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Flashcards in Skeletal Muscle Contraction Deck (29)
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what does the I band contain?

(isotropic light bands) only actin thin filaments, from Z line to center of the sarcomere


what does the A band contain?

(anisotropic dark bands) myosin thick filaments


what is the H zone?

no overlap between actin and myosin


what is the M line?

the center of the sarcomere, where the thick filaments are linked with each other


how is the skeletal muscle organized?

muscle > fasicle > fiber/cell > myofibril > myofilament > sarcomere


myosin molecule in muscle

6 polypeptide chains
-2 heavy chains (230KD) intertwined as double helix and ending in 2 globular heads, with a double-coiled helix tail
-4 light chains (20KD) each in head region


myosin heavy chain (not the same as thick filament)

single PRO that contains globular region that binds both actin and hydrolyzes ATP during muscle contraction
-contians hinge region and extended tail region made of two heavy chains wound together


regulatory light chain (RLC)

phosphorylated in striated muscles by Ca++/calmodulin-dependent myosin light chain kinase
-maintained in fast-twitch after tetanus or low-frequency repetitive stimulation
-phosphorylation correlates with potential of the rate in development and max extent of isometric twitch tension


essential/alkali light chain (ELC)

provides fine tuning of the myosin motor function, regulated in an isoform and tissue-dependent manner


myosin/thick filament

1.6 micron length (equal to A-band) made of 200+ individual myosin molecules that point outward from central H-zone
-successive myosin heads are axially displaced from previous by 120 degrees, so heads protrude in all directions from the tail
-each myosin head has an ATPase catalytic site and actin binding site


outline of excitation contraction coupling

1. motor ATP travels along motoneuron to motor endplate at neuromuscular junction
2. nerve endings secrete ACh that acts on local area of sarcolemma to open numerous ACh-gated ion channels
3. Na+ flows into muscle to depolarize muscle membrane potential, initiating AP to propagate along membrane
4. AP propagates down T-tubule into interior of muscle fiber to triad junction, where it causes release of Ca++ ions that have been sequestered in longitudinal SR
5. increased [Ca++] causes actin and myosin filaments to interact w/ each other, causing sliding motion to shorten length of sarcomere
6. Ca++ are pumped back into SR by Ca-ATPase ion pump in SR membrane, reducing [Ca++] in sarcoplasm, allowing relaxation
7. lengthening of muscle due to antagonistic muscle contraction (biceps VS triceps)


what is a triad made of?

2 cisternae and 1 T-tubule (both from sarcoplasmic reticulum)



alpha-helical rod that covers the myosin binding sites on the thin filament in resting muscle
blocks myosin from binding to the actin thin filament
-bound to by troponin T


troponin and its components

complex of 3 PRO subunits that binds tropomyosin to thin filament
-C - binds Ca++
-I - inhibits actomyosin ATPase and binds to actin
-T - binds to tropomyosin
-when C binds Ca++, tropomyosin moves and uncovers active sites in actin, allowing interaction


crossbridge cycle steps

1. ATP binds to myosin causing tilted X-bridge to separate from actin
2. myosin ATPase cleaves ATP, but hydrolysis products ADP and phosphate remain bound to myosin
-cleavage of ATP causes X-bridge, still separated from actin, to change conformation to perpendicular "cocked" orientation
3. "X-bridge" forms as myosin head binds to actin
4. myosin head then releases phosphate, causing conformational change in X-bridge to tilted position, allowing power stroke that drags actin filament towards M-line
5. ADP released in final step of the cycle


how much of the energy stored in ATP is transformed into mechanical work?

30% of energy


isometric contractions

occur at constant muscle length


how to measure force generated during isometric twitch?

muscle is fixed so force measured w/o muscle shortening
-stimulate electrically with single AP, and force generated is measured as a function of time
-latent period between stimulation and contraction (time delay between AP and activation of X-bridge cycle)
-tension builds during contraction phase of twitch and tension declines during relaxation phase


what do the contraction and relaxation phases of muscle closely parallel?

the levels of Ca++ in sarcoplasm that surrounds sarcomere


what is a "muscle twitch"?

contraction generated by a single AP
-basis of muscle contraction and heart contracts by "twitch" only


fast and slow twitch muscle

number of factors dictate different kinetics between isometric twitches including type of myosin heavy chain expressed and speed of sarcoplasmic Ca++ elevation and clearance
-fast twitches develop and relax quickly


slow twitch (type I) MYH genes

fatigue-resistant, red myoglobin, oxidative metabolism, high mitochondria and low glycogen


fast twitch (type IIa and IIb) MYH gene

a: MYH2; fatigue-resistant, red myoglobin, oxidative metabolism, most mitochondria and high glycogen
b: MYH4; susceptible to fatigue, white b/c low myoglobin, glycolytic metabolism, few mitochondria, and high glycogen


what does MYH mean?

myosin II heavy chain gene


what does the amount of tension generated reflect?

the degree of overlap of thick and thin filaments
-tension increases as degree of overlap of thin and thick filaments increases
-if sarcomere stretches too far, there are fewer X-bridges and thus less force generated (less tension)
--also if muscle shortened below optimal length, or actin crosses M-line and interferes with formation of X-bridges on other side of sarcomere


when is the muscle at its optimal length/tension?

when the number of active X-bridges is greatest (maximal thick/thin filament overlap without interference)


when is there no tension in muscle?

thick filament is completely compressed, or there is no thin-thick filament overlap


when is there slightly less tension in muscle?

thin filament interference, thick filaments hit the z-line, or intermediate thick/thin filament overlap


myostatin gene

controls muscle fiber growth
-if inhibited, then causes uncontrolled muscle hypertrophy b/c satellite cell activation is increased

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