Skeletal Muscle Cell and Contraction Flashcards Preview

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Flashcards in Skeletal Muscle Cell and Contraction Deck (29):

sarcolemma membrane

skeletal muscle cell membrane
contains T-tubles = invaginations



dihydropyridine receptors = Ca channels
cell surface on T-tubules


sarcoplasmic reticulum

intracellular calcium storage space
ryanodine receptors = Ca channels


skeletal muscle cell contractile apparatus




H-zone = only myosin thick filament (length changes with contraction)
A-band = length of the myosin thick filament (remains constant)
I band = contains actin thin filament (length changes with contraction)
Z-lines = demarcate sarcomere borders


A band

length of myosin thick filament
DOES NOT change in length


H zone

area of only myosin thick filament
length changes with contraction as Z-lines come together


I band

contains actin thin filament
length changes with contraction as filaments move together


skeletal muscle cell contraction

AP from nerve --> opens VG-Ca channels --> ACh released into synapse
ACh binds ACh receptors on muscle cell (muscle cell end plate)
muscle cell depolarizes --> travels down cell to T-tubules --> open dihydropyridine receptors


dihydropyridine receptor

voltage-gated Ca channel activates and opens after depolarization of muscle cell from AP
causes Ca induced Ca release from the sarcoplasmic reticulum (ryanodine receptor activation)


ryanodine receptor activation

increase in Ca release from sarcoplasmic reticulum where Ca is being stored
Ca leaves SR through ryanodine receptors


Calcium in muscle cell contraction

Ca binds to troponin C
tropomyosin moves --> allows actin and myosin to bind each other = myosin-actin binding site (actin cross-bridge) revealed
myosin cross-bridge binds to actin cross bridge


resting muscle

tropomyosin blocks actin-myosin binding site


phases of actin-myosin crossbridging

1. resting muscle = actin-myosin unbound
2. binding of cross bridge to actin (Ca-binding to troponin causes conformational change in tropomyosin = exposes cross bridging site)
3. power stroke
4. release


muscle cell contraction

I band = shortens
H zone = shortens
actin filaments pulled closer together
sarcomere length shortens


power stroke muscle contraction

myosin in cocked state by binding ATP and hydrolyzes to ADP and inorganic phosphate


dissociation of actin and myosin

binding of ATP to cross bridge causes loss of affinity for actin


rigor mortis

stiffened state after death
absence of ATP in the dead = muscle remains contracted because myosin can't release from actin


Type I muscle fibers

slow twitch - red muscle fibers
long term aerobic metabolism - low ATPase activity
increased myoglobin (red color)
increased mitochondrial content
best for slow, posture-maintaining muscles (ex: back)


Type II muscle fibers

fast twitch fibers - fast contraction
high ATPase activity - increased capacity for anaerobic glycolysis
decreased mitochondrial content
decreased myoglobin (white color0
best for fast, short-term, skilled muscles of eye, sprinter's legs, hands
hypertrophies with weight training


skeletal muscle denervation atrophy

muscle tissue atrophies
muscle fiber type grouping on histology and occurs with reinnervation (nerve repair) - Type I and Type II muscle fibers grouped together


skeletal muscle disuse atrophy

prolonged disuse (bedridden)
angular atrophy - smaller muscle fibers with angular shape
primarily type II


smooth muscle contraction

AP --> opens VG-Ca channels in sarcolemma
hormones and NTs --> open VG-Ca channels in SR


Cardiac muscle contraction

inward Ca current during plateau -->
Ca release from SR


phosphorylated myosin

more likely to interact with actin = more likely to have muscle contraction


smooth muscle contraction Ca increase

1. increased intracellular Ca
2. Ca binds calmodulin
3. Ca-calmodulin bind to and activates myosin light chain kinase (MLCK)
4. myosin is phosphorylated
5. myosin-P binds actin and shortening occurs
6. dephosphorylation of myosin --> relaxation (by myosin light chain phosphatase)


effect of alpha 1 and M3 muscarinic receptor stimulation on smooth muscle

increases IP3
increases intracellular Ca
smooth muscle contraction


beta 2 stimulation effect on smooth muscle contraction

increases cAMP
inhibits MLCK (myosin light chain kinase)
smooth muscle relaxation


nitrate effects on smooth muscle contraction

nitrates converted to nitric oxide (NO)
NO activates guanylate cyclase
increase cGMP
cGMP causes smooth muscle relaxation of blood vessels