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MUSCULAR SYSTEM

 Body movement (locomotion)


 Maintenance of posture
 Respiration (diaphragm and intercostal contractions)
 Communication (Verbal and Facial)
FUNCTIONS
 Constriction of organs and vessels (peristalsis of intestinal tract; vasoconstriction of blood
vessels & other structures [pupils])
 Heartbeat
 Production of body heat (Thermogenesis) (e.g. sweating (skin & shivering, goosebumps (skin))
1. EXCITABILITY: capacity of muscle to respond to a stimulus
2. CONTRACTILITY: ability of muscle to shorten and generate pulling force
PROPERTIES OF MUSCLE
3. EXTENSIBILITY: muscle can be stretched back to its original length
4. ELASTICITY: ability of muscle to recoil to original resting length after stretched.
TYPES OF MUSCLE (according to function)
A. SKELETAL MUSCLE SKELETAL- attached to bones
 Makes up 40% of body weight; makes up great mass of the somatic musculature
 Responsible for locomotion, facial expressions, posture, respiratory movements,
other types of body movement
 Voluntary in action; controlled by somatic motor neurons.
 Skeletal muscles are made up of thousands of muscle fibers
 A single motor neuron (where the action potential will go down) may directly control a few
fibers or hundred to thousands of muscle fibers
 All of the muscle fibers controlled by single motor neuron constitute a motor unit.
 The size of the motor unit determines how fine the control of movement can be-
o Small motor units – precise control (eye muscles)
o Large motor units – gross control (leg muscles)
 Recruitment is the ability to activate more motor units as more force (tension) needs to be
generated.
 There are always some motor units active, even when at rest. This creates a resting tension
known as muscle tone which helps stabilize bones and joints and prevents atrophy.
o Atrophy: it doesn’t contract properly because there’s a decrease in the original size
thus declining its function; decrease in size

 Isotonic contraction: as tension increases (more motor units recruited, length of muscle
changes usually resulting in movement of a joint. The tension (load) on a muscle stays
constant (iso= same, tonic=tension) during a movement. (E.g. lifting a baby, picking up object,
walking)

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 Isometric contraction: no change in length of muscle even as tension increases. The length of
a muscle stays contestant (iso=same, metric=length) during a contraction (E.g. holding a baby
at arm’s length, pushing against a closed door). Necessary in everyday life to counteract
effects of gravity (e.g. postural muscles keeping a head up.)

 A motor unit is a motor neuron and all the muscle fibers it supplies; consists of somatic motor
neuron
 The number of muscle fibers per motor unit can vary from a few (4-6) to hundreds (1200-
1500)
 Muscles that control fine movements (fingers, eyes) have small motor units.
MOTOR UNIT: The Nerve Muscle  Large weight-bearing muscles *thighs, hips) have large motor units.
Functional Unit  Muscle fivers from a motor unit are spread throughout the muscle (not confined to one
fascicle)
 Therefore, contraction of a single motor unit causes weak contraction of the entire muscle.
 Stronger and stronger contractions of a muscle require more and more motor units being
stimulated (recruited).

o SMOOTH – cells are not striated


 Fibers smaller than those in skeletal muscle
 Spindle-shaped; single; central nucleus; more actin than myosin
 No sarcomeres
i. Not arranged as symmetrically as in skeletal muscle thus no striations.
 Caveolae: indentions in sarcolemma; may act like T tubules.
 Dense bodies instead of Z disks.
 Have noncontractile intermediate filaments.
 Grouped into sheets in walls of hollow organs (GIT, intestine)
a. Longitudinal layer: muscle fibers run parallel to organs long axis
B. SMOOTH MUSCLE
b. Circular layer: muscle fibers run around circumference of the organs
Both layers participate in peristalsis
 It is innervated by autonomic nervous system (ANS)
 Visceral or unitary smooth muscle
o Only a few muscles fibers innervated in each group
o Impulse spreads through gap junctions
o Whole sheet contracts as a unit
o Often autorhythmic
 Multiunit: cells or groups of cells act as independent units
 Arrector pili of skin and iris of eyes.

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3. CARDIAC MUSCLE
o Found only in heart where it forms a thick layer called the myocardium
o Striated fibers that branch
o Each cell usually has one centrally located nucleus.
o Fibers joined by intercalated disks.
C. CARDIAC MUSCLE
a. IDs are composites of desmosomes and gap junctions
b. Allow excitation in one fiber to spread quickly to adjoining fibers
o Under control of the ANS (involuntary) and endocrine system (hormones)
o Some cells are autorhythmic (fibers spontaneously contract aka Pacemaker cells)
o Cardiac Muscle have striated fibers that branch out.
SUMMARY [ TYPES OF MUSCLE]
SMOOTH CARDIAC
SKELETAL - In the walls of hollow organs, blood - Heart: major source of movement of blood
- Responsible for locomotion, facial vessels, eye, glands, uterus, skin - Autorhythmic
expressions, posture, respiratory - Some functions: propel urine, mix food in - Controlled involuntarily by endocrine and
movements, other types of body digestive tract, dilating/constricting pupils, autonomic nervous system
movement regulating blood flow
- Voluntary in action - In some location, autorhythmic
- Controlled by somatic motor neurons - Controlled involuntarily by endocrine and
autonomic nervous system

A. EPIMYSIUM
- Dense regular connective tissue surrounding entire muscle
CONNECTIVE TISSUE SHEATS OF A MUSCLE - Separates muscle from surrounding tissues and organs
- Connected to the deep fascia
 Collagen fibers of all 3 layers come together at B. PERIMYSIUM
each end of muscle to form a tendon or - Collagen & elastic fibers surrounding a group of muscle fibers called a fascicle
aponeurosis. - Contains blood vessels and nerves
 Osteons (from skeletal system) vs. Endomysium C. ENDOMYSIUM
(muscle system): the muscle systems aim to be - Loose connective tissue that surround individual muscle fibers
extensible (stretchable) - Also contains blood vessels, nerves and satellite cells (embryonic stem cells; function
in repair of muscle tissue).

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A. Motor Neurons (each muscle fibers are recruited to move as one by motor neurons)
 Stimulate muscle fibers to contract
 Neuron axons branch so that each muscle fiber (muscle cells) is innervated
 Form a neuromuscular junction (= myoneural junction)
NERVE AND BLOOD VESSEL SUPPLY
B. Capillary beds surround muscle fibers
 Muscles require large amounts of energy
 Extensive vascular network delivers necessary oxygen & nutrients and carries
away metabolic waste produced by muscle fibers.
A. Muscle Attachments
a. Most skeletal muscles run from one bone to another
b. One bone will move- other bone remains fixed
i. Origin: less movable attachment
ii. Insertion: more movable attachment
BASIC FEATURES OF A SKELETAL MUSCLE c. Muscles attach to origins and insertions by connective tissue
i. Fleshy Attachments: connective tissue fibers are short
ii. Indirect Attachments: connective tissue forms a tendon or
aponeurosis
d. Bone markings pre sent where tendons meet bones
i. Tubercles, trochanters & crests
SKELETAL MUSCLE STRUCTURE o Composed of muscle cells (fibers), connective tissue, blood vessels

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o Fibers are long, cylindrical and multinucleated
o Tend to be smaller diameter in small muscled and larger in large muscle (1mm – 4 cm
in length)
o Develop from myoblasts; numbers remain constant
o Striated appearance
o Nuclei are peripherally located
A. SARCOLEMMA- cell membrane
o Surround sarcoplasm (cytoplasm of fiber)
a. Contains many of the same organelles seen in other cells
b. An abundance of the oxygen-binding protein myoglobin
o Punctuated by opening called transverse tubules (T-tubules)
a. Narrow tubes that extend into the sarcoplasm at right angle to the surface
b. Filled with extracellular fluid
B. MYOFIBRILS (cylindrical structures within muscle fibers)
o Bundles of protein filaments (= myofilaments)
o 2 TYPES OF MYOFILAMENTS
1. ACTIN FILAMENTS (thin filaments)
2. MYOSIN FILAMENTS (thick filaments)
o At each end of the fiber, myofibrils are anchored to the inner surface of the
MUSCLE FIBER ANATOMY
sarcolemma
o When myofibril shortens, muscle shortens (contracts)
C. SARCOPLASMIC RETICULUM (SR)
o It is an elaborate, smooth endoplasmic reticulum
i. Runs longitudinally and surrounds each myofibril
ii. Form chambers called terminal cisternae on either side of the T-
tubules.
o A single T-tubule and the 2 terminal cisternae form a triad
o It stores Ca2+ when muscle not contracting
i. When stimulated, calcium released into sarcoplasm (from
cytoplasmic reticulum)
ii. It has Ca2+ pumps that function to pump Ca2+ out of the
sarcoplasm back into the SR after contraction
SARCOMERES o (repeating/functional units of a myofibril)
o About 10 000 sarcomeres per myofibril; end to end
o Each is about 2um long
o Differences in size, density, and distribution of thick and thin filaments gives the
muscle fiber a banded or striated appearance

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o A BANDS: a dark band; full length if thick (myosin) filament
o M LINE: protein to which myosin attach
o H ZONE: thick but NO thin filaments
o I Bands: a light band; from Z disks to ends of thick filaments; thin but NO thick
filaments; extends from A band of one sarcomere to A band of the next
sarcomere.
o Z disk: filamentous network of protein; serves as attachment for actin
myofilaments
o Titin filaments: elastic chains of amino acids; keep thick and thin filaments in
proper alignment

MYOSIN (thick) FILAMENT


o Many elongated myosin molecules shaped like golf clubs
o Single filament contains roughly 300 myosin molecules
o Molecule consist of two heavy myosin molecules wound together to form a rod portion lying parallel to the myosin myofilament and
two heads that extend laterally
o Myosin heads
1. Can bind to active sites on the actin molecules to form cross-bridges (actin binding site)
2. Attached to the rod portion by a hinge region that can bend and straighten during contraction.
3. Have ATPase activity that breaks down adenosine triphosphate (ATP); releasing energy, part of the energy is used to
bend the hinge region of the myosin molecule during contraction.

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ACTIN (thin) FILAMENT
o Thin filament composed of 3 MAJOR PROTEINS:
1. F (FIBROUS) actin
2. Tropomyosin
3. Troponin
o Two strands of fibrous actin form a double helix extending the length of the myofilament; attached at either end at sarcomere
 Composed of G actin monomers each of which has a myosin-binding site
 Actin cite can bind myosin during muscle contraction
o Tropomyosin, an elongated protein which along the groove of the F actin double helix.
o Troponin is composed of three subunits
1. Tn-A: binds to actin
2. Tn-T: binds to tropomyosin
3. Tn-C: binds to calcium ions.
SLIDING FILAMENT MODEL OF CONTRACTION o Thin filaments slide past the thick ones so that the actin and myosin filaments overlap
 Skeletal muscle shortens during contraction to a greater degree
because the thick and thin filaments slide pasts o In the relaxed state, thin and thick filaments overlap only slightly
one another o Upon simulations, myosin heads bind to actin and sliding begins.
o Each myosin head binds and detaches several times during contraction, acting like a
ratchet to generate tension and propel the thin filaments t the center of the
sarcomere
o As this event occurs throughout the sarcomeres, the muscle shortens.
o As sarcomere shorten, myofibril shortens. As myofibrils shorten so does muscle fiber.
o Once a muscle fiber, begins to contract, it will contract maximally
o This is known as the “all or none” principle.
STEP 1: Arrival of an action potential at the synaptic terminal: An action potential (AP), an
electrical impulse, travels down the axon of the motor neuron to the end bulbs (synaptic
terminals)
STEP 2: Release of Acetylcholine: The AP causes the vesicles in the synaptic terminal fuse with
the (end bulb) neuronal membrane to release acetylcholine and dump their contents into the

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synaptic cleft.
STEP 3: Acetylcholine binding at the motor end plate: The membrane of Acetylcholine to the
receptors increases the membrane permeability to sodium ions. Sodium ions then rush into
the cell.
 Acetylcholine diffuses across the synaptic cleft and binds to Ach receptors on the
motor end plate.
STEP 4: Appearance of an action potential in the sarcolemma: An action potential spreads
across the surface of the sarcolemma. While this occurs, Acetylcholineesterase (AChE)
removes the acetylcholine (ACh)
 The bind of ACh to its receptors causes a new AP to be generated along the muscle
cell membrane.
 Immediately after it binds to its receptors, ACh will be broken down by the AChE- an
enzyme present in the synaptic cleft).
o Calcium triggers the contraction of the muscles.
1. ATP HYDROLYSIS
2. Attachment of myosin to actin
THE CONTRACTION CYCLE
3. Power Stroke
4. Detachment of myosin from actin
EXCITATION-CONTRACTION COUPLING - Ca2+ concentration in the sarcoplasm starts muscle contraction
sequence of events that links excitation (a muscle action
potential) to contraction (sliding of the filaments)
 How the forcefulness of muscle contraction depends on the length of the sarcomere
LENGTH-TENSION RELATIONSHIP
b4 contraction begins.
1. Release of acetylcholine
2. Activation of ACh receptors
NEUROMUSCULAR JUNCTION
3. Production of muscle action potential
4. Termination of ACh activity
o Skeletal muscle require stimulation from the nervous system in order to contract
PHYSIOLOGY OF SKELETAL MUSCLE CONTRACTION
o Motor neurons are the cells that cause muscle fibers to contract.
NEUROMUSCULAR JUNCTION o The neurons are not actually attached to the sarcolemma.
Somatic motor neurons: neurons that stimulate skeletal 1. Release of acetylcholine (Ach)
muscle fibers to contract. 2. Activation of Ach receptors.
Neuromuscular junction: synapse between a somatic 3. Production of muscle action potential.
motor neuron and a skeletal muscle fiber. 4. Termination of Ach activity
Synaptic cleft: separates 2 cells

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 Synaptic end bulbs- neural part of NMJ
 Acetylcholine- the neurotransmitter released at NMJ
 Motor End plate: opposite the synaptic end bulbs in
sarcolemma

o Muscle tissues experience few disorders.


a. Heart muscle is the exception
b. Skeletal muscle: remarkably resistant to infection
c. Smooth muscle: problems stem from external irritants (Ulcer, acidity)
1. MUSCULAR DYSTROPHY: a group of inherited muscle destroying disease
 Affected muscle enlarge with fat and connective tissue
 Muscle degenerate
ii. Types of muscular dystrophy
DISORDER OF MUSCLE TISSUE 1. Duchenne muscular dystrophy
2. Myotonic dystrophy
2. MYOFASCIAL PAIN SYNDROME- pain is caused by tightened bands of muscle fibers
3. FIBROMYALGIA – a mysterious chronic pain syndrome; affects mostly women
 SYMPTOMS: fatigue, sleep abnormalities, severe musculoskeletal pain, headache
4. FIBROSIS: condition marked by increase of interstitial fibrous tissues.
5. FIBROSITIS: rheumatic disorder of fibrous tissue.
6. MYASTHENIA GRAVIS: long term neuromuscular disease leading to skeletal muscle
weakness.
o Cardiac and skeletal muscle become amitotic but can lengthen and thicken
o Myoblast-like satellite cells show very limited regenerative ability
DEVELOPMENTAL ASPECT: REGENERATION
o Cardiac cells lack satellite cells.
o Smooth muscle has good regenerative ability.
DEVELOPMENTAL ASPECTS: MALE AND FEMALE o These differences are due primarily to the male sex hormone testosterone
o With more muscle mass, men are generally stronger than women

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o Body strength per unit muscle mass, however is the same in both sexes.
1. TENDONS: muscle to bone
2. Muscle attaches directly to the bone or to soft tissues
MUSCLE ATTACHMENTS
3. APONEUROSIS: flat, sheet like fascia that connects muscle to muscle or muscle to
bone.
 Related to contraction
 Artery and 1or 2 veins accompany each nerve
NERVE & BLOOD SUPPLY o Each muscle cell is in contact with capillaries
 Each muscle cell is in contact with a portion of a nerve cell
o Neuromuscular junction (NMJ)
 Exert force on tendons
 Attached to articulating bones forming a joint
 When muscle contracts, one bone moves toward the other
HOW SKELETAL MUSCLES PRODUCE MOVEMENT  ATTACHMENTS:
1. ORIGIN: attachment to stationary bone
2. INSERTION: attachment to moveable bone
3. BELLY: fleshy portion of muscle between tendons
 AGONIST or PRIME MOVER- causes desired action
GROUP ACTIONS  ANTAGONIST- effect is opposite to agonist
 SYNERGIST or FIXATOR: assists agonist
 Bones = levers, joints = fulcrums
 Levers are acted upon by resistance & effort
 TYPES OF LEVER
1. 1st class lever: fulcrum is placed between effort and resistance (e.g. neck)
LEVER SYSTEMS 2. 2nd class lever: fulcrum is at one end, effort is at the opposite end, resistance is in
between (e.g. heel, up & down)
3. 3rd class lever: fulcrum is at one end, resistance is at the opposite end, effort is in
between. (e.g. arm)
 Leverage is responsible for a muscle’s strength and range of movement.
 Direction of muscle fibers: orientation of muscle fascicles relative to the body’s
midlines
 Location: structure near which a muscle is found.
 Size: relative to the size of the muscle
NAMING OF SKELETAL MUSCLES
 Number of origins: number of tendons of origin.
 Shape: relative shape of the muscle
 Origin & insertion: sites where muscle originates and inserts
 Action: principal action of the muscle

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1. At About age 40, the number & diameter of muscle fibers decrease, Muscle fibers are
gradually replaced with connective tissues, By age 80, about 50% of the muscle mass
MUSCULAR CHANGES AS WE AGE
has been lost.
2. Motor neurons are gradually lost.

PHYSIOLOGY OF SKELETAL MUSCLE CONTRACTION


STEOS THAT START A CONTRACTION  Once an action potential (AP) is generated at the motor end plate it
STEP 1: ACh releases, binding to a receptor. will spread like an electrical current along the sarcolemma of the
STEP 2: Action Potential reaches T tubule muscle fiber.
STEP 3: Sarcoplasmic reticulum releases Ca 2+
 The AP will also spread into the T-tubules, exciting the terminal
STEP 4: Active-site exposure, cross-bridge formation cisternae of the sarcoplasmic reticula.
STEP 5: Contraction begins.  . This will cause Calcium (Ca2+) gates in the (SR) to open, allowing
STEP 6: ACh removed by AChE (Ca2+) to diffuse into the sarcoplasm
STEP 7: Sarcoplasmic reticulum recaptures Ca 2+  Calcium will bind to troponin (on the thin myofilament) causing it to
STEP 8: Active sites covered, no cross-bridge interaction. change its shape. This then pulls tropomyosin away from the active
STEP 9: Contraction ends sites of actin molecules.
STEP 10: Relaxation occurs, passive return to resting length.  The exposure of the active sites allows the sliding of the filaments.
 Calcium gates in the SR open, allowing (Ca 2+) to diffuse into the
sarcoplasm
 Myosin heads are energized by the presence of ADP + PO4 -3 at the
ATP binding site (energy is releases as phosphate bond of ATP
breaks)
 Once the active sites are exposed, the energized myosin heads hook
into actin molecules forming cross-bridges
 If there are no longer Aps generated on the motor neuron, no more
ACh will be released.
 AChE will remove ACh from the motor end plate, and AP
transmission on the muscle fiber will end.
 Ca2+ gates in the SR will close & Ca2+ will be actively transported back
into the SR
 With Ca2+ removed from the sarcoplasm (& from troponin),
tropomyosin will recover the active sites of actin.
 No more cross-bridge interactions can form.
 Thin myofilaments slide back to their resting state.
KEY NOTES:
 Skeletal muscle fibers shorten as thin filaments interact with thick filaments and sliding occurs.

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 The trigger for contraction is the calcium ions released by the SR when the muscle fiber is stimulated by its motor neuron.
 Contraction is an active process; relaxation and the return to resting length is entirely passive.

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