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
• HEAD OF EMBRYO
• EXCEPT FOR HEAD
DEVELOPS FROM
AND LIMBS -GENERAL MESODERM
DEVELOP FROM
SOMITES
• LIMBS DEVELOP FROM
MESODERMAL
• SOMITES MASSES OF
MESODERMAL CELLS CONDENSATIONS
ALONG VERTEBRAE • SOME PROBABLY
MIGRATE TO LIMBS
• MYOTOMES
FROM MYOTOMES
DIFFERENTIATE TO
MUSCLE CELLS
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
SKELETAL MUSCLE
GROSS ANATOMY OF
SKELETAL 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
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
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 ALONG 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
• GLYCOSOMES STORE 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
WAVE SUMMATION
MULTIPLE MOTOR UNIT
SUMMATION
TETANUS
ASYNCHRONOUS MOTOR
UNIT SUMMATION
DEVELOPMENT OF MUSCLE
TENSION
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-SLOW OXIDATIVE 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-FAST OXIDATIVE 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-FAST GLYCOLYTIC
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 CAPSULE RECEPTORS
BELOW CONCIOUSNESS
CLINICAL CONDITIONS
MUSCLE ATROPHY
CRAMPS
MUSCULAR DYSTROPHY
MYASTHENIA GRAVIS
AGING OF THE MUSCULAR
SYSTEM
SMOOTH MUSCLE
SMOOTH MUSCLE
ARRANGEMENTS
• SINGLE UNIT
• MULTIUNIT
• MIX OF BOTH
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
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