Transcript 14 muscles
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 SHAPED MULTINUCLEATE LARGEST OF MUSCLE FIBER TYPES STRIATED VOLUNTARY 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 LARGEST A 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=d etail&mid=BD481F1B29FC2BF8421DBD481F1B29FC2BF8421D Muscle http://www.bing.com/videos/search?q=YouT ube+Muscle+Contraction&FORM=RESTAB #view=detail&mid=27DFE0C5623BB0825B 6327DFE0C5623BB0825B63 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 ISOTONIC CONTRACTIONS SAME TONE OR TENSION BENDING KNEE SMILING MOVEMENT OCCURS 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 NEUROMUSCULAR 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 MEDICAL TERMINOLOGY PLEASE KNOW THE TERMS ON PAGES 181 AND 182