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Discuss control of autonomic nervous system functioning.
HYPOTHALAMUS = main integrative center of ANS activity; it controls activity of brain stem and spinal cord
influences blood pressure, rate and force of heartbeat, digestive tract motility, eye pupil size, and other visceral activities
subconscious cerebral input via limbic lobe connections influences hypothalamic function
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How is equilibrium sensed?
- - sensory receptor for dynamic equilibrium
- - endolymph moves inside the semicircular canals in the direction opposite the rotation; the flow bends the cupula and excites the hair cells
- - bending in the opposite direction from acceleration inhibits the hair cells
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What does tilting the head left compared to right do?
- - bending in the opposite direction hyperpolarizes vestibular nerve fibers and reduces the rate of impulse generation
- - hairs bending away from kinocilium inhibit nerve fiber and decrease the action potential frequency
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How are balance and movement detected?
- - semicircular canals: receptors respond to angular movements of the head
- - maculae in the utricle respond to horizontal movements and tilting the head side to side
- - maculae in the saccule respond to vertical movements
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What are the homeostatic imbalances of hearing?
- Conduction Deafness
- - blocked sound conduction to the fluids of the internal ear
- - results from impacted earwax, perforated eardrum
- Sensorineural Deafness
- - damage to the neural structures at any point from the cochlear hair cells to the auditory cortical cells
- Tinnitus
- - ringing or clicking sound in the ears in the absence of auditory stimuli
- - results from cochlear nerve degeneration
- Meniere's Syndrome
- - labyrinth disorder that affects the cochlea, semicircular canals
- - causes vertigo, nausea, and vomiting
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How does auditory processing occur?
- - impulses from specific hair cells are interpreted as specific pitches
- - loudness is detected by increased numbers of action potentials that result when the hair cells experience larger deflections
- - localization of sound depends on relative intensity and relative timing of sound waves reaching both ears
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What makes endolymph so unique? What's the excitation of hair cells in the spiral organ?
- - stereocilia: protrude into endolymph
- - bending stereocilia: opens mechanically gated ion channels, inward potassium and calcium current greater graded potential and release glutamate
- - cochlear fibers transmit impulses to the brain
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How does resonance differ along the basilar membrane?
- LOW FREQUENCY: displace basilar membrane near the base
- MEDIUM FREQUENCY: displace basilar membrane near the middle
- HIGH FREQUENCY: displace basilar membrane near the apex
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How does sound travel?
- - sound waves vibrate the tympanic membrane
- - auditory ossicles vibrate, amplifying pressure
- - pressure waves move through fluid in the scala vestibuli
- - sounds in the hearing range vibrate the basilar membrane and deflect hairs on inner hair cells
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What are the properties of sound waves?
FREQUENCY: the number of waves that pass a given point in a given time
WAVELENGTH: the distance between two consecutive crests
AMPLITUDE: the height of the crests
PITCH: perception of different frequencies; the higher the frequency, the higher the pitch
LOUDNESS: interpretation of sound intensity (normal range is 0-120 decibels)
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What are the three parts of the ear and what are their general functions?
- EXTERNAL
- - transfers sound energy
- - localizes and amplifies sound
- MIDDLE
- - equalizes pressure
- - vibrations!
INNER- balance
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What influences taste?
- - taste is 80% smell
- - thermoreceptors, mechanoreceptors, nociceptors in the mouth
- - temperature and texture
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What is the taste transduction for the tastes we can sense?
- Gustatory cell depolarization by:
- sodium = salty tastes (direct depolarization)
- hydrogen = sour tastes (by opening cation channels)
- G protein gustducin = sweet, bitter, umami tastes (by releasing calcium, opening cation channels)
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What is the physiology of the chemical senses?
- their chemoreceptors respond to chemical in aqueous solution
- SMELL
- - dissolved odorants bind to receptor proteins
- - G protein is activated, produces cAMP as a second messenger
- - cAMP opens sodium and calcium channels, causing depolarization of the receptor membrane- depolarization triggers an action potential
- TASTE
- - in order to be tasted, a chemical must be dissolved in saliva and touch gustatory hairs
- - binding of the chemical depolarizes the taste cell membrane, releasing a neurotransmitter that elicits and action potential
- - travels to hypothalamus and limbic system
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How and why do we have depth perception?
- - both eyes view the same image from different angles; it's a cortical fusion of slightly different images
- - it helps us locate objects in space
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Compare light adaptation to dark adaptation.
- Darkness => Bright Light
- - large amounts of pigments are broken down instantaneously => glare
- - pupils constrict; rod function ceases
- - cones and neurons rapidly adapt
- - acuity improves over 5-10 minutes
- Bright Light => Darkness
- - cones stop functioning
- - pupils dilate
- - rhodopsin accumulates and retinal sensitivity increases within 20-30 minutes
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Compare signal transmission in the retina in the dark and in the light.
(1) In the LIGHT, the photoreceptor hyperpolarizes because cGMP-gated channels are closed and a cation influx stops. (2) Voltage-gated Ca2+ channels close and (3) no glutamate (an inhibitory transmitter) is released. (4) There's not IPSP in the bipolar cell, so the cell is depolarized, (5) opening Ca2+ channels and releasing a neurotransmitter that generates an (6) EPSP in the ganglion cell. (7) Action potentials propogate along the optic nerve.
In the DARK, the photoreceptor depolarizes because cGMP channels are open. Glutamate IS released continuously, causing IPSPs in the bipolar cell, which results in hyperpolarization. The hyperpolarization closes voltage-gated calcium channels and inhibits excitatory neurotransmitter release and therefore, inhibit the action potential.
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What are some problems of refraction?
- MYOPIA
- - nearsightedness
- - focal point is in front of the retina; longer than normal eyeball
- - corrected with a concave lens
- HYPEROPIA
- - farsightedness
- - focal point is behind the retina; shorter than normal eyeball
- - corrected with a convex lens
- ASTIGMATISM
- - unequal curvatures in different parts of cornea/lens
- - corrected with cylindrically ground lenses, laser procedures, etc.
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How does focusing differ between distant and close vision?
- DISTANT Vision
- - objects are nearly parallel at the eye and need little refraction beyond what occurs at rest
- - ciliary muscles are relaxed
- - lens is stretched flat by tension in the ciliary zonule
- CLOSE Vision
- - light diverges at it approaches the eye
- - requires accomodation (change in lens shape by ciliary muscles), constriction (pupil constriction), and convergence (medial rotation of eyeballs toward object)
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What is the pathway of light entering the eye?
cornea => aqueous humor => lens => vitreous humor => neural layer of retina => photoreceptors
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How does light focus on the retina?
light is refracted (1) at the cornea, (2) entering the lens, (3) leaving the lensthe change in lens curvature allows for fine focusing of an image
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Compare rods and cones.
- RODS
- - more numerous at the peripheral region of the retina- operate in dim light
- - provide indistinct, fuzzy, non-color peripheral vision
- CONES
- - found in the macula lutea and are concentrated in the fovea centralis
- - operate in bright light
- - provide high-acuity color vision
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What is the influence of the autonomic nervous system on the senses?
The PARASYMPATHETIC nervous system causes the sphincter pupillae to DECREASE pupil size.
The SYMPATHETIC nervous system cause the dilator pupillae to INCREASE pupil size.
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What are G protein-linked receptors and what is the related mechanism?
- (1) neurotransmitters binds to G protein-linked receptor
- (2) G protein is activated
- (3) activated G protein controls production of second messengers
- (4) second messengers open/close ion channels, activate kinase enzymes, phosphorylate channel proteins, activate genes and induce protein synthesis
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How is skeletal muscle innervated?
- - by the somatic nervous system
- - one motor neuron to skeletal muscle cells, ALWAYS EXCITATORY
- - to contract muscle cell, activate motor neuron, to relax, don't
- - cerebellum critical to motor coordination: feedback control of motor function, contributes to muscle tone, stores programs for remembered activities
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How is control of the heart done by pacemakers?
- - 1% of cardiac cells are autorhythmic cells; they have pacemaker
- - spontaneous depolarizations caused by closing K+ channels and/or opening 2 types of channels
- - I(f) channels: sodium and potassium, net depolarization
- - Ca2+ channels: further depolarization
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Discuss the form and function of cardiac muscle.
- - cardiac action potentials may be spontaneous due to pacemaker cells
- - intercalated disks: gap junctions allow the muscle to contract as unit; desmosomes provided resistance to mechanical stress
- - aerobic muscle
- - growth by HYPERTROPHY; NO cell division after infancy
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What are the types of smooth muscle?
- SINGLE-UNIT
- - lines smaller blood vessels, urinary tract, digestive tract
- - sheets contract rhythmically as a unit (gap junction)
- - exhibit spontaneous action potential
- - arranged in opposing sheets and exhibit stress
- -relaxation response
- MULTI-UNIT
- - located in large airways, large arteries, arrector pili muscles, and iris of eye
- - few gap junctions
- - graded contractions occur in response to neural stimuli
- - arranged in motor units
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What are the special features of smooth muscle contraction compared to skeletal and cardiac muscle?
- stress-relaxation response: retains ability to contract on demand, responds to stretch briefly, then adapts to new length- length and tension changes- hyperplasia: smooth muscle cells can divide and increase their numbers
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What are the events of SMOOTH muscle contraction and relaxation?
- CONTRACTION
- (1) Ca2+ is released from the sarcoplasmic reticulum into the cell.
- (2) Ca2+ binds to calmodulin, which activitates myosin light chain kinase (MLCK)
- (3) MLCK phosphorylates light chains in myosin heads, increasing myosin ATPase activity.
- (4) Active myosin crossbridges slide along actin, creating muscle tension.
- RELAXATION
- (1) Ca2+ is pumped out of the cell or back into the sarcoplasmic reticulum
- (2) Ca2+ unbinds from calmodulin.
- (3) Myosin phosphatase removes phosphate removes phosphate from myosin, decreasing myosin ATPase activity
- (4) Less myosin ATPase results in decreased muscle tension
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What are the developmental aspects of muscles?
- - they develop from myoblasts
- - muscular development reflects the level neuromuscular coordination, which develops head-to-toe and proximal-to-distal
- - growth factor agrin stimulates clustering of ACh receptors at neuromuscular junctions
- - smooth muscle regenerates throughout life
- - peak natural neural control occurs by midadolescence
- - with age, connective tissue decreases and muscle fiber mass decreases
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What are the diseases related to muscles?
muscular dystrophy: group of inherited muscle-destroying diseases, muscle fibers atrophy, victims usually die of respiratory failure
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What are the effects of exercise of muscle on skeletal muscle?
- aerobic (endurance) exercise leads to increased muscle capillaries, number of mitochondria, myoglobin synthesis
- greater endurance, strength, and resistance to fatigue
- fast glycolytic fibers => fast oxidative fibers
- resistance exercise leads to muscle hypertrophy, and increased mitochondria, myofilaments, glycogen storage, and connective tissue
muscles must be overloaded to produce further gains, but there should be intervals of rest
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What are the different muscle fiber types?
In order of recruitment:
- SLOW OXIDATIVE FIBERS
- - slow contraction
- - aerobic pathway for ATP synthesis
- - low glycogen stores
- - slow to fatigue
- - best for endurance-type activities
- FAST OXIDATIVE FIBERS
- - fast contraction
- - mostly aerobic pathway for ATP synthesis
- - intermediate glycogen stores
- - moderately fatigue-resistant
- - best for sprinting, walking
- FAST GLYCOLYTIC FIBERS
- - fatigue quickly
- - fast contraction
- - low myoglobin, low mitochondria, fewer capillaries
- - synthesize ATP through anaerobic glycolysis
- - best for short-term intense or powerful movements
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What causes muscle fatigue?
- decline in a muscle's ability to maintain a constant force of contraction during repetitve stimulation
- high intensity exercise => build up of lactic acid, compression of blood vessels, depletion of acetylcholine
- oxygen deficit: O2 is needed for replenishment of oxygen reserves, glycogen stores, ATP and CP reserves AND conversion of lactic acid to pyruvic acids, glucose, glycogen
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Where does the energy for contraction come from?
ATP needs to be constantly regenerated by:
- Anaerobic Pathway
- glucose breaks down by glycolysis => PYRUVIC ACID converts to [lactic acid and 2 ATP per glucose], which diffuses into the bloodstream and is used as fuel by the liver, kidneys, and heart
- the liver converts it back to pyruvic acid
- Direct Phosphorylation
- CREATINE PHOSPHATE => couples with ADP => 1 ATP per CP
- doesn't last very long
- Aerobic Pathway
- produces 95% of ATP during rest and light to moderate exercise
- glucose => pyruvic acid => AEROBIC RESPIRATION => 32 ATP per glucose, CO2, H2O
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How do muscles adapt to use?
- a change in muscle size is due to the change in size of individual cells
- hypertrophy: increase myofibrils/increase in size and increase production of actin and myosin
- disuse atrophy: lose myofibrils/decrease in size
- denervation atrophy: motor neuron is destroyed; atrophy due to lack of use
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What influences the velocity and duration of a contraction?
- - muscle fiber type
- - load
- - recruitment
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How does load influence contraction?
A higher load means a longer latent period, a slower contraction, and a shorter duration of contraction.
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What does force-generating capacity depend on?
- The number of crossbridges in each sarcomere and geometrical arrangement of sarcomeres:
- more crossbridges/sarcomeres => more force
- more sarcomeres in parallel => more force
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What factors increase contractile force?
- large number of muscle fibers activated
- large muscle fibers activated
- high frequency of stimulation
- muscle and sarcomere stretched to slightly over 100% of resting length
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What is recruitment?
aka multiple motor unit summation
it brings more and more muscle fibers into action; starts with small fibers and moves up to bigger ones as stimulus intensity increase
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Related a graded response to level of contraction.
- Responses are variations in the degree of muscle contraction and are graded by (1) changing the frequency of the stimulation and (2) changing the strength of the stimulus.
- They're required for proper control of skeletal movement.
(1) Temporal or wave summation means that later contractions (from calcium release) create a stronger reaction because the muscle is already partially contracted from the first contraction. Unfused tetanus = hilly graph; fused tetanus = stimuli are close enough together that it's a mountain; tetany results
(2) As stimulus strength is increased above threshold (where the first observable contraction occurs), the muscle contracts more vigorously. Contraction force is precisely controlled by recruitment.
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What occurs at the neuromuscular junction?
- (1) Action potential arrives at terminal buoton, opening voltage-gated calcium channels
- (2) Calcium enters the cell and triggers the release of Ach
- (3) Ach diffuses across the cleft and binds to receptors on the motor end plate
- (4) Ach triggers opening of sodium and potassium channels
- (5) the movement of the positive charge creates depolarization. The resulting action potential spreads through muscle causing contraction.
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What is the role of calcium in skeletal, cardiac, and smooth muscle contractions?
- SMOOTH
- Calcium ions enter the *cytosol from calcium channels and bind to/activate *calmodulin*, which activates myosin light chain kinase enzymes. Those enzymes catalyze the transfer of phosphate to myosin, which can then form bridges with actin.
- CARDIAC
- Calcium interacts with troponin on actin-containing thin filaments
- SKELETAL
- Calcium interacts with troponin on actin-containing thin filaments
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Discuss excitation-contraction coupling.
- - sequence of events whereby an action potential (electrical signal) in the sarcolemma causes contraction
- - dependent on *neural input* from motor neuron
- - requires *calcium release* from the sarcoplasmic reticulum
(1) Acetylcholine is released from a motor neuron and binds to receptors, triggering an action potential that is propagated along the sarcolemma and down the T-tubulues
(2) Voltage-sensitive tubule proteins respond to AP and change shape, opening Ca2+ release channels in the sarcoplasmic reticulum. Massive amounts of Ca2+ flow into the cytosol within a millisecond.
(3) Calcium binds to troponin, causing it to change shape, remove blocking action of tropomyosin, and expose myosin binding sites.
(4) Myosin binds to actin, forming cross bridges and crossbridge cycling begins.
Ca2+ levels drop immediately afterwards.
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What is contraction?
The generation of force. Shortening occurs when tension generation by crossbridges exceeds forces opposing shortening.
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Discuss muscle cell metabolism.
- ATP is used by the muscle during the crossbridge
- - myosin ATPase splits ATP
- - binding of fresh ATP to myosin the cause dissociation
Active transport of calcium into sarcoplasmic reticulum leads to relaxation
Na+/K+ pump maintains ion gradients and membrane potential (needed for action potentials)
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Discuss the crossbridge cycle.
- *Ca2+ signal and adequate ATP must be present*
- * Ca2+ ions bind to regulatory sites on troponin, which reshapes the troponin to roll away from the binding sites*
- (1) Cross bridge formation: *energized* myosin head attaches to actin myofilament forming a crossbridge.
- (2) The power (working) stroke: Pi is released, causing the myosin head to bend to its low-energy state. This pulls on the actin filament and draws it toward the M-line.
- (3) ADP detaches from myosin head, moving it to a low-energy state.
- (4) Cross bridge detachment: ATP attaches to MYOSIN, which detaches from actin after the link weakens.
- (5) ATP hydrolyzes ADP and Pi and the myosin returns to its cocked position.
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Discuss the sliding filament model.
- - during contraction, (1) myosin heads bind actin, (2) detach, (3) bind again => to propel the thin filaments towards the M line
- - as H zones shorten and disappear, sarcomeres shorten, muscle cells shorten, whole muscle shortens
- - BUT thick and thin filaments OVERLAP, not shorten
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How is force generated in muscle?
Through the "Sliding Filament Model," the "Crossbridge Cycle," "Muscle Cell Metabolism," and "Excitation-Contraction Coupling."
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What is a motor unit?
- - one motor neuron and the muscle fibers it innervates
- - when a motor neuron transmits and action potential, all of the fibers it innervates contract
- - muscle exerting fine control have small motor units; "heavier" muscles have large motor units
- - muscle fibers in a single motor unit are spread throughout the muscle
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What are the form and function of thick filaments?
- MYOSIN
- - protein composing thick filaments
- - tails contain: 2 interwoven, heavy polypeptide chains
- - heads contain: 2 smaller, light polypeptide chains that acts as crossbridges, binding sites for actin of thin filaments, ATP, and ATPase enzymes
- - heads face thin filaments
- TITIN
- - support protein
- - anchors thick filaments between M-line and Z-line
- - provides structural support and elasticity
- NEBULIN
- - support protein that binds to actin which is localized to the I-band
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What are the form and function of thin filaments?
- ACTIN
- - has binding sites for myosin
- TROPOMYOSIN
- - regulatory protein
- - overlaps binding sites on actin for myosin
- TROPONIN
- - regulatory protein
- - complex of three proteins (attaches actin and tropomyosin, and binds calcium reversibly)
- - calcium binding to troponin regulates skeletal muscle
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What are the components of sarcomeres?
- thick and thin myofilaments made of contractile proteins
- it's the smallest contractile unit
- region of a myofibril between two successive Z discs
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What are the components of a muscle fiber?
- surrounded by connective tissue
- multinucleated = lots of DNA = ability to make a lot of protein
- sarcoplasm = cytoplasm
- sarcoplasmic reticulum = ER
- contains many mitochondria
- transverse tubules = T tubules, glycosomes for glycogen storage, myoglobin for O2 storage
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What are the connective tissue sheaths for muscles?
- epimysium (surround entire muscle)
- perimysium (surround fasicles)
- endomysium (surround each muscle fiber)
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What are the components of a muscle?
Fasicles, which are made of fibers, which are made of fibrils.
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What are the special characteristics of muscle tissue?
Each muscle is served by one or more VEINS, one ARTERY, one NERVE
- EXCITABILITY: by neuronal stimulation, leading to contraction; ability to receive/send stimulus
- CONTRACTIBILITY: ability to shorten when stimulated
- EXTENSIBILITY: ability to be stretched
- ELASTICITY: the ability to recoil to resting length
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Compare in detail the three types of muscle tissue.
- Skeletal Muscle Tissue
- - attached to bones and skins
- - striated
- - voluntary
- - powerful
- Cardiac Muscle Tissue
- - only in the heart
- - striated
- Smooth Muscle Tissue
- - in the walls of hollow organs: stomach, urinary bladder, and airways
- - not striated
- - involuntary
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