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characteristics of muscle tissue
- differentiated cells in parallel array
- contractile proteins
- sacroplasm: filled with aligned myofilaments
- - thin filaments (actin)
- -thick (myosin 2)
cell membrane + external lamina
classification of muscle tissue:
1) skeletal - striated (stripes), nucleie shoved to side b/c full of fibers, voluntary contraction, strong quick and discontinuous contraction, multinucleted, muscle cell = muscle fiber
2) cardiac - striated, nuclei in middle but still bundles of fibers (strong quick involuntary contraction)
3) smooth - not ordered regularly to get striations (weak, slow involuntary contraction)
connective tissue that continues at end of muscle
- functional unit of muscle
- - group of muscle fibers
why do my arms get bigger after i go surfing?!! (what what?!)
satellite cells/stem cells are triggered to divide and fuse (located in between muscle fibers)
that is why you get bigger when you work out
as long as you have external lamina then you are o.k. it can regenerate, but if you damage your muscles TOO MUCH fibroblasts will come in and connective tissue scarring :( not cool...
3 layers of connective tissue:
- epimysium - surrounds whole muscle (dense CT)
- perimysium- CT surrounds fasicle (bundle of fibers)
- endomysium - CT around each cell, small blood vessels in them
what else is in the sarcoplasm?
glycogen: energy depot
myoglobin: O2 binding protein, why muscles are red, necessary for high oxidative phosphorylation level, present in deep diving mammals
- - each one contracts causing whole fiber to contract, organized together
- basic contractile unit of myofibril
- from Z line to Z line
- draw one!!!
- I band: only actin
- H band: only myosin
- A band: overlap
- thick filament
- has a tail with 2 globular heads (actin/ATP binding site)
structure of thin filaments (actin)?
- - 2 beaded strings wrapped around each other
- plus end is bound to the Z line
- tropomyosin - forms filmaent that lies in groove
- troponin (3 subunits) TrC = binds calcium, causing conformational change exposing TrI , TrT binds to tropomyosin linking complex to filament
functions of accessory proteins and what are they?
- regulate spacing
- regulate alignment
titin, nebulin, tropomodulin, myomesin
super long protein, forms elastic matrix that prevents excessive stretching
anchors actin to Z line
anchors free portion of thin filament, stabilizes it (bc they normally keep growing) keeps it at a certain length
keeps myosin right in the middle
sliding filament hypothesis
shortening of sarcomere (muscle) due to increase in areas of overlap
5 stages of contraction cycle
- 1) attachment - RIGOR CONFO no atp bound, myosin head bound tightly to actin filament (why you have brief moment rigor mortis before you die where muscles are very tight)
- 2) release - atp binds,change in confo reduces affinity for actin so you get a release
- 3) bending - atp hydrolyzes to ADP, confo change bends myosin head, rate of atp hydrolysis is slow (requires actin as a cofactor
- 4) force generation - adp gives confo change, get a weak binding to new spot on actin, release of inorganic P, increases affinity to new binding site increases so bind more tightly! myosin moves back to original unbent position (power stroke) then releases ADP and takes back original position
- 5) reattachment - rigor conformation, each shortening provides for alignment of new actin myosin bridges
regulation of contraction
Ca binds to TnC - exposes myosin binding site on actin - atp hydrlysis produces movement of myosin head - contraction activity will continue till ca ions are removed
where is all the Calcium stored?
where do ca ions come from?
sacroplasmic reticulum and transverse system - rapid delivery and removal
SR: repeating system of networks organized in specific way with T tubules (invaginations of plasma membrane taht occur at A/I junction) this means 2 T tubules/sarcomere
voltage sensor proteins
in t tubules, sense voltage change
what is the triad?
terminal cisternae, t tubule, terminal cisternae
what do terminal cisternae contain?
- Ca release channels
- large numbers of mitochondria and glycogen granules
mechanism of transverse system?
- neuronal impulse t - release of Ach - attach to Ach receptors that trigger action potential (Na+ gates open) to plasma membrane of muscle cell - depolarization of muscle cell through t tubules, triggers voltage sensor proteins in terminal cisternae, open up Ca gated channels, once Ca channels open up its passive diffusion out of channels
- when depolarization ends active transport of Ca back inside SR cell will stop contraction
what part does the neuron play in this?
nerve impulse travels down axon - ach released from neuromuscular junction and binds to Ach receptor - triggers voltage gated Na+ channels to open up (gradient set up by NaKATPase pump so normally low Na inside the cell) - wave of depolarization - goes down t tubule - Ca released - binds to TrC - once neuro stimulation stops, sodium channels close, membrane potential goes back to what it was and Ca goes back through calcium activated ATPase pump
what is a motor unit?
a single motor neuron and all the muscles it innervates
- individual muscle fibers contract all the way or not at all
how can you vary the force of contraction?
- break up muscles into motor units
- vary number of motor units used
- graded innervation (how long innervation lasts)
(ex: delicate eye movements, neurons connected to few amount of muscle fibers because so exact)
vs. courser movements (100s of fibers - postural muscles of back)
whats meant by use it or lose it - with muscles?
muscles will atrophy if they dont get constant stimulation
what is muscular dystrophy?
progressive degeneration of skeletal muscle fibers, so constant demand on satellite cells (the pool gets exhausted)
rate of degeneration exceeds rate of regeneration (loss of muscle function)
what is a satellite cell?
muscle stem cell, will differentiate and form muscle fibers when you need them
whats the same with CARDIAC MUSCLE?
- -Thick and thin filaments, sarcomere,
-A band, I band, Z line = same
- cross striations are the same
whats diff about cardiac muscle?
- -Triglyceride droplets in cardiac muscle because need a
- lot of energy
-Even more mitochondria than muscle cells and also has more glycogen granules between myofibrils because heart never stops beating
- -each cell contains 1 or 2 centrally located nuclei
- (instead of polynucleated)
- -Each muscle cell has only 1 or 2 nuclei that are right in center, so myofibrils go around
- the nucleus)
what is the function of intercalated discs?
turn the muscle cells into branched fibers! instead of connected end to end, they are connected almost side to side so that they can communicate - functional unit
structure of intercalated discs?
- transverse component: end to end
- lateral component: parrallel to fibers
what are the types of junctions in the intercalated discs?
- fascia adherens - adhere cells together at ends to form long fiber
- macula adherens - strengthens that interaction (desmosomes are transverse and lateral)
- gap junctions = allow cells to communicate (only lateral)
why does skeletal muscle not have intercalated discs?
because they dont need gap junctions, they already share cytoplasm
what are the differences with cardiac SR?
- - larger T tubules
- external lamina
- t tubules are at z line instead of A/I junction
- diad, not triad
- more mitochondria and lipid droplets in cytoplasm
- SR not as well organized, no discrete bundles
is cardiac muscle stimulated by a motor neuron?
pacemaker/SA node --> perkinje fibers trigger the heartbeats (spontaneous rhythmic contraction)
what is the source of calcium for cardiac muscle?
wave of depolarization - open voltage sensor proteins (but cant store Ca as well as in skeletal muscle) so its a combo of intracellular and extracellular calcium!
extracellular and intracellular Ca?
voltage sensor proteins are calcium channels themselves! so ca moves in from the outside first which triggers Ca activated calcium release channels on the inside (intracellular)
structure of smooth muscle
- bundles or sheets of elongated, fusiform cells (fibers)
- lots of gap junctions
what causes the uniform force?
non striated, each cell enclosed by basal lamina and reticular fibers
- = combined force generated by each into concerted action
- good for continuous contractions of low force
other names for smooth muscle?
- visceral muscle
- involuntary muscle
where is it in body?
viscera (blood vessels), GI tract, uterus, urinary bladder, male genital tract, gallbladder
structure of filaments:
- contractile apparatus of thin and thick filaments
- cytoskeleton of desmin and vimentin intermediate filaments
- remaining sarcoplasm: thin filaments and thick myosin filaments scattered throughout
- thin filaments are attached to dense bodies
LOOK AT PAGE 334
what are the 2 proteins that block myosin binding site?
caldesmin and calponin
how does tropomyosin get shifted? like troponin shifts to open up binding site?
calcium leads to phosphorylation of myosin heads
role of dense bodies?
- (like the Z line)
- - contains alpha actinin (and other attachement proteins) that anchor thin filaments and intermediate filaments to sarcolemma
mechanism of smooth muscle contraction?
different stimuli increase calcium - binds to calmodulin - ca2+ calmodulin complex + MLCK - phosphorylates myosin which means that myosin can then bind actin - when ATP is present the head bends producing contraction
what can stimulate the smooth muscle contraction?
- action potential
- or hormonal stimulation
- parasympathetic nervous system
why does whole muscle cell shrink instead of shorten?
contractions (sliding filaments) happen in different directions
desmin or vimentin
actin thin filament anchored to intermediate filaments
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