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excitability (responsiveness)
respond to stimulus
to chemical signals, stretch, and electrical changes across the plasma membrane
conductivity
stimulus transmitted from cell to cell to cell …
local electrical excitation sets off a wave of excitation that travels along the muscle fiber
NOT IN SKELETAL MUSCLE (must be connected to a nerve cell); only cardiac & smooth (gap junctions)
contractility
shortens when stimulated
extensibility
capable of being stretched (w/out damage) between contractions
elasticity
returns to its original rest length after being stretched
Endomysium
connective tissue around muscle cell
inner most layer
on top of sarcolemma
Perimysium
connective tissue around muscle fascicle
Epimysium
connective tissue surrounding entire muscle
myoglobin
red pigment- gives red color
provides some oxygen needed for muscle activity
Aponeurosis
flat tendon, connected to fat muscles
myofibril
organelle present within a muscle cell
long protein cords occupying most of sarcoplasm
myofilament
contractile protein of organelle
sarcolemma
plasma membrane of a muscle fiber
sarcoplasm
cytoplasm of a muscle fiber
flooded with calcium
attached to TnC
glycogen
carbohydrate stored to provide energy for exercise
Multiple nuclei
flattened nuclei pressed against the inside of the sarcolemma
Mitochondria
packed into spaces between myofibrils
Sarcoplasmic reticulum (SR)
smooth ER that forms a network around each myofibril
functions: storage, conc. of calcium
releases calcium through channels to activate contraction
Terminal cisterns
Terminal cisterns
dilated end-sacs of SR which cross the muscle fiber from one side to the other
T tubules
tubular infoldings of the sarcolemma which penetrate through the cell and emerge on the other side
continuous with sarcolemma
transfers action potentials deep into the cell
Triad
a T tubule and two terminal cisterns associated with it
needed for muscle contraction
calcium
resting cell membrane potential
intracellular memb. is slightly negative
hyperpolarization
polarity increases (more negative)
depolarization
polarity decreases (more positive)
thick filaments
made of several hundred myosin molecules
shaped like a golf club
two chains intertwined to form a shaft-like tail
double globular head
heads directed outward in a helical array around the bundle
heads on one half of the thick filament angle to the left, while heads on the other half angle to the right
bare zone with no heads in the middle
head of myosin
active binding site for actin (high affinity site)
binding sites for ATP
are an ATPase (ATP is broken down to ADP + energy)
extends
high energy state of head (movement)
bends
low energy state of head (movement)
thin filaments
structural & regulatory proteins
Fibrous (F) actin
two intertwined strands
string of globular (G) actin subunits each with an active site that can bind to head of myosin molecule
Tropomyosin molecules
each blocking six or seven active sites on G actin subunits
fibrous protein, parallel to F actin
coveres myosin binding site → prevents myosin + actin from attaching
Troponin molecule
small, calcium-binding protein on each tropomyosin molecule
has 3 subunits (TnT, TnC, TnI)
cross bridge formation
calcium binds
troponin changes shape
pull tropomyosin off actin’s binding site
myosin can attack
TnT
tropomyosin
TnC
binds to calcium, comes from terminal cisterae
TnI
binds to G-actin, inhibitory
dystrophin
links actin in outermost myofilaments to membrane proteins that link to endomysium
transfers forces of muscle contraction to connective tissue ultimately leading to tendon
genetic defects in dystrophin produce disabling disease muscular dystrophy (MD)
deficient dystrophin
striations
result from the precise organization of myosin and actin in cardiac and skeletal muscle cells
altering A-bands (dark) and I-bands (light)
A band
dark, anisotropic
darkest part where thick filaments overlap a hexagonal array of thin filaments
H band: not as dark; middle of A band; thick filaments only
M line: middle of H band
I band
light, isotropic
the way the bands reflect polarized light
Z disc: provides anchorage for thin filaments and elastic filaments
Bisects I band
sarcomere
segment from Z disc to Z disc
functional contractile unit of muscle fiber
synapse
point where a nerve fiber meets its target cell
connection of neuron to another cell
Neuromuscular junction (NMJ)
when target cell is a muscle fiber
Axon Terminal
swollen end of nerve fiber
contains synaptic vesicles with acetylcholine (ACh)
synaptic cleft
gap between axon terminal and sarcolemma
motor endplate
area of sarcolemma where folds are in close proximity
excitation
process in which nerve action potentials lead to muscle action potentials
excitation-contraction coupling
events that link the action potentials on the sarcolemma to activation of the myofilaments, thereby preparing them to contract
contraction
step in which the muscle fiber develops tension and may shorten
relaxation
when stimulation ends, a muscle fiber relaxes and returns to its resting length, stopping interaction
Action potential (nerve impulse)
depolarization
repolarization
hyperpolarization
spastic paralysis
state of continual contraction (stimulated and stay contracted) of the muscles; possible suffocation
Tetanus (lockjaw)
a form of spastic paralysis caused by toxin Clostridium tetani
not due to synaptic influence
Flaccid paralysis
a state in which the muscles are limp and cannot contract
paralyze target’s competitive inhibitor, ACh can’t activate channels & stimulate muscle
botulism (botox)
type of food poisoning caused by neuromuscular toxin secreted by the bacterium Clostridium botulinum
blocks release of ACh causing flaccid paralysis (doesn’t attach to receptors, muscle ins’t stimulated)
cosmetic injections used for wrinkle removal
rigor mortis
hardening of muscles and stiffening of body beginning 3-4 hours after death
cross bridge forms, can’t separate bc ATP is used up
peaks about 12 hours after death, the diminishes over the next 48-60 hours
Length-tension relationship
the amount of tension generated by a muscle depends on how stretched or shortened it was before it was stimulated
weak contraction
result of an overly shortened or too stretched muscle before it was stimulated
myogram
a chart of the timing and strength of a muscle’s contraction
activity of muscle plotted on graph
Treshold
minimum voltage necessary to generate an action potential in the muscle fiber and produce a contraction
sub-threshold
subminimal, no muscles stimulated= no contraction
twitch
a quick cycle of contraction and relaxation when stimulus is at threshold or higher
muscle response to single stimulus
7-100 ms
maximal stimulus
all muscle and muscle fibers stimulated, provides the max amount of force it can
beyond maximal stimulus
doesn’t change force of contraction
latent period
very brief delay between stimulus and contraction
time required for excitation and tensing of elastic components of muscle
contraction phase
time when muscle generates external tension
force generated can overcome the load and cause movement
relaxation phase
time when tension declines to baseline
SR reabsorbs Ca2+, myosin releases actin and tension decreases
takes longer than contraction
cross bridge cycle diminishes
motor unit
motor neuron and all the muscle fibers it innerrates
identical twitches
low frequency stimuli produce…
temporal (wave) summation
higher frequency stimuli (ex: 20 stimuli/s) produce …
treppe (staircase effect)
each new twitch rides on the previous one generating higher tension
complete (fused) tetanus
unnaturally high stimulus frequencies cause a steady contraction
no relaxation in between
smooth contraction
muscle stimulated at high rate
isometric muscle contraction
length of muscle stays same while muscle contracts, muscles have to contract to maintain posture
muscle produces internal tension but external resistance causes it to stay the same length
can be a prelude to movement when tension is absorbed by elastic component of muscle
important in postural muscle function and antagonistic muscle join stabilitation
isotonic muscle contraction
force stays same as muscle contracts
muscle changes in length with no change in tension
concentric contraction
muscle shortens as it maintains tension (ex: lifting weight)
eccentric contraction
muscle lengthens as it maintains tension (ex: slowly lowering weight
myokinase and creatine kinase
enzyme systems that control phosphate transfers
myokinase
transfers phosphate from one ADP to another, converting the latter to ATP
creatine kinase
obtains phosphate from a phosphate-storage molecule creatine phosphate (CP) and gives it to ADP
Phosphagen system
the combination of ATP and CP which provides nearly all energy for short bursts of activity
after stored ATP is used up
enough energy for 6 seconds of sprinting
anaerobic threshold (lactate threshold)
point at which lactate becomes detectable in the blood
faster but less efficient
produces enough ATP for 30-40 seconds of maximum activity
lactic acid
stalls conversion of glucose to ATP
aerobic respiration
produces more ATP per glucose than glycolysis does (another 30 ATP per glucose)
more efficient for prolonged exercise
excess postexercise oxygen consumption (EPOC)
aka oxygen debt
returns cells back to normal oxygen rate
replenishes ATP sources → convert back to resting state
needed for:
aerobically replenish ATP
replace oxygen reserves on myoglobin
provide oxygen to many cells that have elevated metabolic rates after exercise
can be 6x basal consumption and last an hour (why we heavy breathe after exercising)