MUSCLES
Chapter 8
“We are made wise not by the
recollection of our past, but the
responsibility for our future.”
George Bernard Shaw
SMOOTH MUSCLES
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Smooth – Hollow organs, blood vessels,
and respiratory passages
Involuntary
Causes wavelike contractions = peristalsis
Look like a toothpick
Uni-nucleate
Triggers: nerve impulse, hormonal
stimulation, stretching and more
CARDIAC MUSCLES
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Found only in heart
Involuntary
Intercalated disc
Uni-nucleate
Striated
Triggers: self-excitatory; nerves and/or
hormones influence rate
SKELETAL MUSCLE
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MUSCLE FIBERS ARE CIGAR SHAPED
MULTINUCLEATE
LARGEST OF MUSCLE FIBER TYPES
STRIATED
VOLUNTARY
MOVES SKELETAL SYSTEM
Triggers: nerve system
MUSCLE FUNCTIONS
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PRODUCES MOVEMENT
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SKELETAL – WALKING, LIFTING
SMOOTH – BLOOD & FOOD MOVEMENT
CARDIAC – PUMPS BLOOD
MAINTAINS POSTURE
STABILIZES JOINTS
GENERATES HEAT
One neuron & all its muscle fibers = one motor unit
MUSCLE COMPOSITION
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Muscle fiber has cell wall called sarcolemma
The sarcolemma is insulated by ENDOMYSIUM
Many groups of endomysium wrapped fibers are
grouped together, wrapped in PERIMYSIUM and
called a FASCICLE.
Many fasicles are wrapped together by EPIMYSIUM
EPIMYSIUM COVERS ENTIRE MUSCLE &
CONTINUES DOWN TO MERGE INTO A TENDON
OR SPREAD INTO AN APONEUROSES
NEUROMUSCULAR JUNCTION
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Impulse from nerve caused a release of
neurotransmitter (acetylcholine – ACh)
via vesicle to exocytose to synaptic cleft.
ACh diffuses across cleft to receptors on
muscle sarcolemma at the motor end
plate.
Muscle must be excitable to begin the
action potential
MUSCLE CONTRACTION
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Must be able to shorten and change its shape
The sarcolemma is filled with MYOFIBRILS
(organelles of the cell)
Each MYOFIBRIL has bands, giving it a striped
look
The bands are actin and myosin filaments.
They are the contractile unit of the sarcomere.
FROM SMALLEST TO LARGEST
A REVIEW……..
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ACTIN & MYOSIN (MICROFILAMENTS)
make up a sarcomere
Many SARCOMERE make a MYOFIBRIL
Many myofibrils are in a cell; the cell wall is
called a SARCOLEMMA
Sarcolemma are covered by ENDOMYSIUM
Several endomysium covered sarcolemma
are wrapped by PERIMYSIUM to make a
FASCICLE
CONTINUED
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Many fasicles are wrapped together by EPIMYSIUM
The epimysium wrapped package of fibers is a
muscle; biceps, triceps, spinator
EPIMYSIUM merges into a tough cord called a
TENDON to connect the biceps to its insertion site
EPIMYSIUM may spread to become an
APONEUOSIS (SHEET) which attaches the muscle
to a bone surface.
BANDING OF SARCOMERE
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BARE ZONE = NO ACTIN PRESENT
AT RELAXATION
DARK AREA = THICK FILAMENT
CALLED MYOSIN
THIN FILAMENT CALLED ACTIN
HOW A CONTRACTION
HAPPENS
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The presence of ACH at the muscle receptor causes a
change in polarity. The change in Na and K balance
causes the ACTION POTENTIAL
Once started, the stimulus is unstoppable and travels
the length of the sarcolemma.
The action potential stimulates the sarcoplasmic
reticulum to RELEASE CALCIUM into the cytoplasm
CALCIUM triggers the opening of the myosin binding
site on the actin filaments by binding to tropinin and
tropomyosin.
You Tube Assistance
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Nerve at Synapse
http://www.bing.com/videos/search?q=Action+Potential+Animation+McGraw+Hill&Form=VQFRVP#view=d
etail&mid=BD481F1B29FC2BF8421DBD481F1B29FC2BF8421D
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Muscle
http://www.bing.com/videos/search?q=YouT
ube+Muscle+Contraction&FORM=RESTAB
#view=detail&mid=27DFE0C5623BB0825B
6327DFE0C5623BB0825B63
CONTINUED
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The cross-bridge heads attach to the open site.
The attachment and release of cross bridges to
actin causes a “rowing motion” of the myosin
heads pulling the actin filament closer together
resulting in a contraction.
During the muscle contraction,
Acetylcholinesterase breaks down ACH to stop
the influx of ions across the sarcolemma
CONTINUED
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THE CELL RETURNS TO RESTING STATE
AS THE SODIUM- POTASSIUM PUMP
RETURNS THE IONS TO ORIGINAL
CONCENTRATION
What kind of movement is this called?
THE ACETYLCHOLINESTERASE HAS
NEGATED THE NERVE IMPULSE UNTIL
THE NEXT NEUROTRANSMITTER RELEASE
IS ACHIEVED
ENERGY FOR CONTRACTIONS
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MUSCLES STORE VERY LITTLE ATP
IT’S GONE IN SECONDS!!!
NEXT, IT LOOKS FOR CREATINE
PHOSPHATE IN MUSCLES
TAKES A PHOSPHORUS MOLECULE
TO RE-ENERGIZE ADP TO ATP
USES ALL CP WITHIN 20 SECONDS!!!
AEROBIC RESPIRATION
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OCCURS IN MITOCHONDRIA
GLUCOSE BROKEN DOWN INTO H2O
& CO2 RELEASING ENERGY
ENERGY CAPTURED AS ATP
GET 36 ATP FOR 1 GLUCOSE
SLOW; NEEDS O2 (FROM
MYOGLOBIN) & NUTRIENT FUELS IN
CONTINUOUS FLOW
ANAEROBIC GLYCOLYSIS
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OCCURS IN CYTOSOL
GLUCOSE BECOMES PYRUVIC ACID &
ENERGY
2 ATP FOR 1 GLUCOSE
PYRUVIC ACID & OXYGEN = ENERGY
PYRUVIC ACID & NO O2 = LACTIC ACID
FASTER; BUT PROMOTES MUSCLE
FATIGUE & SORENESS
MUSCLE FATIGUE
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FATIGUE = UNABLE TO CONTRACT
EVEN THOUGH STIMULATED
CONTRACTION BECOMES WEAKER
UNTIL STOPS
USUALLY DUE TO O2 DEBT OF
PROLONGED MUSCLE ACTIVITY
CAN HAPPEN TO MARATHON
RUNNERS
O2 DEBT MUST BE PAID BACK
EFFECTS OF EXERCISE ON
MUSCLES
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USE IT OR LOSE IT!!!!!!!
EXERCISE INCREASES SIZE, STRENGTH
& ENDURANCE
AEROBIC EXERCISE = INCREASED
RESISTANCE TO FATIGUE, IMPROVES
METABOLISM & DIGESTION, INCREASES
COORDINATION, MAKES SKELETON
STRONGER, LUNGS MORE EFFICIENT,
CLEANS FAT DEPOSITS FROM BLOOD
VESSEL WALLS
ISOTONIC CONTRACTIONS
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SAME TONE OR TENSION
BENDING KNEE
SMILING
MOVEMENT OCCURS
ISOMETRIC CONTRACTION
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SAME MEASUREMENT
INCREASES THE TENSION ON THE
MUSCLE
NO MOVEMENT
MUSCLES vs IMMOVABLE OBJECT
RESISTANCE EXERCISES
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BODY BUILDERS USE THIS
MAKING MUSCLES CONTRACT WITH
AS FORCE AS POSSIBLE ENLARGES
THE MUSCLE CELL
USE ISOTONIC FOR HEALTH
USE ISOMETRIC FOR DEFINITION OF
MUSCLES
MUSCLE TONE
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SOME MUSCLE FIBERS ARE ALWAYS
CONTRACTING EVEN WHEN WE ARE
RELAXED
MAKES MUSCLE FEEL FIRM
CONTINUOUS PARTIAL
CONTRACTIONS = MUSCLE TONE
MOVEMENT NAMES
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FLEXION – DECREASE ANGLE OF JOINT
EXTENSION – ENLARGES ANGLE
ROTATION – MOVING BONE AROUND
LONGITUDINAL AXIS
ABDUCTION – AWAY FROM MIDLINE
ADDUCTION – TOWARD MIDLINE
CIRCUMDUCTION – PROXIMAL END IT
STABLE, DISTAL END MOVES IN A CIRCLE
SPECIAL MOVEMENTS
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DORSIFLEXION – STAND ON HEELS
PLANTAR FLEXION – POINT TOES
INVERSION – TURN SOLE MEDIALLY
EVERSION – TURN SOLE LATERALLY
SUPINATION – PALM FACES ANTERIORLY
PRONATION – PALM FACES DORSALLY
OPPOSITION – THUMBS TO FINGER TIPS
INTERACTIONS of MUSCLES
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PRIME MOVER – MAJOR MUSCLE
CAUSING MOVEMENT
ANTAGONIST- REVERSES MOVEMENT
OF PRIME MOVER
SYNERGISTS – HELPS PRIME MOVER
OR STABILIZES JOINT
FIXATORS – STABILIZE ORIGIN OF
PRIME MOVER OR HOLDS BONE STILL
NAMING MUSCLES
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DIRECTION OF THE FIBERS
SIZE OF MUSCLE
LOCATION
NUMBER OF ORIGINS
SHAPE
ACTION
LOCATION OF ORIGIN & INSERTION
ARRANGEMENT OF FASCICLES
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CIRCULAR – SPHINCTERS
CONVERGENT – MEET IN ONE SPOT
PARALLEL – EVEN TO LONG AXIS
• FUSIFORM – LIKE PARALLEL WITH WIDE CENTER
PENNATE- FEATHERLIKE PATTERN, ENTERS
THE TENDON
• UNIPENNATE, BIPENNATE, MULTIPENNATE
FACIAL MUSCLES
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FRONTALIS
ORBICULARIS OCULI
ORBICULARIS ORIS
BUCCINATOR
ZYGOMATICUS
CHEWING MUSCLES
• MASSETER
• TEMPORALIS
NECK MUSCLES
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PLATYSMA – SHEET OF MUSCLE
FROM CHEST TO MANDIBLE- PULLS
CORNER OF MOUTH DOWN = SAG
STERNOCLEIDOMASTOID – COME
FROM STERNUM AND CLAVICLE TO
INSERT ON MASTOID
ANTERIOR TRUNK MUSCLES
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PECTORALIS MAJOR
INTERCOSTALS
ABDOMINAL GIRDLE
• RECTUS ABDOMINUS – STRAIGHT FROM PUBIS
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TO RIB CAGE
EXTERNAL OBLIQUE – SIDES TO CENTER
DOWNWARD
INTERNAL OBLIQUE – SIDES TO CENTER UP
TRANSVERSE ABDOMINUS – LOWER RIBS AND
ILIAC CREST ACROSS ABDOMEN
POSTERIOR MUSCLES
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TRAPEZIUS – TRIANGULAR IN UPPER
BACK
LATISSIMUS DORSI – LOWER BACK
ERECTOR SPINAE – ALONG SPINE
DELTOID – TRIANGULAR IN
SHOULDER/ UPPER ARM
MUSCLES CAUSING HIP
MOVEMENT
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GLUTEUS MAXIMUS – FORMS BUTTOCKS,
HIP EXTENSOR
GLUTEUS MEDIUS – HIP ABDUCTOR,
STEADIES PELVIS DURING WALKING
ILIOSPOAS – HIP FLEXOR, PREVENTS
HYPEREXTENSION
ADDUCTOR MUSCLE – ADDUCT HIP
MUSCLES & KNEE JOINTS
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HAMSTRING GROUP – POSTERIOR THIGH,
HAVE LARGE TENDON BY KNEE
SARTORIUS - WEAK THIGH FLEXOR;
SYNERGISTICS TO SIT LIKE AN INDIAN
QUADRICEPS –
• RECTUS FEMORIS – EXTENDS KNEE & FLEX HIP
• 3 VASTUS MUSCLES – HELP EXTEND KNEE
MUSCLES AND ANKLE/ FOOT
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GASTROCNEMIUS IS MOST
IDENTIFIABLE AS THE CALF MUSCLE
CAUSES PLANTAR FLEXION OF
FOOT AND FLEXES THE KNEE
DEVELOPMENTAL ASPECTS OF
MUSCLES
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MUSCULAR DYSTROPHY – MUSCLES
ENLARGE DUE TO FAT & CONNECTIVE
TISSUE DEPOSITS BUT THE MUSCLE
FIBERS ARE DEGENERATING
• DUSCHENNE’S MD – DX BY AGE 2-6
• W/C BY 10 -12
• DEATH IN YOUNG ADULTHOOD
CONTINUED
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MYASTHENIA GRAVIS – A SHORTAGE
OF ACH RECEPTORS AT NEUROMUSCULAR JUNCTION DUE TO
ANTIBODIES AT RECEPTOR SITES.
MUSCLE CELLS HAVE POOR
STIMULATION & WEAKEN. DEATH
RESULTS FROM RESPIRATORY
FAILURE.
AGING
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LOSE MUSCLE MASS AND
STRENGTH AS WE AGE UNLESS WE
EXERCISE TO KEEP FIRM
LOSE 50% OF STRENGTH BY AGE 80
DISORDERS OF ASSOCIATED
STRUCTURES
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BURSITIS
TENDONITIS
BUNIONS
TENOSYNOVITIS
SHINSPLINTS
CARPAL TUNNEL SYNDROME
MEDICAL TERMINOLOGY
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PLEASE KNOW THE TERMS ON
PAGES 181 AND 182