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DESCRIPTION
SKELETAL MUSCLE ATTACHES TO BONES OF SKELETON EXERT FORCES TO CAUSE MOVEMENT VOLUNTARY--NORMALLY UNDER CONSCIOUS CONTROL REGULATED BY SOMATIC NERVOUS SYSTEM STRIATED MULTIPLE, PERIPHERAL NUCLEITRANSCRIPT
MUSCLE ANATOMY AND PHYSIOLOGY
• MOVEMENT• ALTERATION OF DIAMETERS• PROPULSION OF MATERIALS• EXCRETION OF MATERIALS• MAINTENANCE OF BODY
TEMPERATURE• MAINTENANCE OF HOMEOSTASIS
MUSCLE TYPES
• SKELETAL MUSCLE• SMOOTH MUSCLE• CARDIAC MUSCLE
SKELETAL MUSCLE• ATTACHES TO BONES OF SKELETON• EXERT FORCES TO CAUSE MOVEMENT• VOLUNTARY--NORMALLY UNDER
CONSCIOUS CONTROL• REGULATED BY SOMATIC NERVOUS
SYSTEM• STRIATED• MULTIPLE, PERIPHERAL NUCLEI
SMOOTH MUSCLE• LACKS STRIATIONS• IN WALLS OF HOLLOW ORGANS, TUBES• CONTRACTION CONTROL MOVEMENT OF
MATERIALS IN BODY• INVOLUNTARY--NOT NORMALLY UNDER
OUR CONTROL• CONTROLLED BY AUTONOMIC NERVOUS
SYSTEM, INTRINSIC FACTORS AND HORMONES
CARDIAC MUSCLE
• SPECIALIZED MUSCLE• FOUND ONLY IN HEART• INVOLUNTARY• CONTROLLED BY AUTONOMIC
NERVOUS SYSTEM, INTRINSIC FACTORS, AND HORMONES
• STRIATED
EMBRYONIC DEVELOPMENT OF MUSCLE
SKELETAL MUSCLE
• EXCEPT FOR HEAD AND LIMBS --DEVELOP FROM SOMITES
• SOMITES MASES OF MESODERMAL CELLS ALONG VERTEBRAE
• MYOTOMES DIFFERENTIATE TO MUSCLE CELLS
• HEAD OF EMBRYO DEVELOPS FROM GENERAL MESODERM
• LIMBS DEVELOP FROM MESODERMAL CONDENSATIONS
• SOME PROBABLY MIGRATE TO LIMBS FROM MYOTOMES
SKELETAL MUSCLE
• MUSCLE FIBERS ARISE FROM MYOBLASTS
• INDIVIDUAL MYOBLASTS FUSE TO FORM MULTINUCLEATED
• AS MATURE FORMS EXTENSIVE MEMBRANE SYSTEM AND CONTRACTILE PROTEINS
SKELETAL MUSCLE
• GENERALLY CANNOT UNDERGO MITOSIS
• HAVE SATELLITE CELLS --INACTIVE MYOBLASTS--THAT CAN DIVIDE
• MORE IN CHILDREN• LOSE AS MUSCLE MATURES• LESS THAN 1% IN MATURE MUSCLE
SMOOTH MUSCLE
• DIGESTIVE TUBE AND BODY ORGANS
• MESODERM MIGRATES AND FORMS THIN LAYER
• DEVELOP INTO SMOOTH MUSCLE
CARDIAC MUSCLE
• FORMATION SIMILAR TO SMOOTH• MIGRATION OF MESODERM TO
HEART TUBE• HAS INTRINSIC CONTRACTION
GROSS ANATOMY OF MUSCLE
• CONNECTIVE TISSUE COVERINGS• ATTACHMENTS• MUSCLE SHAPE
CONNECTIVE TISSUE COVERINGS
• MUSCLE HAS MANY INDIVIDUAL MUSCLE FIBERS HELD TOGETHER BY FASCIA
• ENDOMYSIUM COVERS INDIVIDUAL MUSCLE FIBERS
• INDIVIDUAL FIBERS ARE BUNDLED INTO FASCICULI BY PERIMYSIUM
• WHOLE MUSCLE IS COVERED BY EPIMYSIUM
SKELETAL MUSCLE ATTACHMENTS
• EXTENSIONS OF ENDOMYSIUM, PERIMYSIUM AND EPIMYSIUM ANCHOR MUSCLE
• CAN BLEND INTO TENDON WHICH IS CONTINUOUS WITH PERIOSTEUM OR PERICHONDRIUM
• SOME TENDONS SHORT -- SOME TENDONS LONGER THAN A FOOT
• BROAD FLAT THIN SHEETS ARE APONEUROSES
SKELETAL MUSCLE ATTACHMENTS
• ORIGIN IS LESS MOVABLE END• INSERTION IS MORE MOVABLE END• BELLY IS IN BETWEEN• MUSCLE ARISES FROM ORIGIN • INSERTS INTO INSERTION• ORIGIN GENERALLY BROADER THAN
INSERTION
SKELETAL MUSCLE SHAPES• ARRANGEMENT OF MUSCLE FIBERS VARIES
GREATLY• MAY BE ARRANGED PARALLEL TO LONG AXIS• GIVES MAXIMUM MOVEMENT BUT LITTLE
POWER• MAY INSERT DIAGONALLY INTO A TENDON• PRODUCES LESS MOVEMENT BUT MORE
POWER
MUSCLE SHAPE• UNIPENNATE--ALL FASCICUL INSERT ON ONE
SIDE OF TENDON• BIPENNATE--FASCICULI INSERT ON BOTH SIDES
OF TENDON• MULTIPENNATE-- SEVERAL TENDONS CONVERGE• CONVERGENT--FASCICULI CONVERGE FROM
BORAD ORIGIN TO SINGLE NARROW TENDON• SPHINCTER--CIRCULAR MUSCLES
MICROSCOPIC ANATOMY OF SKELETAL MUSCLE
COMPOSITION OF THE MYOFILAMENTS
• MULTINUCLEATE, 10 TO 100 MICRONS IN DIAMETER, MANY CENTIMETERS LONG FIBER HAS SEVERAL HUNDRED TO SEVERAL THOUSAND MYOFIBRILS
• ALTERNATE LIGHT AND DARK BANDS
ISOTROPIC BANDS
• ALSO CALLED I BANDS OR LIGHT BANDS
• DENSE Z LINE OR Z DISC CROSSES CENTER
• Z LINES DIVIDE INTO SARCOMERES• Z LINE CONTAINS ALPHA-ACTININ
PROTEIN
ANISOTROPIC BANDS
• LESS DENSE H ZONE IN CENTER• H ZONE HAS M LINE
TYPES OF MYOFILAMENTS
• THICK FILAMENTS• THIN FILAMENTS
MYOSIN--THICK FILAMENTS
• MADE OF SIX POLYPEPTIDE CHAINS• TWO HEAVY CHAINS--FOUR LIGHT CHAINS• LOOKS LIKE GOLF CLUBS WITH LONG
HANDLES• HAS ABOUT 200 MYOSIN MOLECULES• CLUB PORTION CALLED CROSS BRIDGES
THICK FILAMENTS
• OCCUR IN A BAND• OVERLAP WITH THIN FILAMENTS• H ZONE ONLY HAS THICK FILAMENTS• M LINE MADE OF FINE FILAMENTS
THAT CONNECT THICK FILAMENTS• M LINE CONTAINS PROTEIN
MYOMESIN
THIN FILAMENTS
• OCCUPY I BAND AND PART OF A BAND
• ATTACH TO Z LINES• MAKE HEXAGONAL ARRANGEMENT
AROUND THICK FILAMENTS
ACTIN, TROPONIN, AND TROPOMYOSIN--THIN FILAMENTS
• ACTIN HAS SUBUNITS OF GLOBULAR (G) ACTIN• G ACTIN ARE HELD TOGETHER BY FILAMENTOUS F
ACTIN• TROPOMYOSIN LIKE END TO END ALONG SURFACE
OF ACTIN• EACH EXTENDS ALON ABOUT SEVEN G ACTIN UNITS• TROPONIN ATTACHES TO BOTH ACTIN AND
TROPOMYOSIN
TRANSVERSE TUBULES
• TUBULAR INVAGINATIONS OF SARCOLEMMA
• EXTEND DEEPLY INTO SKELETAL MUSCLE FIBER
• IMPORTANT FOR TRANSMISSION OF ACTION POTENTIAL
SARCOPLASMIC RETICULUM
• SIMILAR TO SMOOTH ENDOPLASMIC RETICULUM• TERMINAL CISTERNAE LIE CLOSE TO TUBULES • NEAR A AND I BANDS OF SARCOMERE• THIS REGION IS CALLED A TRIAD• CONTAINS HIGH LEVELS OF CA++ IONS• IONS ARE BOUND TO CALSEQUESTRIN• WHEN STIMULATED CALCIUM IONS ARE
RELEASED AND CAUSE CONTRACTIONS
SKELETAL MUSCLE CONTRACTION
• EXPERIMENTALLY ARE TWO TYPES OF CONTRACTIONS WE CAN SEE
• ISOTONIC• ISOMETRIC• IN REALITY BOTH OCCUR AND ARE
HARD TO SEPARATE
ISOMETRIC
• LENGTH OF MUSCLE STAYS CONSTANT
• DEVELOPS FORCE AND TENSION• OCCUR WHEN LIFT OBJECTS TO
HEAVY OR FIXED IN PLACE
ISOTONIC
• MUSCLE SHORTENS UNDER A CONSTANT LOAD
• EVEN THOUGH NOT PURE --WALKING, RUNNING, LIFTING ARE CALLED ISOTONIC
SKELETAL MUSCLE CONTRACTION
• OCCURS AT CELLULAR LEVEL• MUST HAVE STIMULATION FROM
NERVOUS SYSTEM• INTERACTION BETWEEN ACTIN AND
MYOSIN• DEVELOP TENSION AND SHORTENS
FIBERS
NEUROMUSCULAR JUNCTION
• MOTOR NEURONS SUPPY INNERVATION
• SPECIALIZED JUNCTIONS --DO NOT TOUCH
• MOST SKELETAL MUSCLE FIBERS HAVE ONLY ONE NEUROMUSCULAR JUNCTION
SKELETAL MUSCLE EXCITATION• BRIEF INTERMITTENT ELECTRICAL IMPULSES
CALLED ACTION POTENTIALS OR NERVE IMPULSES• NERVE IMPULSE DOES NOT DIRECTLY STIMULATE
SKELETAL MUSCLE FIBER• MUST CROSS SYNAPTIC CLEFT• ACETYLCHOLINE (ACh) CROSSES FROM NEURON
TO SARCOLEMMA• BINDS TO RECEPTORS AND CAUSES MEMBRANE
PERMEABILITY TO INCREASE
EXCITATION-CONTRACTION COUPLING• PROPOGATED ACTION POTENTIAL CAUSES
INTERACTIONS BETWEEN THICK AND THIN FILAMENTS
• ACTION POTENTIAL TRAVELS DOWN SARCOLEMMA INTO T TUBULES AND INTO CENTER OF MUSCLE FIBER
• TRIGGERS RELEASE OF CALCIUM IONS FROM TERMINAL CISTERNAE
• CALCIUM BINDS TO TROPONIN CAUSING INTERACTIONS BETWEEN THICK AND THIN FILAMENTS
CONTRACTION MECHANISMS• REQUIRED ENERGY FROM ATP• ATP OCCUPIES BINDING SITE ON MYOSIN
GLOBULAR HEAD• MYOSIN HAS ENZYME ACTION• SPLITS ATP TO ADP AND PHOSPHATE• ADP AND PHOSPHATE STAY ATTACHED TO
MHYOSIN HEAD• REACTION RELEASES ENERGY• LEADS TO A HIGH ENERGY MYOSIN MOLECULE
CONTRACTION MECHANISMS• MYOSIN HEAD ALSO HAS BINDING SITE THAT
COMBINES WITH COMPLEMENTARY SITE ON ACTIN
• HIGH ENERGY MYOSIN LIKES TO BIND TO ACTIN• TROPOMYOSIN PREVENTS THIS IN RESTING
MUSCLE• STIMULATED MUSCLE RELEASES CA++ WHICH
OPENS TROPONIN AND CAUSE TROPOMYOSIN TO MOVE OUT OF WAY
CONTRACTILE MECHANISMS
• BINDING OF CALCIUM IONS TO TROPONIN WEAKENS LINK BETWEEN TROPONIN AND ACTIN
• THIS ALLOWS TROPOMYOSIN TO MOVE AWAY FROM ITS POSITION
• ALLOWS HIGH ENERGY MYOSINS TO BIND TO ACTIN
CONTRACTION MECHANISMS
CONTRACTION MECHANISMS• INITIAL BINDING WEAK BETWEEN MYOSIN AND ACTIN• BINDING CAUSES RELEASE OF PHOSPHATE BOUND TO
MYOSIN• RELEASE CAUSES MYOSIN TO BIND TIGHTLY TO
ACTIN• ENERGY IN MYOSIN RELEASED CAUSING MYOSIN
HEAD TO MOVE• MYOSIN HEAD SWIVELS TOWARD CENTER PULLING
ON THIN FILAMENT
CONTRACTION MECHANISMS• ADP IS RELEASED FROM MYOSIN BUT MYOSIN
IS STILL ATTACHED TO ACTIN• ANOTHER ATP MOLECULE ATTACHES TO
MYOSIN CAUSING RELEASE OF ACTIN• MYOSIN SPLITS ATP INTO ADP AND PHOSPHATE• PRODUCING HIGH ENERGY MYOSIN THAT
ATTACHES TO ACTIN • AND SO ON
CONTRACTION MECHANISMS
• DURING CONTRACTION ABOUT 50 PERCENT OF MYOSIN HEADS ARE ATTACHED TO ACTIN SUBUNITS
• REST ARE AT INTERMEDIATE STAGES• TWO HEADS OF MYOSIN MOLECULES
ARE THOUGHT TO CYCLE SEPARATELY
CONTRACTION MECHANISMS
• FORCE OF MYOSIN HEADS PULLING ON ACTIN FILAMENTS IS TRANSFERED TO PLASMA MEMBRANE AND EVENTUALLY TO LOAD
• MUST OVERCOME RESISTANCE OF LOAD• IF DO WILL PULL Z LINES CLOSER
TOGETHER AND SHORTEN MUSCLE FIBER
CONTRACTILE REGULATION
WHY DON’T INTERACTIONS BETWEEN THICK AND THIN FILAMENTS OCCUR INDEFINITELY?
• CALCIUM IONS RELEASED FOR ONLY SHORT PERIOD• ACTIVE TRANSPORT REMOVE IONS • BACK TO SARCOPLASMIC RETICULUM• TROPONIN STRENGTHENS HOLD ON ACTIN• DOES NOT ALLOW INTERACTIONS BETWEEN MYOSIN AND
ACTIN• CONTRACTILE PROCESS STOPS• RAPID SUCCESSION OF ACTION POTENTIALS CAN KEEP
CALCIUM FROM BEING TOTALLY REMOVED• CALCIUM IONS ARE AVAILABLE AND FIBER DOES NOT
RELAX UNTIL IMPULSES STOP
ENERGY SOURCES FOR MUSCLE CONTRACTION
• ATP IS IMMEDIATE ENERGY SOURCE• ONLY HAVE ENOUGH ATP TO
CONTRACT MUSCLE FOR FEW SECONDS
• MUST HAVE AN ADDITIONAL ENERGY SUPPLY
CREATINE PHOSPHATE• FOUND IN SKELETAL MUSCLE• ALLOWS RAPID ATP FORMATION• PHOSPHATE AND ENERGY CAN BE TRANSFERRED TO ATP• CREATINE KINASE • SKELETAL MUSCLE CONTAINS MORE CREATINE
PHOSPHATE THAN ATP• CREATINE PHOSPHATE ADDS JUST A FEW MORE
SECONDS OF CONTRACTION• IMPORTANT JUST AFTER INITIATION OF MUSCLE
CONTRACTION
NUTRIENTS• METABOLIC BREAKDOWN OF GLUCOSE, GLYCOGEN,
AND FATTY ACIDS PROVIDE ATP FOR CONTINUED MUSCULAR ACTIVITY
• RESTING AND SLIGHTLY ACTIVE MUSCLES USE FATTY ACIDS
• WITH INCREASE IN ACTIVITY MUSCLES USE MORE AND GLYCOGEN AND GLUCOSE FOR ENERGY
• GLYCOGEN STORED IN MUSCLES• GLUCOSE AND FATTY ACIDS BROUGHT BY BLOOD
STREAM
AEROBIC METABOLISM• MUST HAVE SUFFICIENT OXYGEN• BREAKS DOWN GLUCOSE, GLYCOGEN AND FATTY ACIDS TO
CARBON DIOXIDE AND WATER• EXERCISE CAUSES RESPIRATION AND BLOOD FLOW TO
SKELETAL MUSCLE TO INCREASE • YIELDS UP TO 38 ATPS FROM ONE MOLECULE OF GLUCOSE• HAS MANY STEPS AND IS VERY SLOW• MUST HAVE AN ADEQUATE AND CONTINUAL SUPPLY OF
OXYGEN• OCCURS DURING LIGHT TO MODERATE EXERCISE--WALKING OR
JOGGING • AEROBIC OR ENDURANCE EXERCISES
ANAEROBIC METABOLISM
• INTENSE MUSCULAR ACTIVITY• OXYGEN CANNOT BE DELIVERED FAST ENOUGH• LACTATE FERMENTATION• PRODUCES ONLY 2 ATP• PROCEED MUCH FASTER• USES LARGE AMOUNTS OF GLUCOSE OR GLYCOGEN• PRODUCES LACTATE AND HYDROGEN IONS• LACTATE CONVERTED BACK TO GLUCOSE IN LIVER
BY CORI CYCLE
MUSCLE FATIGUE
• INTENSE MUSCLE ACTIVITY CANNOT CONTINUE FOREVER
• INABILITY OF A MUSCLE TO MAINTAIN A PARTICULAR STRENGTH OF CONTRACTION OR TENSION OVER TIME
MUSCLE FATIGUE• NOT WELL UNDERSTOOD• APPEARS TO DIFFER WITH TYPES OF EXERCISE• MAJOR FACTOR IS THE INABILITY OF MUSCLE TO
GENERATE ENERGY AT HIGH ENOUGH RATE• MAY BE DUE TO DEPLETION OF METABOLIC
RESERVES• A BUILD UP OF HYDROGEN IONS• PSYCHOLOGICAL FATIGUE CAN CAUSE A PERSON
TO QUIT
OXYGEN DEBT
• WHEN MUSCLE CONTRACTION ENDS CREATINE PHOSPHATE LEVEL MUST BE REINSTATED
• LACTIC ACID MUST BE RETURNED TO GLUCOSE• GLYCOGEN LEVELS MUST BE REPLENISHED• THESE REQUIRE ATP• AEROBIC PROCESSES PROVIDE ENERGY• TO SUPPYL OXYGEN REATHING CONTINUES AT
INCREASED RATE FOR SOME TIME AFTER EXERCISE
MOTOR UNITS• MUSCLE HAS MORE FIBERS THAT NEURONS• EACH NEURON BRANCHES TO SUPPLY SEVERAL
MUSCLE• SINGLE NEURON AND ALL THE MUSCLE FIBERS
IT SUPPLIES• FUNCTIONAL UNIT OF MUSCLE• MUSCLES OF FINE MOVEMENT HAVE LOW RATIO• MUSCLES OF GROSS MOVEMENTS HAVE HIGH
RATIO
SKELETAL MUSCLE RESPONSES
• MOTOR UNITS COMBINE TO CAUSE CONTRACTION OF THE MUSCLE AS A WHOLE
• CONTRACTIONS WILL VARY IN BOTH STRENGTH AND DURATION
MUSCLE TWITCH
GRADED MUSCULAR CONTRACTIONS
MULTIPLE MOTOR UNIT SUMMATION
WAVE SUMMATION
TETANUS
ASYNCHRONOUS MOTOR UNIT SUMMATION
DEVELOPMENT OF MUSCLE TENSION
CONTRACTILE AND SERIES ELASTIC ELEMENTS
MUSCLE TENSION AND SERIES ELASTIC ELEMENTS
TYPES OF TENSION ACHIEVED IN SKELETAL
MUSCLE
LENGTH OF MUSCLE AND MUSCLE TENSION
LOAD AND VELOCITY OF SHORTENING
ACTION OF MUSCLE
LEVERS AND MUSCLES
CLASSES OF
LEVERS
CLASS I LEVERS
CLASS II LEVERS
CLASS III LEVERS
LEVERS AND MOVEMENT
SKELETAL MUSCLE FIBER TYPES
SLOW TWITCH, RED, FATIGUE RESISTANT FIBERS
• TYPE I FIBERS• SPLIT ATP AT SLOW RATE• SLOW CROSS-BRIDGE CYCLING• MANY MITOCHONDRIA• HIGH CAPCITY FOR AEROBIC RESPIRATION• SURROUNDED BY MANY CAPILLARIES• LARGE AMOUNTS OF MYOGLOBIN• EXTREMELY RESISTANT TO FATIGUE
FAST TWITCH, RED, FATIGUE RESISTANT FIBER
• TYPE II a FIBERS• MANY MITOCHONDRIA--HIGH CAPACITY FOR AEROBIC
RESPIRATION• WELL SUPPLIED WITH BLOOD VESSELS• LARGE AMOUNTS OF MYOGLOBIN• SPLIT ATP AT RAPID RATE• FAST CROSS BRIDGING• CAN SUPPLY MOST OF THEIR NEEDS BY OXIDATIVE
RESPIRATION• QUITE RESISTANT TO FATIGUE
FAST TWITCH, WHITE, FATIGABLE FIBER
• TYPE II b FIBERS• FEWER MITOCHONDRIA• NOT WELL SUPPLIED BY BLOOD VESSELS• LITTLE MYOGLOBIN• SPIT ATP RAPIDLY• GEARED FOR ANAEROBIC RESPIRATION• FATIGUE EASILY
UTILIZATION OF FIBERS IN SKELETAL MUSCLE
EXERCISE AND ITS EFFECT ON THE SKELETAL
MUSCLES
MUSCLES AND NERVOUS SYSTEM
SOMATIC MOTOR SYSTEM
PYRAMIDAL VS EXTRAPYRAMIDAL TRACTS
PYRAMIDAL TRACTS
• ORIGINATE IN PRECENTRAL GYRUS• PRIMARY MOTOR CORTEX• ARISE FROM PYRAMIDAL CELLS• PROVIDES VOLUNTARY CONTROL
OVER SKELETAL MUSCLES
EXTRAPYRAMIDAL TRACTS
• ARISE IN ANY AREA OTHER THAN THE PRECENTRAL GYRUS
• MODIFY OR DIRECT MUSCLE CONTRACTIONS
PROPRIOCEPTION
• KINESTHETIC SENSE• PROPRIOCEPTORS MONITOR
POSITION OF JOINTS, TENSION IN TENDONS AND LIGAMENTS AND STATE OF MUSCLE CONTRACTION
MAJOR PROPRIOCEPTORS
• MUSCLE SPINDLES• GOLGI TENDON ORGANS• JOINT CAPUSLE RECEPTORS• BELOW CONCIOUSNESS
CLINICAL CONDITIONS
MUSCLE ATROPHY
CRAMPS
MUSCULAR DYSTROPHY
MYASTHENIA GRAVIS
AGING OF THE MUSCULAR SYSTEM
SMOOTH MUSCLE
SMOOTH MUSCLE ARRANGEMENTS
SINGLE-UNIT SMOOTH MUSCLE
• VISCERAL SMOOTH MUSCLE• MOST COMMON ARRANGEMENT• FOUND IN SMALL ARTERIES, VEINS,
INTESTINES, UTERUS AND OTHER STRUCTURES
• CONNECTED BY GAP JUNCTIONS• MANY CELLS RESPOND AS A UNIT
PACEMAKER ACTIVITY
• RESULT OF AUTOMATIC CHANGES IN THE PERMEABILITY OF ION CHANNELS IN THE PLASMA MEMBRANE
• WHEN THRESHOLD IS REACHED AN ACTION POTENTIAL OCCURS
SLOW WAVE POTENTIALS
• RESULT OF CYCLIC CHANGES IN RATE OF SODIUM ION TRANSPORT
• CAUSES CYCLIC CHANGES IN SODIUM MEMBRANE POTENTIAL
MULTIUNIT SMOOTH MUSCLE
• LESS COMMON • PRESENT IN LARGE ARTERIES, LARGE
AIRWAYS TO LUNGS, AND OTHER STRUCTURES
• FEW GAP JUNCTIONS• EACH CELL OR SMALL GROUP OF CELLS
RESPONDS INDEPENDENTLY• GENERALLY NOT SELF EXCITABLE
EXTERNAL FACTORS AND SMOOTH MUSCLE CONTRACTION
• NEURAL ACTIVITY• HORMONES• OTHER CHEMICALS
MECHANICS OF SMOOTH MUSCLE CONTRACTION
• CROSS BRIDGES BETWEEN MYOSIN AND ACTIN CREATE FORCES
• CALCIUM COMES FROM EXTRACELLULAR AND INTRACELLULAR SOURCES
• CALCIUM BINDS TO CALMODULIN• ACTIVATES MYOSIN LIGHT CHAIN KINASE• LIGHT MYOSIN CHAINS PHOSPHORYLATED
CONTRACTION AND RELAXATION OF SMOOTH MUSCLE DEPENDS ON THE
ACTIVITY OF MYOSIN LIGHT CHAIN KINASE AND
MYOSIN LIGHT CHAIN PHOSPHATASE
SPEED AND COST OF SMOOTH MUSCLE
CONTRACTION• SMOOTH MUSCLE CAN GENERATE
AS MUCH CONTRACTILE TENSION AS SKELETAL
• USES MUCH LESS ATP• CONTRACTS MORE SLOWY
STRESS RELAXATION RESPONSE
• SMOOTH MUSCLE CAN BE STRETCHED MORE BEFORE SEEING INCREASE IN TENSION
• ALLOWS HOLLOW ORGANS TO EXPAND WITH OUT APPRECIABLE CHANGES IN PRESSURE ON CONTENTS
CONTRACTION WHEN STRETCHED
• CAN UNDERGO GREATER STRETCHING
• DUE TO ARRANGEMENT OF THIN AND THICK FILAMENTS
AMOUNT OF SHORTENING DURING CONTRACTION
• CAN SHORTEN MORE • CAN CONTRACT FROM TWICE ITS
NORMAL LENGTH TO 1/2 ITS NORMAL LENGTH
• ALLOWS YOU TO VARY DIAMETER OF LUMENS
SMOOTH MUSCLE TONE
• LOW LEVEL OF MUSCLE TENSION• DUE TO PRESENCE OF CALCIUM
IONS• IMPORTANT IN CARDIOVASCULAR
SYSTEM
CARDIAC MUSCLE
• CARDIOCYTES• CARDIAC MYOCYTES• 10-20 MICRONS IN DIAMETER• 50-100 MICRONS IN LENGTH• ONE TO TWO CENTRAL
NUCLEUS/NUCLEI
STRUCTURE OF CARDIAC MUSCLE
SHORT AND BROAD T TUBULES
NO TRIADS
T TUBULES SURROUND THE SARCOMERES AT Z LINES
NO TERMINAL CISTERNAE IN SARCOPLASMIC
RETICULUM
SARCOPLASMIC RETICULUM TUBULES
CONTACT T TUBULES AND CELL MEMBRANE
ACTION POTENTIAL TRIGGERS RELEASE OF CALCIUM IONS
FROM SARCOPLASMIC RETICULUM AND THE ENTRY OF CALCIUM IONS FROM THE
EXTRACELLULAR FLUIDS
INTERCALATED DISCS
• INTERTWINING OF CELL MEMBRANES
• BOUND BY GAP JUNCTIONS AND DESMOSOMES
MAJOR FUNCTIONAL CHARACTERISTICS OF
CARDIAC MUSCLE• AUTORYTHMICITY
– PACEMAKER CELLS• AUTONOMIC NERVOUS SYSTEM
AFFECTS RATE OF CONTRACTION• CONTRACTIONS LAST LONGER• NO WAVE SUMMATION• NO TETANIC CONTRACTIONS
THE COST OF CONTRACTION
• ALMOST TOTALLY DEPENDENT ON AEROBIC RESPIRATION
• LOTS OF MITOCHONDRIA• LOTS OF MYOGLOBIN• GLYCOGEN AND LIPID INCLUSIONS