contractions (e.g., thigh muscles).
- Used in movements like lifting a
backpack.
 Eccentric Contractions: Muscle tension
Force of Contraction in Individual Muscle Fibers
maintained, resistance causes muscle to
 Muscle contractions can vary in strength, from lengthen.
weak to strong, based on the response to stimuli. - Seen in controlled weight lowering.
Muscles can lift heavy weights because - Can lead to muscle injury during
individual muscle fibers generate different repetitive eccentric exercise.
amounts of force. This force depends on cross-
bridges formed within the fiber. More cross- 7.6 MUSCLE FIBER TYPES
bridges mean stronger contractions, similar to  Two main types of skeletal muscle fibers:
multiple people lifting together. Frequency of - slow-twitch
stimulation increases cross-bridge formation. At - fast-twitch.
low frequencies, muscle twitches are all-or-
 Skeletal muscles vary in function due to
none, but with higher frequencies, twitches
differing muscle fiber composition.
merge into wave summation, incomplete
 Muscle fibers contain distinct forms of
tetanus, and complete tetanus due to longer
myosin.
mechanical versus electrical events. This leads
 Slow-twitch myosin: contracts slowly,
to sustained contractions without relaxation
fatigue-resistant.
between twitches.
 Fast-twitch myosin: contracts quickly,
fatigues rapidly.
 Proportion of fiber types varies within
muscles.

When the frequency of signals to muscles goes up from 1 to 4, relaxation

between signals decreases. At frequency 1, muscles twitch and relax fully. At
frequencies 2-3, relaxation decreases, causing incomplete tetanus. At
frequency 4, there's no relaxation, causing complete tetanus.

Contractions in Whole Muscles Slow-Twitch Muscle Fibers

Muscle Tone:  Type I muscle fibers contract slowly, resist
Constant tension in muscles over time. fatigue.
 Have better blood supply, more mitochondria.
 Keeps back, lower limbs straight, head  Break down ATP slowly, myosin heads have
upright, abdomen flat. slow ATP enzyme.
 Depends on a small percentage of motor  Produce ATP using O2, called oxidative fibers.
units contracting out of phase.  Contain myoglobin for O2 storage during
 Nerve impulse frequency causes incomplete activity.
tetanus, maintaining tension.
 ANATOMY AND PHYSIOLOGY
Fast-Twitch Muscle Fibers o Anaerobic ATP production during intense
short-term exercise.
 Type II muscle fibers contract quickly, fatigue
o Aerobic ATP production during most
faster.
exercise and normal conditions.
 Myosin heads have fast ATP enzyme for rapid
 Pathways operate at different timeframes:
cross-bridges.
1. Immediate upon contraction
 Fewer mitochondria, less myoglobin, more
2. Short-term contraction
glycogen.
3. Prolonged contraction over hours.
 ATP produced quickly without O2.
 Type IIa use ATP with and without O2, IIb use
ATP without O2.
Adenylate Kinase and Creatine Kinase
Distribution of Fast-Twitch and Slow-Twitch Adenylate Kinase and Creatine Kinase in Muscle
Muscle Fibers Fibers:
 Animal muscles: fast-twitch are pale, slow-
 Enzymes for quick ATP production.
twitch are dark.
 Add 15 seconds of contraction beyond initial 5–
 Human muscles have both fiber types, ratio
6 seconds from stored ATP.
varies.
 Adenylate kinase transfers phosphate from one
 Training enlarges and enhances both fiber types.
ADP to another, forming ATP and AMP.
 Intense exercise: weight lifting grows fast-
 Creatine kinase transfers phosphate from
twitch, vascularity.
creatine phosphate to ADP to create ATP.
 Exercise with O2: slow-twitch grows, endurance
improves.
ATP Production in Skeletal Muscle:
 Adenylate kinase converts ADP to ATP (few
Exercise Effects
seconds).
 Muscle hypertrophy (increase in size and  Creatine kinase uses creatine phosphate for
strength) with exercise. ATP (5-6 seconds).
 Muscle atrophy (decrease) with lack of use.  Anaerobic respiration for intense exercise
 Muscle fiber number remains relatively (additional 40 seconds).
constant.  Aerobic respiration for prolonged exercise
 Nuclei added through satellite cells in response (hours).
to exercise.
 Improved endurance due to better metabolism,
Anaerobic Respiration:
circulation, capillaries, respiration, heart
capacity.  No O2 required.
 Glucose breakdown produces ATP and
lactate
 Provides ATP for 30–40 seconds.
 Begins with glycolysis, forming pyruvate
7.7 ENERGY SOURCES FOR MUSCLE
and then lactate.
CONTRACTION
 Skeletal muscle fibers use three main ATP-
dependent proteins: myosin head, Na+/K+ Aerobic Respiration:
pump, and Ca2+ pump.
 Requires O2.
 Muscle contraction and relaxation need ATP.
 Glucose breakdown produces ATP, CO2,
 Muscle fibers store limited ATP for about 5-6
and H2O.
seconds of contraction.
 Supplies 95% of ATP for a cell.
 Four processes for ATP production in muscle
fibers:  More efficient than anaerobic respiration.
o Adenylate kinase converts 2 ADP to 1  Up to 36 ATP from one glucose molecule.
ATP and 1 AMP.  Occurs in mitochondria.
o Creatine kinase transfers phosphate from
creatine phosphate to ADP, forming ATP.
 ANATOMY AND PHYSIOLOGY
ATP Production as Exercise Progresses
 Initial ATP reserve depletes quickly.
 Adenylate kinase and creatine kinase
produce ATP.
 Anaerobic respiration dominant after initial
ATP depletion
 Fast-twitch fibers break down glucose to
lactate.
 Lactate shuttled to slow-twitch fibers for
ATP or to blood for energy elsewhere.
 Fast-twitch anaerobic and slow-twitch
aerobic pathways work together.
Muscle Fatigue
 Temporary reduced work capacity.
 Mechanisms:
1. acidosis and ATP depletion
2. oxidative stress
3. local inflammation.
Acidosis and ATP Depletion:
 Anaerobic respiration breaks down glucose
to lactate and protons, reducing pH.
 Lowered pH leads to decreased Ca2+
effectiveness on actin and reduced Ca2+
release.
 Lactic acidosis from reduced lactate
clearance due to liver dysfunction or
increased anaerobic respiration.
 Muscle fatigue correlates with localized ATP
decreases or specific transport system
changes.
Oxidative Stress:
 Intense exercise increases ROS, breaking
down proteins, lipids, nucleic acids.
 ROS triggers IL-6, causing inflammation
and muscle soreness.
Inflammation:
 Exercise activates immune system, T
lymphocytes migrate to worked muscles.
 Immune system intermediates increase pain
perception.
Muscle Fatigue:
 Physiological contracture due to low ATP
binding to myosin, preventing muscle
relaxation.
 Psychological fatigue involves CNS
perception of muscle contraction
impossibility.
Oxygen Deficit and Excess Postexercise Oxygen
Consumption:
 Oxygen deficit: insufficient O2
consumption at exercise onset, repaid
during and after exercise.
 Excess postexercise oxygen consumption:
elevated O2 consumption after exercise,
restores homeostasis.
Muscle Soreness:
 After intense exercise, muscle pain due to
inflammatory chemicals affecting fibers.
 Enzymes from injured fibers detected in
extracellular fluid, collagen fragments
indicate damage.
 Rest periods aid muscle tissue repair.
7.8 SMOOTH MUSCLE AND CARDIAC
MUSCLE
 Smooth muscle cells: small, spindle-shaped,
one nucleus, less actin/myosin.
 No sarcomere organization, not striated,
slower contraction, no oxygen deficit.
 Involuntary control, hormone-stimulated
contraction, some autorhythmicity.
 Layers with gap junctions for synchronized
contraction.
 Cardiac muscle cells: long, striated,
branching, one nucleus.
 Sarcomeres present but less uniform, less
distinct striation.
 Contraction rate between smooth and
skeletal muscle.
 Autorhythmic, sustained by aerobic
respiration, connected by intercalated disks.
 Involuntary control, hormone influence.
 ANATOMY AND PHYSIOLOGY
7.9 GENERAL PRINCIPLES OF SKELETAL 5. Origin and Insertion: Origin and insertion points
MUSCLE ANATOMY (e.g., sternocleidomastoid).
6. Number of Heads: Number of origins (e.g.,
biceps - two heads).
7. Function: Reflects muscle's action (e.g.,
abductors move away from midline).
Understanding these traits simplifies learning
muscle names.

 Muscles extend between bones and cross joints,

connected by tendons.
 Tendons come in various forms: long, broad
(aponeuroses), or short.
 Retinaculum holds tendons at wrists and ankles.
 Muscle contraction moves bones at joints,
causing body movement.
 Some muscles attach to skin, like facial muscles
during smiling.
 Muscle attachment points: origin (stationary
end) and insertion (moving end).
 Multiple origins are called heads; insertion
attached to moving bone.
 The muscle belly is between origin and
insertion.
 Muscle action causes specific body movement.
 Muscles work in groups: agonists (cause action)
and antagonists (oppose action).
 Synergists work together in muscle groups for
movements.
 Prime mover is the main muscle causing desired
movement.
 Fixators stabilize bones during distal bone
movement.
 Some muscles belong to multiple groups based
on movement type.

Muscle Names
Muscle Naming Criteria:
1. Location: Muscle named after where it is
situated (e.g., pectoralis in the chest).
2. Size: Reflects muscle size (e.g., gluteus
maximus - large, gluteus minimus - small).
3. Shape: Describes muscle shape (e.g., deltoid -
triangular).
4. Fascicle Orientation: Fascicle direction relative
to associated structure (e.g., rectus - straight).
 ANATOMY AND PHYSIOLOGY
 Muscles around the mouth contribute to lip and
skin movements:
1. Orbicularis oris encircles the mouth.
2. Buccinator is in cheek walls; used in
puckering and flattening cheeks
(whistling/blowing)
 Smiling involves zygomaticus muscles lifting
upper lip and mouth corner.
 Sneering is done by levator labii superioris
raising one side of the upper lip.
 Frowning and pouting involve depressor anguli
oris, depressing mouth corner.

 Surface anatomy aids in understanding muscle

anatomy.
 Visible muscles in upper and lower limbs
identified.
 Muscle details in head, neck, trunk, and limbs
explained later.
 Chapter tables provide summary for studying
muscular system.
 Locate muscle on figure, then find description in
table.
 Group muscles by actions, practice actions to
remember details.
 Study one muscle table at a time for better
understanding.

7.10MUSCLES OF THE HEAD AND NECK

The muscles of the head and neck include those
involved in forming facial expressions, chewing,
moving the tongue, swallowing, producing sounds,
moving the eyes, and moving the head and neck.
Facial Expression
 Human facial expressions are crucial for
nonverbal communication.
 Muscles around the eyes and eyebrows play a
role in facial movements:
1. Occipitofrontalis raises eyebrows.
2. Orbicularis oculi tightly closes eyelids
and creates wrinkles at eye corners.
Mastication
 Mastication involves chewing with strong
muscles.
 Four pairs of chewing muscles:
1. Temporalis muscle
2. Masseter muscle
3. Pterygoid muscles (two pairs)
 Temporalis and masseter muscles visible on
head's side during chewing.
 Pterygoid muscles beneath the mandible.
 ANATOMY AND PHYSIOLOGY
 Lateral/posterior neck muscles rotate and
laterally flex head.
 Key muscle: sternocleidomastoid (SCM).
 SCM contraction: one side rotates head, both
sides flex/extend head-neck.

Tongue and Swallowing Muscles

 Tongue's importance: mastication and speech.
 Tongue's functions: moves food, holds food with
buccinator muscle, initiates swallowing.
 Tongue muscles:
1. intrinsic (inside tongue, shape change),
2. extrinsic (outside, move tongue).
 Swallowing involves:
1. hyoid muscles,
2. soft palate,
3. pharynx, (throat)
4. larynx (voicebox)
 Hyoid muscles
- suprahyoid (above hyoid bone),
- infrahyoid (below hyoid bone).
 Suprahyoid muscles stabilize hyoid, infrahyoid
muscles elevate larynx during swallowing.
 Soft palate and pharynx muscles prevent food
entering nasal cavity, elevate and constrict
during swallowing.
7.11 TRUNK MUSCLES
 Pharyngeal elevators lift pharynx,
 Pharyngeal constrictors push food down Trunk muscles include those that move (1) the
esophagus. vertebral column, (2) the thorax, (3) the abdominal
 Pharyngeal muscles also open auditory tube to wall, and (4) the pelvic diaphragm and perineum
equalize ear pressure (e.g., chewing gum when Vertebral Column Muscles
changing altitude).
 Erect posture in humans maintained by strong
back muscles.
 Erector spinae group of muscles on each side of
the back: main role in keeping back straight and
body erect.
 Deep back muscles between spinous and
transverse processes: responsible for vertebral
column movements - extension, lateral flexion,
rotation.
 Abnormal stretching or tearing of deep back
muscles: muscle strains, ligament sprains in
lumbar region, leading to low back pain.
Neck Muscles  Treatments: anti-inflammatory medication,
RICE (rest, ice, compression, elevation).
 Deep neck muscles:  Low back exercises beneficial for addressing the
1. neck flexors issue.
2. neck extensors.
 Flexors originate on front vertebral bodies.
 Extensors originate on back vertebral bodies.
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2. Internal abdominal oblique
3. Transversus abdominis
 Muscle layers contract to flex/rotate vertebral
column or compress abdominal contents.

Thoracic Muscles
 Thoracic Muscles are primarily responsible for
breathing.
 External intercostals: Elevate ribs during
inhalation.
 Internal intercostals: Depress ribs during forced
exhalation.
 Diaphragm: Dome-shaped muscle, contracts to
flatten, increasing thoracic cavity volume for
inhalation.
 Diaphragm's contraction leads to inspiration in
quiet breathing.
Pelvic Diaphragm and Perineal Muscles
 The pelvis is a ring of bone with an opening
closed by a muscular floor.
 This floor is known as the pelvic diaphragm.
- It comprises the coccygeus
muscle and the levator ani
muscle.
 Below the pelvic diaphragm lies the perineum,
shaped like a diamond.
 The perineum is divided into the urogenital
triangle (front) and anal triangle (back).
 Pregnancy can stretch the pelvic diaphragm and
urogenital muscles.
 Special exercises can strengthen these muscles
during pregnancy.

Abdominal Wall Muscles

 Anterior abdominal wall muscles: Flex and
rotate vertebral column, compress abdominal
cavity, protect organs.
 Linea alba: Tendinous area, white connective
tissue, runs from sternum to pubis.
 Rectus abdominis: Straight muscle, tendinous
intersections create segmented appearance.
 Muscle layers lateral to rectus abdominis:
1. External abdominal oblique
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Arm Movements
 Pectoralis major and latissimus dorsi muscles
attach arm to thorax.
 Pectoralis major: Adducts and flexes shoulder,
extends from flexed position.
 Latissimus dorsi: Medially rotates, adducts arm,
and extends shoulder.
- Latissimus dorsi known as
"swimmer's muscle" due to its
role in freestyle stroke.

7.12 UPPER LIMB MUSCLES

Upper limb muscles attach the limb and pectoral
girdle to the body. They are found in the arm,
forearm, and hand.
Scapular Movements
 Upper limb connected to body by muscles:
1. Trapezius: Shoulder to neck, upper line.
2. Levator scapulae: Raises scapula.
3. Rhomboids: Scapular attachment.
4. Serratus anterior: Scapular origin, lateral
thorax.
5. Pectoralis minor: Scapular attachment.
 Muscles act as fixators for scapular stability.
 Scapular muscles allow various positions and
upper limb movement.
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 Rotator cuff muscles stabilize shoulder joint,

especially during arm abduction.
 Form a cuff over proximal humerus.
 Rotator cuff injury involves damage to these
muscles/tendons.
 Deltoid muscle: Attaches humerus to
scapula/clavicle, major upper limb abductor.
 Pectoralis major: Upper chest, deltoid: Rounded
shoulder mass.
 Deltoid often used for injections.

Forearm Movements
 Arm divided into anterior and posterior
compartments.
 Posterior compartment: Triceps brachii, primary
elbow extensor.
 Anterior compartment:
1. Biceps brachii: Primary elbow flexor.
2. Brachialis: Primary elbow flexor.
 Brachioradialis: Assists in elbow flexion,
despite being a posterior forearm muscle.
Supination and Pronation
 Supination: Turning flexed forearm with palm
up.
o Muscles: Supinator, Biceps Brachii (also
flexes elbow).
 Pronation: Turning forearm with palm down.
o Muscles: Two pronator muscles.
Wrist and Finger Movements
 Forearm muscles can be divided into
anterior and posterior groups.
 Anterior forearm muscles flex the wrist and
fingers, while posterior forearm muscles
extend them.
 The retinaculum is a fibrous tissue that
holds flexor and extensor tendons in place
around the wrist.
 Carpal tunnel syndrome can result from
limited retinaculum flexibility.
 Flexor carpi muscles flex the wrist;
extensor carpi muscles extend it.
 Flexor carpi radialis tendon helps locate the
radial pulse.
 Overuse of wrist extensor muscles can lead
to "tennis elbow."
 Flexor digitorum facilitates finger flexion;
extensor digitorum handles extension.
 Intrinsic hand muscles are within the hand,
responsible for various thumb and finger
movements.
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 Interossei muscles between metacarpal
bones manage finger abduction and
adduction.
 Intrinsic muscles contribute to thumb and
finger movements and fleshy areas between
thumb and little finger, and between thumb
and index finger.
7.12LOWER LIMB MUSCLES
The muscles of the lower limb include those located
in (1) the hip, (2) the thigh, (3) the leg, and (4) the
foot.
Thigh Movements
 Hip muscles attach to femur via hip bone
 Iliopsoas flexes hip
 Posterior and lateral hip muscles: gluteal
muscles and tensor fasciae latae.
 Tensor fasciae latae tenses iliotibial tract to
stabilize femur-tibia standing.
 Gluteus maximus: extends, abducts, laterally
rotates thigh (buttocks mass).
 Gluteus medius: abducts, medially rotates thigh
(smaller mass above maximus).
 Optimal gluteus maximus function: hip
extension with flexed thigh at 45-degree angle.
 Thigh muscles also connect to hip bone, moving
thigh:
1. Anterior: flex hip.
2. Posterior: extend hip.
3. Medial: adduct thigh.
Leg Movements
 Anterior Thigh Muscles:
 Quadriceps femoris (four muscles)
 Primary knee extensors
 Common insertion: patellar tendon
 Patellar ligament extension onto tibial
tuberosity
 Vastus lateralis used for injections
 Sartorius:
o Longest muscle in body
o Flexes hip and knee
o Rotates thigh laterally for cross-
legged sitting
 Posterior Thigh Muscles (Hamstrings):
 Responsible for knee flexion
 Easily felt tendons on medial and lateral
posterior knee
 Named after hog tendons used to hang
hams
 Wolves disable prey by biting hamstrings
 Medial Thigh Muscles (Adductors):
 Adduct the thigh
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Ankle and Toe Movements
 Leg muscles categorized into three groups:
anterior, posterior, and lateral.
 Anterior muscles involved in foot dorsiflexion
and toe extension.
 Posterior muscles (gastrocnemius, soleus) in
calf, flexors for foot plantar flexion.
 Deep posterior muscles responsible for foot
inversion, toe flexion.
 Lateral fibularis muscles aid foot eversion and
plantar flexion.
 Intrinsic foot muscles (20 in total) control toe
movements: flexion, extension, abduction,
adduction.
 Intrinsic foot muscles organized similarly to
hand's intrinsic muscles.
REPRESENTATIVE DISEASES AND
DISORDERS: Muscular System