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attachments between muscle and bone
continuous with collagen fibers of tendons
somewhat extensible and elastic
stretches slightly under tension and recoils when released
resists excessive stretching and protects muscle from injury
returns muscle to its resting length
contributes to power output and muscle efficiency
unspecialized myoblasts remaining between the muscle fiber and endomysium
play a role in regeneration of damaged skeletal muscle tissue
smooth ER that forms a network around each myofibril
acts as a calcium reservoir; releases calcium through channels to activate contraction
made up of several hundred myosin molecules
each molecule is shaped like gold club
two chains intertwined to form a shaft-like tail
double globular head
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
when relaxed, each blocking six or seven active sites on G actin subunits
Troponin molecule: small, calcium-binding protein on each troponin molecule
titin: huge, springy protein that makes elastic filament
run through cord of thick filament and anchor it to z disc and M line
help stabilize and position the thick filament
prevent overstretching and provide recoil
tropomyosin abd troponin
act like a switch that determines when fiber can (and cannot) contract
contraction activated by release of calcium into scar plasm and its binding to troponin
troponin changes shape and move tropomyosin off the active sites on actin
clinically important protein
links actin in outermost myofilamnets 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
result from the precise organization of myosin and actin in cardiac and skeletal muscle cells
alternate A-bands (dark) and I-bands (light)
middle of A band
thick filaments only
not as dark
the way bands reflect polarized light
Z disc: provides anchorage for thin filaments and elastic filaments
z disc bisects I band and “zig-zags”
segments from z disc to z disc
functional contractile unit of muscle fiber
dystrophin and linking proteins
transfers pull to extracellular tissue
axons lead to the skeletal muscle
each nerve fiber branches out to a number of muscle fibers
each muscle fiber is supplied by only one motor neuron
dispersed throughout muscle
contact in unison
produce was contraction over wide area
provide ability to sustain long-term contraction as motor units take turns contracting
effective contraction usually requires contraction of several motor units at once
control degree of control
three to six muscle fibers per neuron
eye and hand muscles
control more strength then control
powerful contractions supplied by large motor units with hundreds of fibers
when target cell is a muscle fiber
each terminal branch of the nerve fiber within the NMJ forms separate synapse with the muscle fiber
the swollen end of nerve fiber
contains synaptic vesicles with acetylcholine (ACh)
the more anions on the inside of the membrane than on the outside
anions make the inside of the plasma membrane negatively charged then to its outer surface
the plasma membrane is electrically polarized with a negative resting membrane potential
there are excess sodium ions in the extracellular fluid
there are excess potassium ions in the intracellular fluid
sodium gates open in the plasma membrane
sodium flows into the cell downs its electrochemical gradient
these cations override the negative charges in the ICF
depolarization: inside of the plasma membrane becomes positive
immediately potassium gates open and potassium rushes out of the cell partly repelled by positive sodium charge and partly because of its concentration
loss of positive potassium ions turns the membrane negative again (repolarization)
one point causes another one to happen immediately in front of it, which triggers another one a little further along and so forth
this wave of excitation is called an impulse
toxins interfering with synaptic function
cholinesterase inhibitors bind to acetylcholinesterase and prevent it form degrading ACh
form of spastic paralysis caused by toxin clostridium tetani
glycine in the spinal cord normally stops motor neurons form producing unwanted muscle contractions
tents toxin blocks glycine release in the spinal cord and causes overstimulation and spastic paralysis of the muscles
type of food poisoning caused by a neuromuscular toxin
blocks release of ACh causing flaccid paralysis
botox cosmetic injections used for wrinkle removal
a weak contractions results, as the minimal overlap between thick and thin filaments, results in minimal cross-bridge formation
optimum resting length produces greatest force when muscle contracts
hardening of muscles and stiffening of the body beginning 3 to 4 hours after death
muscle relaxation requires ATP, and ATP production is no longer produced after death
rigor mortis peaks about 12 hours after death, then diminishes over the next 48 to 60 hours
deteriorating sarcoplasmic reticulum releases calcium
deteriorating activates sarcolemma allows calcium to enter cytosol
calcium activates myosin-actin cross-bridging
muscle contracts, but cannot relax
very brief delay between stimulus and contraction
time required for excitation, excitation-contraction coupling, and tensing of elastic components of muscle
time when muscle generate external tension
force generated can overcome the load and cause movement
time when tension declines to baseline
SR reabsorbs calcium, myosin releases actin and tension decreases
takes longer than contraction
the muscles starting length influences tension generation
muscles fatigue after continual use
warmer muscles’ enzymes work more quickly
muscle cell’s hydration level influences cross-bridge formation
with subthreshold stimuli- no contraction at all
at threshold intensity and above- twitch produced
cites more nerve fibers which stimulate more motor units to contract
more motor units come play with stronger stimuli
muscle produces internal tension but external resistance causes it to stay the same length
important in postural muscle function and antagonistic muscle joint stabilization
muscle changes in length with not change in tension
creates concentric and eccentric contraction
isometric phase
muscle tension rises but muscle does not shorten
tension stopes increasing
muscle begins to shorten and move the load (isotonic phase)
anaerobic fermentation
aerobic respiration
enables cells to produce ATP in the absence of oxygen
yields little ATP and lactate, which needs to be disposed of by the liver