CHAPTER 9: MUSCLE Flashcards
cardiac and smooth muscle cells generally have how many nuclei?
a single nucleus
skeletal muscle fibers have how many nuclei?
multiple nuclei (multi-nucleated)
characteristics of a skeletal muscle fiber
-multi-nucleated
-contains T-tubules
-contains myofibrils and sarcomeres
-sarcolemma (plasma membrane)
-sarcoplasm (cytoplasm)
-sarcoplasmic reticulum (smooth ER)
-
if skeletal muscle fibers are damaged, they undergo a repair process involving what?
satellite cells: undifferentiated stem cells
the satellite cells are normally inactive, but they become active following _____ …
muscle strain/injury and undergo mitotic proliferation
epineurium surrounds outer surface of _____
nerve
perineurium surrounds outer surface of ______
fasicles (bundle of muscle fibers)
endoneurium surrounds the individual ______
axons
epimysium
sheath of fibrous elastic tissue covering entire muscle
perimysium
a sheath of connective tissue surrounding each fascicle (bundle of muscle fibers)
endomysium
connective tissue covering each muscle fiber
myofibrils
structures that give skeletal and cardiac muscle their characteristic “striated appearance”
how are thick (myosin) and thin (actin) filaments arranged?
hexagonal arrangements
___ thin filaments surround each thick filament, and ____ thick filaments surround each thin filament
6 thin (actin), 3 thick (myosin)
contraction refers to…
the activation of the force-generating sites within the muscle fibers—the cross-bridgers (ex: holding a dumbell at a constant position requires muscle contraction)
sliding filament mechanism
force generation produces shortening of a skeletal muscle fiver, the overlapping thick and thin filaments in each sarcomere move past each other, propelled by movements of the cross-bridges
what does the ability of a muscle fiber to generate force and movement depend on?
it depends on the interaction of the contractile proteins actin and myosin
cross-bridges in the thick filaments bind to the actin in the thin filaments and undergo a conformational change that…
… propels the thin filaments towards the center of the sarcomeres
troponin
-regulatory protein
-forms a complex with other proteins of the thin filament
-troponin binds Ca2+ reversibily
-Ca2+ binding to troponin regulated skeletal muscle contraction because it moves the tropomyosin away and allows myosin and actin to interact
troponin C
binds to calcium ions to produce conformational chage in T and I
troponin T
binds to tropomyosin, interlocking them to form a tropinin-tropomyosin complex
troponin I
binds to actin in thin myofilaments to hold troponin-tropmyosin complex in place
cross-bridge cycle steps
1) binding (of actin with myosin + ADP, Pi)
2) movement of CB & release ( of ADP, Pi)
3) dissociate (actin from myosin & bind to new ATP)
4) energize (myosin hydrolysis of ATP)
*results in myosin + ADP, Pi
sarcoplasmic reticulum
a muscle homologous to ER found in most cells
-ca2+ is stored and released following membrane excitation
t-tubules and SR are connected with junctions called…
junctional feet/foot processes
these junctions involve 2 integral membrane proteins, one in t-tubule membrane and the other in the SR membrane
the protein connected to the t-tubule is a ____, which acts as a voltage sensor
a modified voltage-sensitive Ca2+ channel known as DHP (dihydropyridine) receptor
sarcoplasmic reticulum forms ______ around each myofibril
sleeve-like segments
motor neurons
nerve cells whose axons innervate skeletal muscle fibers
axons of motor neurons are _____ and are the ____-diameter axons in the body
myelinated, largest-
what does propagating action potentials at high velocities mean?
it means that signals from the CNS can travel to skeletal muscle fibers with minimal delay
motor unit
motor neuron and the skeletal muscle fibers it innervates
one motor neuron innervates _____ muscle fibers, one muscle fiber is innervated by _____ motor neuron
many, only one
tension
force exerted on an object by a contracting muscle
load
the force that a muscle fiber generates a force called tension to oppose
twitch
the mechanical response of a muscle fiber to a single action potential
latent period
period of time from the action potential to the onset of contraction (time delay is due to excitation-contraction coupling)
contraction phase
time that tension is developing due to the cross-bridge cycling
relaxation phase
time that the tension is decreasing and is longer than the contraction phase (result of the amount of time it takes to get all of Ca2+ returned to lateral sacs of SR)
isometric twich
generates tension but does not shorten the muscle (load > force generated by muscle)
contraction time
time interval from beginning of tension development and end of latent period
when tension exceeds the load, this type of shortening occurs
concentric contraction
when unsupported load is greater than the tension generated by CBs
eccentric contraction
isotonic twitch
shortens the muscle
three ways a muscle fiber can form ATP
1) phosphorylation of ADP by creatine phosphate
2) oxidative phosphorylation of ADP in mitochondria
3) phosphorylation of ADP by glycolytic pathway in cytosol
sarcomeres
repeating, striated pattern of light of light and dark bands (skeletal muscle fibers)
which neurotransmitter do the vesicles in the motor neuron contain?
acetylcholine (Ach)
neuromuscular junction
junction of axon terminal with the motor end plate
events that occur at neuromuscular junction that lead to an action potential:
1) action potential arrives at axon terminal & depolarizes plasma membrane
2) also opens ca2+ channels and allows calcium ions to flow in from EC fluid
3) ca2+ binds to proteins that enable membranes of ACh-contianing vesicles to fuse with neuronal plasma membrane
4) ACh is released into EC cleft separating axon terminal and motor end plate
5) ACh diffuses from axon terminal to motor end plate, where it binds to ionotropic receptors
6) that binding opens an ion channel in receptor proteins (allows Na+ and K+ to flow in)
7) because more Na+ moves in than K+ out –> local depolarization (…)
end-plate potential
local depolarization of the motor end plate as a result of difference in electrochemical gradient because more Na+ goes in than K+ goes out
which is more sufficient to depolarize muscle membrane adjacent to end-plate membrane to its threshold potential?
excitatory postsynaptic potential (EPSP) or end-plate potential (EPP)
end-plate potential (EPP)
all neuromuscular junctions are _______ (inhibitory or excitatory)
excitatory
what neurotransmitter breaks down ACh?
acetylcholinesterase
(result: choline is transported back into axon terminal to be reused in synthesis of new ACh & ion channels in plate CLOSE)
curare
a deadly poison (arrowhead) that binds strongly to nicotinic ACh receptors so ACh cannot bind to them anymore –> results in no EPP in motor end plate and no contraction
antidote for organophosphate an nerve gas include _____, a drug that reactivates acetylcholinesterase, and _____, a receptor antagonist
pralidoxime and atropine
excitation-contraction coupling
sequence of events by which an action potential in plasma membrane activates force-generating membranes
tropomyosin
rod-shaped molecule with polypeptides intertwined that partially covers the myosin-binding site on each actin monomer, which prevents cross-bridges from making contact with actin
how to get tropomyosin molecules to move away from their blocking positions on actin?
Ca2+ must bind to specific binding sites on binding subunit of troponin –> changes shape of troponin, which allows tropomyosin to move away from binding site on actin
steps of release of Ca2+ by SR during contraction
1) action potential propagated along muscle cell membrane and into T-tubules
2) Ca2+ released from terminal cisternae
3) Ca2+ binding to troponin removes blocking action of tropomyosin
4) cross-bridges bind, rotate, and generate force
5) Ca2+ transported back into SR
6) Ca2+ removal from troponin restores tropomyosin blocking action
do lengths change in thick and thin filaments due to shortening of a skeletal muscle fiber?
no
power stroke
movement of bound cross-bridge when binding of myosin to actin triggers release of strained conformation of energized CB
rigor mortis
gradual stiffening of skeletal muscles that begins several hours after death and reaches a maximum after about 12 hours
difference between concentric and isometric contraction in step 2 of cross-bridge cycle:
in concentric, the CBs bound to actin rotate through their power stroke, causing sarcomere shortening
in isometric, bound CBs do exert a force on thin filaments but cannot move them (rotation is absorbed by sarcomere/muscle)
fast-twitch fibers vs slow-twitch fibers
fast-twitch fibers have short contraction times, slow-twitch fibers have longer contraction times
as load increases, shortening velocity…
decreases (hyperbolic curve)
summation
increase in muscle tension from successive action potentials occurring during phase of mechanical activity
tetanus
maintained contraction in response to repetitive stimulation
difference between unfused and fused tetanus
unfused = tension may oscillate as muscle fiber partially relaxes b/t stimuli
fused = no oscillations, produced at higher stimulation frequencies
why is tetanic tension much greater than twitch tension?
because during tetanic contraction, the successive Aps each release Ca2+ from SR before all Ca2+ from previous AP has been pumped back into SR –> results in persistent elevation of cytosolic Ca2+ concentration, so more available binding sites = more CBs become bound to thin filaments
optimal length
length at which the fiber develops the greatest isometric active tension
stretching a fiber beyond optimal length or decreasing it below that will decrease the tension generated because…
…of reduced CB access to thin filaments
when chemical bond b/t creatine and phosphate is broken…
the energy (+ phosphate group) can be transferred to ADP to form ATP using enzyme creatine kinase (enzymatic reaction)
during first 5-10 minutes, breakdown of muscle glycogen to glucose provides major fuel contributing to…
oxidative phosphorylation
sources of glucose for glycolysis
1) blood
2) stores of glycogen within contracting muscle fibers
at end of muscle activity, creatine phosphate and glycogen concentrations in muscle have..
decreased (must replace these to return fiber back to og state)
oxygen debt
increased oxygen consumption following exercise repays this by increased in ATP via O.P.
muscle fatigue
decline in muscle tension as a result of previous contractile activity
fatigue develops more slowly with ____-intensity & ____-duration exercise (ex: long-distance running)
low intensity and long-duration
central command fatigue
when appropriate regions of cerebral cortex fail to send excitatory signals to the motor neurons
can cause a person to stop exercising even if muscles aren’t fatigued
fatigue results from:
-decrease in ATP [ ]
-increase in ADP, Pi, Mg, H, oxygen free radicals [ ]s
metabolic changes can:
-decrease rate of Ca2+ release, reuptake, and storage by SR
-decrease sensitivity of thin filament proteins
-directly inhibit the binding and power-stroke motion of CBs
fast-twitch (type 2) fibers contain myosin with 4x _____ ATPase activity than slow-twitch (type 1)
greater
subtypes of fast-twitch fibers:
2A and 2X (& 2B)
(2X is faster)
oxidative fibers
fibers with numerous mitochondria and a high capacity for oxidative phosphorylation
AKA red muscle fibers because myoglobin gives them a dark red color
myoglobin
oxygen-binding protein that increases rate of oxygen diffusion into the fiber and provides small store of oxygen
(oxidative fibers have a lot)
glycolytic fibers
fibers with few mitochondria but a high [ ] of glycolytic enzymes and a large store of glycogen
AKA white muscle fibers because of lack of myoglobin
slow-oxidative (type 1) fibers characteristics
low myosin-ATPase activity and high oxidative capacity
fast-oxidative-glycolytic fibers (type 2A) characteristics
high myosin-ATPase activity and high oxidative capacity and intermediate glycolytic capacity
fast-glycolytic (type 2X) fibers
low myosin-ATPase activity and high glycolytic capacity
number of fibers contracting at any time depends on what two factors?
1) number of fibers in each motor unit
2) # of active motor units
total tension of a muscle depends upon what two factors?
1) amount of tension developed by each fiber
2) # of fibers contracting at any time
greater diameter of a single fiber = ______ force
greater force
activating a fast-glycolytic motor unit will produce _____ force than activating a slow-oxidative motor unit
more force
recruitment
process of increasing # of motor units that are active in a muscle at any given time –> increases amount of tension and rate of shortening
(smaller motor neurons are recruited first)
neural control of whole-muscle tension involves:
1) frequency of APs in individual motor units
2) recruitment of motor units
shortening velocity depends on what factors?
1) load on the fiber
2) speed of myosin type expressed in fiber
denervation atrophy
when denervated muscle fibers (deprived of neural supply) become smaller and amt of contractile proteins increases because neyrons to skeletal muscle are destroyed or the junctions become nonfunctional
disuse atrophy
when muscle hasn’t been used for a long time
explain the switch of myosin composition from type 2X to type 2A
occurs during low intensity but long duration of exercise, where # of mitochondria and capillaries increases –> increase ability to sustain muscle contraction/increased capacity for endurance, minimum fatigue
explain the switch of myosin composition from type 2A to type 2X
occurs during high-intensity but short duration exercise, where fast-twitch fibers increase (hypertrophy) and more myofibrils form –> strengthens muscle, but little capacity for endurance, fatigue quicker
myostatin
regulatory protein produced by skeletal muscle cells and binds to receptors on those same cells
exerts negative feedback to prevent hypertrophy
explain soreness
-result of structural damage to muscle cells + membranes
-results from eccentric contractions (lengthening of a muscle fiber by external force produces greater muscle damage)
flexion
bending of a limb at a joint
extension
straightening of a limb
antagonists
group of muscles that produce oppositely directed movements at a joint
lever action of muscles
requires tension to be far greater than load to sustain a load in isometric contraction
poliomyelitis
paralysis of skeletal muscle
muscle cramps
involuntary tetanic contractions related to heavy exercise –> due to dehydration + electrolyte imbalances in fluid around muscle and nerve fibers
hypcalcemic tetany
excessive muscle contractions caused when EC Ca2+ decreases below normal (Na+ channels open)
muscular dystrophy
genetic disorder that results from defects of muscle-membrane-stabilizing proteins like dystrophin –> associated with degeneration of muscle fibers
myasthenia gravis
autoimmune disorder in which destruction of ACh receptors of motor end plate causes progressive loss of ability to activate skeletal muscles –> muscle fatigue
smooth muscle characteristics
-lack a cross-striated pattern
-nerves to them are part of autonomic division of PNS
-INVOLUNTARY
-smaller than other muscles
-have a single nucleus and capacity to divide throughout life of an individual
dense bodies
thin filaments that are anchored to either plasma membrane or to cytoplasmic structures (in place of sarcomeres) & next to Z lines
difference between smooth and skeletal muscle in terms of force
in smooth muscles, significant force is generated over a broad range of muscle lengths (good b/c they usually surround hollow structures than change in volume)
smooth muscles don’t contain what that other muscle types do?
no sarcomeres! (still use sliding filament mechanism though) + no troponin
what happens after an increase in cytosolic Ca2+ in smooth muscle fiber?
1) Ca2+ binds to calmodulin, a Ca2+ binding protein that is present in the cytosol of all cells
2) the complex binds to myosin light-chain kinase, which activates the enzyme
3) active myosin light-chain kinase uses ATP to phosphorylate myosin light chains in the globular head of myosin
4) phosphorylation of myosin drives the cross-bridge away from thick filament backbone -> binds to actin
5) CB’s go through repeated cycles of force generation as long as myosin light chains are phosphorylated
what is needed to relax a smooth muscle?
first myosin must be dephosphorylated because it needs to be unable to bind to actin –> mediated by enzyme myosin light-chain phosphatase
when cytosolic Ca2+ [ ] increases, rate of myosin phosphorylation…
exceeds the rate of dephosphorylation –> produces an increase in tension
latch state
condition where stimulation is persistent and Ca2+ [ ] remains elveated, so rate of ATP hydrolysis by CBs declines even though isometric tension is maintained
sources of Ca2+
1) sarcoplasmic reticulum
2) EC Ca2+ entering the cell through the plasma membrane Ca2+ channels
smooth muscle tone
when the Ca2+ [ ] is sufficient to maintain a low level of basal cross-bridge activity in the absence of external stimuli
inputs that influence smooth muscle contractile activity
-spontaneous electrical activity in plasma membrane of muscle cell
-neurotransmitters released by autonomic neurons
-hormones
-changes in chemical composition of EC fluid
-stretching
what can smooth muscle cytosolic Ca2+ [ ] be increased/decreased by?
graded depolarizations/hyperpolarizations in membrane potential
–> these increase/decrease # of open Ca2+ channels
pacemaker potential
membrane potential change occurring during spontaneous depolarization to threshold (refer to graphs in doc pg 15)
slow waves
periodic fluctuations in membrane potential due to regular variation in ion flux across membrane
(see how excitatory input affects in graphs in doc pg 15)
smooth muscle cells do not have a specialized _____
motor end-plate region
varicosities
-swollen regions on branches of axons of postganglionic autonomic neurons
-contain vesicles filled with neurotransmitters
key difference between smooth and skeletal muscles in regards to neural contractile activity
skeletal can only receive excitatory input (increase) from motor neurons, SMOOTH MUSCLE TENSION CAN BE INCREASED OR DECREASED by neural activity
what local factors can alter smooth muscle tension?
-paracrine signals
-acidity
-oxygen and CO2 [ ]
-osmolarity
-ionic composition of EC fluid
(most induce relaxation)
single-unit smooth muscle characteristics
-whole muscle tissue responds to stimulation (elec + mech)
-each muscle cell is linked to adjacent fibers by GAP JUNCTIONS –> allows APs to propagate to other cells
-ex) pacemaker cells –> spontaneously generate APs
-contractile response can be induced by stretching muscle tissue
multiunit smooth muscle
-no or few gap junctions
-APs do not occur in the cells of most multiunit SMs
-innervated by autonomic nerves
-circulating hormones can increase or decrease contractile activity in multiunit SM (not stretching though!)
cardiac muscle characteristics
-striated muscle with regularly repeated sarcomeres composed of myosin-containing thick filaments
-contain troponin and tropomyosin and T-tubule system
intercalated disks
structures where adjacent cardiac muscle cells that are joined end to end to + contain gap junctions (see page 17 of doc)
how are cardiac muscle cells arranged?
they are arranged in layers and surround hollow cavities (blood-filled <3 chambers)
L-type Ca2+ channels
specialized channels where there is an influx of Ca2+ resulting in depolarization during cardiac muscle cell APs
what is cardiac muscle contraction dependent on? (this differs from skeletal)
movement of EC Ca2+ into cytosol because cytosolic Ca2+ [ ] needs to be restored to its original resting value
why can’t multiple cardiac APs be initial during the time frame of a single twitch?
because the heart’s function must alternate between being relaxed (and filling with blood) and contracting to eject blood
what initiates action potentials in cardiac muscle?
certain cardiac muscle cells exhibit pacemaker potentials that generate APs spontaneously & it propagates rapidly throughout ENTIRE heart
