connects thick filaments to Z lines and recoils after stretching
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sliding filament theory
when muscles contract, thin filaments slide over thick filaments
* H & I bands get smaller, zones of overlap get larger * Z lines move closer together, A band is unchanged * sliding occurs in all sarcomeres in each myofibrl
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membrane potential
unequal distribution of changes on either side of plasma membrane = potential difference
* exists because plasma membrane contains leak channels that are always open (K+ & Na+)
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chemical gradient
concentration gradient for an ion across the plasma mebrane
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electrical gradient
created by the attraction between opposite charges and repulsion of like charges
* rush of positive Na+ ions into cell * depolarization: change of membrane potential to positive
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action potential step 3
membrane potential reaches to +30 mV
* Na+ channels close * K+ channels open & K+ leaves cells * repolarization: membrane potential returns to polarized state
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action potential step 4
repolarization continues to hyperpolarization
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action potential step 5
membrane potential stabilizes
* K+ channels close at resting potential * Na+/K+ pump restores original distribution * refractory period: time needed to reach original distribution * membrane cannot respond to another stimulus until after refractory period
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neuromuscular junction
location where motor neuron controls a skeletal muscle fiber
* there’s one NMJ per muscle fiber * a motor neuron may control multiple muscle fibers
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axon terminal (synaptic terminal) of motor neuron
contains vesicles with Acetylcholine (ACh)
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motor end plate of muscle fiber
* has junctional folds that increase # of ACh receptors * contains Acetylcholinesterase (AChE) * breaks down ACh
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synaptic cleft
space between axon terminal and motor end plate
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neuromuscular junction action step 1
electrical impulse arrives at axon terminal
* change in membrane permeability causes ACh vesicles to fuse with neuron plasma membrane * ACh released (exocytosis)
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neuromuscular junction action step 2
ACh diffuses across synaptic cleft
* binds ACh receptor membrane channels at motor end plate * changes sarcolemma Na+ permeability\\ * Na+ enters muscle fiber sarcoplasm
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neuromuscular junction action step 3
Na+ influx generates action potential in sarcolemma
* ACh diffuses away or breaks down (AChE) * ACh receptor membrane channels close
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neuromuscular junction action step 4
action potential generated at motor end plate immediately spreads across sarcolemma
* ACh cleared from receptor * no other stimulus occurs until AP occurs
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neuromuscular junction action step 5
action potential moves down T tubules between terminal cisternae of sarcoplasmic reticulum
* changes permeability of SR
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neuromuscular junction action step 6
sarcoplasmic reticulum releases stored Ca2+ into sarcomeres and begins contractions
* excitation contraction coupling: action potential is coupled with contraction
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muscle fiber contraction cycle step 1
resting sarcomere
* myosin heads are energized or “cocked” * cocking head requires breakdown of ATP
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muscle fiber contraction cycle step 2
contraction cycle begins
* calcium ions arrive from sarcoplasmic reticulum
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muscle fiber contraction cycle step 3
active sites exposed
* calcium binds to troponin * troponin changes position, moves tropomyosin and exposes active sites on actin
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muscle fiber contraction cycle step 4
cross-bridges form
* myosin heads bind to exposed active sites on actin * forms cross-bridges
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muscle fiber contraction cycle step 5
myosin heads pivot
* cross-bridge formation causes myosin heads to pivot toward M line (center of sarcomere) * power stroke * ADP and P release
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muscle fiber contraction cycle step 6
cross-bridges detach
* a new ATP attaches to each myosin head, myosin releases from actin * released energy used to recock myosin head
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troponin
protein or protein complex that assists is skeletal muscle contractions
* promotes muscle contractions
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mV
threshold: -55 mV
depolarizatiom: +30 mV
resting: -85 mV
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muscle twitch
single stimulus contraction relaxation sequence in a muscle
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fasciculation
involuntary muscle twitch under skin
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motor unit
group of muscle fibers controlled by single motor neuron
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myogram
shows development of muscle tension
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muscle twitch phase 1
latent period
* action potential stimulates sarcolemma * calcium released from sarcoplasmic reticulum * no tension yet
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muscle twitch phase 2
contraction phase
* calcium binds to troponin * cross-bridge cycling * start of tension development to peak tension
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muscle twitch phase 3
relaxation phase
* calcium drops; cross-bridges detach; active sites covered * tension returns to resting level * from peak tension to end of twitch
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peak tension
depends on the frequency of stimulation and the number of muscle fibers stimulated
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treppe
stimulation of muscle fiber immediately after relaxation phase produces increasing maximum tension
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wave summation
addition of one twitch to another
* stimulation of muscle fiber before relaxation phase ends produces increasing maximum tension
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incomplete tetanus
rapid cycle of contraction/relaxation producing near peak tension
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complete tetanus
higher stimulation frequency eliminates relaxation phase
* results in peak tension * no calcium ions return to SR
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motor unit recruitment
activation of more motor units to produce more tension
* smaller motor units activated first, then large motor units * smooth, steady increase in muscle tension
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asynchronous motor unit summation
motor units activated on rotating basis to maintain sustained contractions
* as muscle shortens, tension remains constant * ex: flexing elbow while holding dumbell
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eccentric contraction
peak tension produced is less than the load; muscle lengthens
* ex: returning dumbell from flexed position to extended
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glycolysis
anaerobic breakdown of glucose to pyruvate
* occurs in cytosol * oxygen in cytosol * produces 2 ATP & pyruvate molecules for each glucose
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aerobic metabolism
* produces 95% of ATP demands of resting cell * occurs in mitochondria * produces 15 ATP for each pyruvate * ATP comes from electron transport chain
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glycogen
the way most energy stored
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free ATP
minimal, supports only \~10 twitches
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creatine phosphate
* supplies energy for 15 seconds * creatine assembled from amino acids
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muscle metabolism at rest
* low ATP demand * mitochondria produces surplus ATP * fatty acids & glucose absorbed from bloodstream * make ATP to convert creatine to creatine phosphate & glucose to glycogen
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muscle metabolism at moderate activity levels
* ATP demand increases * relies on anaerobic metabolism of pyruvate to make ATP * increased oxygen consumption
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muscle metabolism at peak activity levels
* enormous ATP demands * mitochondria at max production produces 1/3 ATP needs * most produced by glycolysis * excess pyruvates to lactate * lactate & H+ increase, drops pH (lactic acidosis) and causes muscle fatigue
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fatigue
muscle can no longer perform at required level
* major factor is decreased pH * decreases calcium/troponin binding * alters enzyme activity
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polio
virus that attacks CNS motor neurons causing atrophy and paralysis
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tetanus
toxin from bacteria suppresses mechanism that inhibits motor neuron activity; causes sustained and powerful muscle contractions
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botulism
toxins from bacteria blocks ACh release at neuromuscular junctions
* paralysis of skeletal muscles * acquired through bacteria-contaminated food
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myasthenia gravis
autoimmune disease causing loss of ACh receptors at neuromuscular junctions
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rigor mortis
generalized muscle contractions shortly after death