Skeletal Muscle Cell and Contraction Flashcards
(29 cards)
sarcolemma membrane
skeletal muscle cell membrane
contains T-tubles = invaginations
T-tubules
dihydropyridine receptors = Ca channels
cell surface on T-tubules
sarcoplasmic reticulum
intracellular calcium storage space
ryanodine receptors = Ca channels
skeletal muscle cell contractile apparatus
sarcomere
sarcomere
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
- resting muscle = actin-myosin unbound
- binding of cross bridge to actin (Ca-binding to troponin causes conformational change in tropomyosin = exposes cross bridging site)
- power stroke
- 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