muscles chapter 8 “we are made wise not by the recollection of our past, but the responsibility...
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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
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
Found only in heart Involuntary Intercalated disc Uni-nucleate Striated Triggers: self-excitatory; nerves and/or
hormones influence rate
SKELETAL MUSCLE
MUSCLE FIBERS ARE CIGAR SHAPEDMULTINUCLEATE LARGEST OF MUSCLE FIBER TYPESSTRIATEDVOLUNTARY MOVES SKELETAL SYSTEM Triggers: nerve system
MUSCLE FUNCTIONS
PRODUCES MOVEMENT• 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
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
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
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 LARGESTA REVIEW……..
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
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
BARE ZONE = NO ACTIN PRESENT AT RELAXATION
DARK AREA = THICK FILAMENT CALLED MYOSIN
THIN FILAMENT CALLED ACTIN
HOW A CONTRACTION HAPPENS
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 Nerve at Synapse
http://www.bing.com/videos/search?q=Action+Potential+Animation+McGraw+Hill&Form=VQFRVP#view=detail&mid=BD481F1B29FC2BF8421DBD481F1B29FC2BF8421D
Muscle http://www.bing.com/videos/search?q=YouTube+Muscle+Contraction&FORM=RESTAB#view=detail&mid=27DFE0C5623BB0825B6327DFE0C5623BB0825B63
CONTINUED
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
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
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
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
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
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
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
ISOMETRIC CONTRACTION
SAME MEASUREMENT INCREASES THE TENSION ON THE
MUSCLE NO MOVEMENT MUSCLES vs IMMOVABLE OBJECT
RESISTANCE EXERCISES
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
SOME MUSCLE FIBERS ARE ALWAYS CONTRACTING EVEN WHEN WE ARE RELAXED
MAKES MUSCLE FEEL FIRM CONTINUOUS PARTIAL
CONTRACTIONS = MUSCLE TONE
MOVEMENT NAMES
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
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
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
DIRECTION OF THE FIBERS SIZE OF MUSCLE LOCATION NUMBER OF ORIGINS SHAPE ACTION LOCATION OF ORIGIN & INSERTION
ARRANGEMENT OF FASCICLES
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
FRONTALIS ORBICULARIS OCULI ORBICULARIS ORIS BUCCINATOR ZYGOMATICUS CHEWING MUSCLES
• MASSETER
• TEMPORALIS
NECK MUSCLES
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
PECTORALIS MAJOR INTERCOSTALS ABDOMINAL GIRDLE
• RECTUS ABDOMINUS – STRAIGHT FROM PUBIS 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
TRAPEZIUS – TRIANGULAR IN UPPER BACK
LATISSIMUS DORSI – LOWER BACK ERECTOR SPINAE – ALONG SPINE DELTOID – TRIANGULAR IN
SHOULDER/ UPPER ARM
MUSCLES CAUSING HIP MOVEMENT
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
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
GASTROCNEMIUS IS MOST IDENTIFIABLE AS THE CALF MUSCLE
CAUSES PLANTAR FLEXION OF FOOT AND FLEXES THE KNEE
DEVELOPMENTAL ASPECTS OF MUSCLES
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
MYASTHENIA GRAVIS – A SHORTAGE OF ACH RECEPTORS AT NEURO- MUSCULAR JUNCTION DUE TO ANTIBODIES AT RECEPTOR SITES. MUSCLE CELLS HAVE POOR STIMULATION & WEAKEN. DEATH RESULTS FROM RESPIRATORY FAILURE.
AGING
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
BURSITIS TENDONITIS BUNIONS TENOSYNOVITIS SHINSPLINTS CARPAL TUNNEL SYNDROME
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