ch 9- muscle n muscle tissue Flashcards

62 slides (120 cards)

1
Q

myo

A

muscle tissue

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2
Q

sarco

A

striped muscle

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3
Q

functions of muscles

A

movement, posture and position, joint stability, maintaining body temperature

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4
Q

muscle characteristics

A

excitebaility, contractility, extensibility, elasticity. all muscles have all 4

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5
Q

skeletal muscle tissue

A

voluntary, control how much and when used. moves body parts, striated and multinucleate. uses skeleton like puppet. creates most force, needs most rest. adaptable to force, we say how much

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6
Q

smooth muscle tissue

A

involuntary, moves fluids and substances, no striations and uninucleate. lines hollow organ

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7
Q

cardiac muscle tissue

A

involunatury muscle tissue, moves blood thru body, pacemaker cells set the rate, striated, uninucleate. ONLY HOLLOW ORGAN WITHOUT SMOOTHMUSCLE TISSUE IS THE HEART

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8
Q

innervation of skeletal muscle tissue

A

each muscle fiber synapses w one motor nerve. but, each muscle can be served by multiple motor neurons. nerve ending controls activity

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9
Q

vascularization of skeletal muscle tissue

A

each muscle has 1 artery and 1 vein, brings nutrients and removes waste, a lot of ATP so a lot of waste

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10
Q

connective tissue sheaths

A

support muscle, hold muscle together

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11
Q

connective tissue layers

A

endomysium (inner most layer isolates individual muscle fibers), perimysium (middle layer, forms fascicles with groups of muscle fibers), epimysium (outermost layer, surrounds entire muscle, continues with tendon to attach bone)

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12
Q

imagine picture of muscle. what is order of stuff in it

A

TENDON TO EPIMYSIUM TO PERIMYSIUM TO ENDOMYSIUM TO MUSLCE FIBER AND ONE MUSCLE FIBERS GOT ALL THOSE MYOFIBRILS

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13
Q

skeletal muscle attachments

A

can be direct or indirect. muscles use our bones like levers, so muscle attaches to bone

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14
Q

direct attachment

A

epimysium of muscle fuses directly to bone or cartilage, no tendon here so prone to damage

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15
Q

indirect attachment

A

has tendons, which are band of connective fibrous tissue connecting muscle to bone.

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16
Q

more common skeletal muscle attachment

A

indirect

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17
Q

points of attachment for bone

A

origin and insertion

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18
Q

origin

A

muscle attaches to less movable bone, proximal portion.

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19
Q

insertion

A

muscle attaches to a moveable bone, distal

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20
Q

myocytes

A

largest/longest cells in body- muscle fibers

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21
Q

sarcolemma

A

plasma membrane of muscle fibers

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22
Q

sarcoplasm

A

cytoplasm of muscle fibers. has many glycosomes and myoglobins

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23
Q

glycosomes

A

organelles that store glycogen, polysaccharide. glycogen is needed to ATP bc it gets turned into glucose.

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24
Q

myoglobin

A

stores oxygen, O2 needed for ATP production. makes it so O2 is available during contraction.

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25
myofilaments
protein filaments in muscle tissue, has thick and thin
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thick filament
myosin
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thin filament
actin
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how is tension created in a muscle
actin and myosin interact!
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myosin filaments whatrthey
thicker, have 2 heavy chains, and myosin head at end of each chain. myosin head has 2 bind sites: 1 head for ATP 1 for actin.the heavy chains twist around each other.
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why r myosin headsneeded
links two myofilaments during contraction
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actin filaments
chains of G protein and myosin binding sites
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actin filament function
myosin head binds myosin site of actin during contraction, regulatory proteins of actin control if or when the myosin head can bind- PREVENTS INAPPROPRIATE MOVEMENT
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regulator proteins in actin filaments
tropomyosin and troponin
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tropomyosin
arranged along length of thin filament, blocks myosin binding sites on actin filament when muscle is relaxed. no bad interactions then!
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troponin
globular protein that is associated w tropomyosin, binds tropomyosin to position it on actin filament. prevents and allows contraction
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myofibrils
rod like organelles inside muscle cells. bands of actin and myosin. each muscle has several myofibrils
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what creates striations on skeletal muscle
myofilament overlap to produce dark bands
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myofibrils r made up of...
A band and I band
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A band
myofibril region where actin and myosin overlap
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I band
ONLY actin filaments here in myofibril.
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Z disc
holds actin filaments in place, prevents movement.
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sarcomere
A and I bands create it, between neighboring Z discs. one of them is an entire A band and 1/2 I band on each side
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why is sarcomere important
smallest contractile unit of skeletal muscle tissue. if it shortens, contraction happens!
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T-tubules
extension of sarcolemma wraps deeper myofibrils, helps stimulate the deep ones. increases SA of sarcolemma, so a change in membrane potential can reach even deep ones
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sarcoplasmic reticulum
wraps myofibrils, stores and releases Ca2+ for muscle contraction and relaxation. forms terminal cisterns. AP travels down to stimulate Ca releasing.
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terminal cisterns
thickening, where Ca is released.
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one skeletal muscle cell is innervated by
one motor neuron
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neuromuscular junction
site of synapse between somatic motor neuron and muscle fiber. releases ACh which will stimulate muscle fiber and depolarize sarcolemma
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first step for stimulation of muscle fiber
motor neuron releases ACh at neuromuscular junction, so ACh can bind to chemically gated ion channels on sarcolemma
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second step for stimulation of muscle fiber
EPP and AP across sarcolemma, ACh opens ion channels on sarcolemma for EPP (end plate potential). EPP is a graded potential for muscle tissue only, it depolarizes sarcolemma- if strong enough AP happens
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third step for stimulation of muscle fiber
AP goes from sarcolemma to t tubules (which r extensions of sarcolemma), Ca2+ released from sarcoplasmic reticulum so it flows into cytosol
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fourth step for stimulation of muscle fiber
cross bridge formation and muscle contraction. Ca2+ now in cytosol, so actin and myosin can interact. cross bridges form.
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cross bridge
attachment of myosin to actin, rolls side to side so binding site shown for contraction. when at rest, tropomyosin blocks that same site
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cross bridge formation process until ADP and Pi
Ca2+ binds troponin, shape change of troponin, tropomyosin rolls to side, myosin binding site on actin is exposed now, myosin head splits ATP into ADP + Pi...
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After ADP + Pi of cross bridge
allow for myosin head to bind actin, ATP now needed , myosin head has changed shape for pulling of actin filament (new each time new ATP molecule comes) toward sarcomere center. myosin binds to another ATP and then myosin head detaches from actin binding site- THIS OCCURS UNTIL ATP OR CA RUNS OUT
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power stroke
myosin head pulls actin filament toward asacromere center.
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what result comes from repeated formation of cross bridges between actin and myosin
myosin crip walks along actin filament, repeated temporary bonds with these filaments bind to new part each time
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how does cross bridge and muscle contraction end
motor impulse sno longer sent to muscle fiber, Ca2+creturned to sarcoplasmic rectiulum, so no more troponin bind, and troponin returns to original shape- tropomyosin covers that active binding site again
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sliding filament model of muscle contraction
actin filaments slide over myosin filaments, because myosin heads form and break multiple cross bridges with actin
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what happens to actin and myosin during sliding model
only actin moves, myosin stays put. the filaments don't change in length, the sarcomere shortens tho and generates that muscle tension. THIS IS WHY MUSCLE FIBERS SHORTEN WHEN THEY CONTRACT!!! BC FILAMENTS PULLED INWARDS AND I BAND IS GONE
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motor units in skeletal muscle
one motor neuron can innervate multiple muscle fibers by branching- but a single muscle fiber is innervated by one motor neuron.
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motor unit
single Motor neuron and all the muscle fibers it innervates, it has rules
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rule 1 of motor unit
when motor neuron fires, all fibers it innvervates will contract. all these fibers r spread out not clumped
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rule 2 of motor unit
number ofmuslce fibers a motor neuron innervates infleiunces movement
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where would you find many fibers innervated by motor neuron
legs, back, not a lot of precise control
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where would you find few fibers innervated by motor neuron
fingers or mouth or face, gives precise control for these fibers only 2/3 fibers at a time
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graded muscle contractions ns does what
muscle contraction is modified by NS for production of various force amounts
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temporal summation
one of then graded muscle contractions,. increases frequency of stimulation of muscle fiber
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motor unit summation
another type of graded muscle contractions, increases number of motor units used
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how does temporal summation happen
increases firing rate of a motor neuron to generate more force by having stimuli fired in rapid succession, second impulse hits muscle fiber before it has relaxed. INCREASE IN MUSLCE TEMSION
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basic temporal summation
RESTING POTENTIAL, STIMULUS, A LITTLE REPOLARIZE, MORE STIMULUS AND AP THEN MORE CA RELEASED SO MORE CROSS BRIDGE AND TENSION
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unfused tetanus
result of temporal summation, muscle fiber has little time to relax before next stimulius-BOMBARD UNTIL IT LEVELS OUT
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fused or complete tetanus
no relaxation occurs in muscle fiber, contractions from individual stimuli fuse to into one contraction. MAX POTENTIAL, SOOOO MUCH ATP CROSS BRIDHE MAX
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motor unit summation
increasing muscle force by increasing motor unit number used during contraction
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size principal of motor unit summation
motor unit with smallest muscle fibers recruit ed first, largest r last, largest create most force tho
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why do motor units recruit asynchronously?
some contract some relax to prevent early fatigue, AP is kept n stored
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muscle tone
relaxed muscles always contracted a little, also no sliding filaments here so no movement
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without muscle tone...
muscle would not respond to stimuli, posture and joint stabilization as well as healthy tissues would not happen
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muscle contraction types
isotonic and isometric
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isotonic contraction
muscle tension develops to overcome load, muscle shortening happens. can be concentric or eccentric (shorten or lengthen)
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why would a bodybuilder focus on eccentric contractions?
the muscle lengthened under the tension, th sliding of filaments is in opposite direction so sarcomere lengthens, this is movement control and takes 50% more force.
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isometric contraction
tension develops in a muscle, but length wont change, no legtnh change bc no movement happens- sarcomere doesn't shorten but cross bridge is still here. ex: planks or wall sits, tension but no sliding
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only source of energy used directly for contractile activity
ATP- needed for any cross bridge
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skeletal muscle stores energy in this form
glycogen
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ATP is regenerated how?
as fast as it is used- so we can use it multiple times
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what is the ATP reserve
glycogen
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3 paths to generate ATP
direct phosphorylation, anaerobic phosphorylation, aerobic pathways
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direct phosphorylation
ATP from ADP and Pi using creatine phosphate (CP). phosphate from CP goes to ADP- so 1 ATP is made per 1 CP. No O2, makes 15s of ATP.
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anaerobic pathways, glycolysis
glucose broken down into ATP and pyruvic acid. doesn't need O2, produces quick ATP. However, only 2 ATP per 1 Glucose, so lactic acid buildup may cause fatigue in muscle or delayed soreness. VERYFAST PROCESS 1 MIN ATP
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when is pyruvic acid used
when there's no O2 it is converted into lactic acid.
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aerobic pathway, cellular respiration
95% of ATP used is created here, to be used by muscle during rest and light or moderate long term exercise. needs consistent O2/mitochondria, produces 30-32 ATP tho!!! its slow, needs glucose and O2 so much - worth it tho for so much ATP from only one glucose.
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muscle fatigue
muscle Is physiologically incapable of contraction. allows time for ATP replenishing for basic survival bc need ATP to survive.
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rate/duration of fatigue depends on
LIIT or HIIT, HIIT has fatigue quickly drains. ATP fast too , LIIT is not as much, but the fatigue duration lasts a while after activity is over.
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force
determined by number of cross bridges formed between actin and myosin filaments, more of these cross bridges mearns more force.
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4 factors that influence force
frequency of stimulation (temporal), number of muscle fibers (motor unit summation), muscle fiber size/hypertrophy, and degree of muscle stretch
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what size muscle fiber will generate more force
large fiber, has more myofibrils and more myofilamenrs so more cross bridges happen
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hypertrophy
size of muscle fibers increase to increase force generated, can increase from resistance training to challenge muscle to grow. rate depends on genetics and sex and neutron.
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degree of muscle estretch
force muscle creates varies based on how much muscle is stretched Stretch- actin and myosin have room to slide, but no overlap so no cross bridge, so tension won't generate Shortened- overlap actin and myosin, but touch at center with no room to slide. not a lot of force here restung legnth- perfect room for overlap for cross bridges and tension ,movement
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length tension relationship
amt of tension a muscle can produce is based on its length
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speed of contraction
depends on how fast ATP is split and electrical activity of motor neurons. faster split means faster cross bridge formation. fast motor neurons means fast contraction
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pathway of ATP production
oxidative fivers use aerobic pathways with O2, glycolytic fibers use anaerobic with no O2. one muscle will have 3 fiber types, but you can train to have more.
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fast glycolytic fibers
contract quickly, use anaerobic path, low myoglobin, low mitochondria and blood supply. EX: weight lifters
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fast oxidative fibers
contract quickly, use aerobic pathways, has some glycogen, much myoglobin, and a lot of mitochondria and blood supply(sprinters and gymnasts)
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slow oxidative fibers
contract slowly, aerobic path, low glycogen, high myoglobin for O2, much mitrochonrdia and blood supply. uses less glycogen and ATP than the fast one (EX: endurance activities)
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why r there no slow glycolytic fibers
glycolysis is too fast for a slow contraction
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smooth muscle tissue
hollow visceral organs have this, and iris and bronchi
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will the 2 layers of muscle tissue ever contract simultaneously ?
NO, never in same part of organ! they have opposite effects- asynchronously
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longitudinal layer of smooth muscle tissue
muscle fibers run length of organ, when it contracts it shortens and widens
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circular layer of smooth muscle tissue
muscle fibers run circumference of organ, deeper, lengthens and narrows the organ.
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skeletal muscle difference with smooth
smooth is shorter and smaller, covered only by endomysium, has no neuromuscular junctions, innervation forms varicosities, smooth muscle fibers have no T tubules n less sarcoplasmic reticulum, and have gap junctions, and no striations or sarcomeres or troponin, and actin n myosin r arranged diagonally.
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varicosities
smooth little bulbs that store n release ACh
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caveolae
invaginations of sarcolemma of muscle fiber, have Ca2+ from dif place.
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gap junctions in smooth muscle cause
spontaneous depolarization bc ions r passed but no stimuli is there
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calmodulin
protein that acts as Ca2+ bind site to make contraction happen. regulatory protein- basically forms cross bridges
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what happens when a muscle fiber contracts in smooth muscle
it twists, like wringing a towel out
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smooth muscle types
unitary, multi unit
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unitary smooth muscle
everything described prior, in hollow organs. extremely common type
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multi unit smooth muscle
no gap junctions, structurally independent, motor units here, graded contractions with NS supply (even tho its autonomic). ONLY IN arrestor pilli, bronchi, and internal eye muscles
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neural regulation
neuropteran from ANS can excite or inhibit smooth muscle tissue, involuntary but still needs regulation
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hormones and local chemical factors
some smooth muscle has no innervation. only local chemical response- while others spontaneously depolarize.