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Smooth muscle
no striation
uninucleated
nucleus centrally located
skeletal muscle
striated
multinucleated
nucleus peripherally located
cardiac muscle
striated
uninucleated or binucleated
nucleus centrally located
epimysium
surround the muscle group
perimysium
surrounds fasicle
endomysium
surrounds muscle fiber/cell
sarcomere
functional unit of muscle
striation
comes from arrangement of myofilaments within myofiber
myofilament
actin and myosin
myofiber
muscle cell
I-band
actin only; light region of sarcomere
A-band
myosin plus overlapping actin; dark region of sarcomere
H-band
myosin only; center of A-band
M-line
center of A band
thick filaments
myosin
thin filaments
actin
z-line
how sarcomeres are divided from each other, found in center of I band
sarcolemma
muscle plasma membrane
T tubules
extension of sarcolemma into muscle fiber; carry action potential to interior myofibrils
Sarcoplasmic reticulum
stores calcium ions
excitation-contraction coupling
pairs depolarization of neuron with depolarization of a muscle cell
steps of excitation-contraction coupling
Ach is released into neuromuscular junction and binds to receptor site on sarcolemma
action potential travels down T tubules causing Ca2+ channels to open
intracellular Ca2+ concentration increases
Ca2+ binds to troponin on thin filaments
Tropomyosin moves away to allow myosin to attach to actin
cross-bridge cycling begins and force is generated
Ca2+ is reaccumulated by SR and muscle relaxes
Ca2+ is low
tropomyosin blocks myosin binding site on actin; no contraction
Ca2+ is present
Ca2+ binds to troponin complex which changes tropomyosin to allow myosin to bind to actin; contraction can occur
sliding filament theory
ATP binds to myosin and causes myosin head to detach
ATP hydrolyzed into ADP and P; myosin is in resting cocked position
myosin binds to actin monomer forming crossbridge
P is released; filaments slide past each other (powerstroke)
ADP is released
motor unit
single motor neuron and the muscle fibers it innervates
small motor units
fine motor activities
large motor units
gross motor activities
recruitment
start using small motor units and add more as needed
isometric action
muscle contract and length remains; force generated is insufficient to overcome load
isotonic action
contraction tension remains constant and muscle changes length and moves the load
concentric action
muscle contracts and shortens
eccentric action
muscle contracts and lengthens
agonist
primary mover
synergist
muscle that assist agonist group
antagonist
muscles that oppose the agonist
Slow Twitch - Type I
mostly aerobic respiration, not large amount of force, fatigue resistant, efficient, lots of mitochondria
endurance athlete
Fast Twitch - Type IIX
anaerobic glycolysis or direct phosphorylation of ADP
less resistant to fatigue, high power output, rich in glycolytic enzymes, small number of mitochondria
100m sprint
Fast Twitch - Type IIA
intermediate fibers, mix of Type I and Type IIX
800m sprint
hypertrophy
increase in muscle fiber diameter due to increase in myofibril size; muscle can exert more force due to proportionality of cross-sectional area and force
Muscle soreness
from microscopic injury to muscle fibers
24-48 hrs after injury
not from lactic acid accumulation
Rigor mortis
postmortem muscle stiffness due to rigor cross-bridges in absence of ATP
Sarcopenia
age related decline in muscle mass beginning around age 25 and occurs across lifespan
slow phase sarcopenia
10% muscle mass loss from age 25-50
rapid phase sarcopenia
additional 40% muscle mass loss from age 50-80
Muscular dystrophy
group of hereditary muscle diseases that weaken skeletal muscle
no cure and respiratory failure usually occurs early in life
lack dystrophin protein
dystrophin protein
helps maintain structural integrity of sarcolemma