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Physio Ch. 12, Muscles

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hrdcorhrvivor's version from 2017-04-18 03:00

Section 1

Question Answer
functions of the muscular systemsupport, movement, maintenance of body temp, regulate organ volumes
skeletal muscle characteristicsstriated, voluntary, attached to bone skin or fascia
cardiac muscle characteristicsstriated, involuntary
smooth muscle characteristicsnonstriated, involuntary, hair follicles in skin and walls of hollow organs
5 properties of muscle tissueexcitability: response to chemicals from nerve cells, conductivity: propagate electrical signals over membrane, contractility: shorten and generate force, extensibility: stretch w/out damage, elasticity: return to original shape
muscle fibers (myofiber)cylindrical, striated, sarcolemma, SR
satellite cellsstem cells, lie outside the myofiber membrane, activate and turn into muscle cells for growth and repair
structure of skeletal muscleepimysium: surrounds muscle, perimysium: fascicles, endomysium: individual muscle fibers
functional organization from largest to smallestmuscle, fascicle, myofiber, myofibril, sarcomere, myofilaments
z discboundaries of sarcomere
a bandactin and myosin overlap
i bandactin only, z discs pass thru center
h zonemyosin only
m linemiddle of sarcomere
myofibrils are build from 3 types of proteins:contractile, regulatory, structural
contractile proteingenerate force during contraction
regulatory proteinturn the contraction process off and on
structural proteinalign thick and thin filaments, elasticity and extensibility, link myofibrils to sarcolemma
actinthin filament, polymer of g-actin forming two strands of f-actin
myosinthick filament, globular heads, ATP and actin binding sites
troponinbinds ca2+
tropomyosinblocks myosin binding site on actin, removed when troponin binds to ca2+
titinstabilizes myosin, most elasticity and extensibility of muscle
nebulinanchor thin filaments to z discs
dystrophinconnects actin to sarcolemma, missing in those with Duchenne's muscular dystrophy
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Section 2

Question Answer
muscle tensionforce created by a muscle when it contracts
loadweight or force that opposes a contraction
contractioncreates tension, muscle shortens
relaxationtension released, muscle returns to original shape
sliding filament model 4 steps1. cocking: myosin hydrolyzes ATP 2. crossbridge formation: myosin binds to actin 3. powerstroke: ADP and Pi leave, confirmation changem myosin bends pulling actin toward midline 4. release: new ATP binds and myosin releases actin
how to regulate a contraction 3 steps1. calcium binds to troponin-c 2. causes a confirmational change moving tropomyosin 3. actin binding sites now available
where does calcium come from?calcium is stored in SR, release is triggered by nervous stimulation
excitation contraction couplingconversion of an electrical stimulus into mechanical work
neuromuscular junctionregion where an axon terminal meets a myobiber at motor end plate
steps to excitation contraction coupling 41. ACh released from somatic motor neuron 2. ACh binds to motor end plate creating APs 3. AP triggers calcium release from SR 4. calcium binds to troponin initiating contraction
end plate potentialwhen ACh binds to receptors on motor end plate, graded potential that always reches threshold and creates an AP
to open a calcium channel you need 2 proteins:DHP receptor: mechanically linked to calcium release channel, only in skel muscle, ryanodine RyR receptor: calcium release channel, AP causes change in DHP and calcium released
relaxation 5 steps1. AP cease 2. AChE breaks down ACh in synaptic cleft 3. sarcolemma AP ceases 4. calcium release channels close 5. calcium ATPase pumps remove calcium from sarcoplasm
rigor mortisstage of death: 3-4 hours postmortem, determines time of death, no ATP, breakdown of tissue from decomp leads to relaxation
phosphocreatineback up energy source for contractions, created from ATP and creatine during rest via creatine phophokinase
energy for contractions with oxygen presentglucose is used in cellular respiration to create ATP
energy for contractions with low oxygen anaerobic respiration, increaded hydrogen ions, lactic acid buildup
stages muscles can go through for energy1. ATP stores 2. phophocreatine 3. anaerobic respiration 4. aerobic respiration
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Section 3

Question Answer
three factor that affect muscle tension in whole muscle1. degree of muscle stretch 2. frequency of stimulation 3. number of motor units recuited
degree of muscle stretchtension developed during twitch directly related to length of sarcomere, if sarcomeres are too far apart filaments barely overlap, if too short too much overlap
frequency of APsincreasing the frequency of stimulus increases force until fatigue
motor unit recuitmentactivation of the motor unit stimulates all myofibers, small mu: more precise, large mu: less precise
continued rapid stimulation results inacidic compounds increase, low levels of ATP, ion imbalance ->fatigue
skeletal muscle fiber classificationsslow twitch (type 1): recruited first, small. fast twitch oxidative glycolytic (type 2A). fast twitch glycolytic (type 2X) recruited last, large
fast twitches2-3x faster because their isoform of myosin cleaves ATP faster, pump calcium back into Sr faster
glycolytic fibers (type 2X)rely on anaerobic glycolysis for ATP production, easier to fatigue, low amount of myoglobin
oxidative fibers (types 1 and 2A)rely on cell respiration to make ATP, more mitochondria and BV, lots of myoglobin
isotonic contractionmuscle will contract and shorten
isometric contractionmuscle will control and not shorten
myasthenia gravisimmune system attacks ACh receptors on motor end plate, muscle fatigue and weakness, anticholinsterase drugs to reduce breakdown of ACh
botoxform of botulism toxin, blocks release of ACh
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Section 4

Question Answer
smooth muscle categorized in 3 wayslocation, contraction pattern, communication with neighboring cells
phasic smooth muscle v tonic smooth musclephasic: alternate between contraction and relaxation (intestinal walls), tonic: continuously contracted (sphincters)
single unit sm v multi unit smsingle: connected via gap junctions, contract as coordinated unit, multi: not electrically linked, must be stimulated individually
sm contraction 4 steps1. increased calcium initiates contraction 2. calcium binds to calmodulin in cytosol 3. creates a signal cascade that ends with phyphorylation of myosin 4. addition of a phosphate enhances myosins ability to hydrolyze ATP
calcium releasecell membrane calcium entry, IP3 activated via GPCR-phospholipase C pathway - calcium released, RyR opens in response to calcium release through calcium induced calcium release, calcium release from SR mediated by RyR receptor channel and IP3 receptor channel
binding of calmodulin and cascadecalcium binds calmodulin, forms calcium calmodulin complex, complex activated myosin light change kinase, phosphorylation increases ability to hydrolyze ATP
relaxationcalcium pumped into Sr and some out of cell, decrease in calcium calmodulin complex, myosin light chain kinase decreases activity, muscle relaxes
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