Exam 3 Study Guide Flashcards
Describe the internal structure of the muscle cell (fiber). What is the difference
between a myofilament and a myofibril?
each muscle cell is long, multinucleated, and cylindrical.
the sarcolemma (plasma membrane) surrounds everything within the muscle cell (called sarcoplasm)
the cells or fiobers are packed with protein rods called myofibrils and mitochondria.
a myofibril is a collection of myofilaments- thick and thin
thick: composed of mysoin, has one tail and two head groups.
head groups: have an actin binding sites and ATP binding sites.
thin: composed of actin, small spherical proteins, have one binding site for myosin.
have two regulatory proteins: tropomyosin and troponin
Functions of Skeletal Muscle
functions for movemement, when muscles contract and use bones as levers so that bones can move.
functions to help maintain posture because of gravity. skeletal muscle is always partially contracted to keep skeleton upright.
functions to stabalize joints; muscles can cross joints and when they contract, they provide that joint with stability.
functions to generate heat when they contract
functional charcateristics of skeltal muscle
exhibits excitability, meaning skeletal muscle is capable of rapidly changing membrane potential (charge difference/difference in ion concentrations cross plasma membrane) in order to send or recieve info from other excitable cells.
contractibility: has the ability to shorten or contract
also able to extend or stretch beyond its resting lenght
elasticity: when strecthed, skeletal muscle has the tendendy to want to go back to its original resting length or recoil.
structural characteristics of skeletal muscle
innervated by the somatic NS (motor division- allows for voluntary movement) and very vascular to fuel cellular activities.
has connective tissue sheaths- epimysium: sheath around the outside entirety of the muscle. dense irregular CT
perimysium- surrounds the fasicle- group of skeletal muscle cells. dense irregular CT
endomysium- surrounds individual muscle cells- aereolar CT
can connect directly or indirectly to bone. if direct, the epimysium is continuous with the periosteum of bone. dense irregular CT
if indirect (via tendons or aponeurosis- a sheet or very wide tendon) dense regular CT
sarcomere
repeating sarcomeres within a myofibril
I bands: only thin filaments
A bands: both filaments, also corresponds to entire length of thick filament
H zone: small region at center of A band, with only thick filaments
sarcomere is from one z-disc or center of I band to the next
role of Ca+
calcium is stored in sarcoplasmic reticulum (specialized type of smooth ER that stores Ca+).
Ca+ being released from SR, it binds to troponin, moves tropomyosin out of the way, exposing binding sites on actin, so mysosin can reach up, bind to actin and form a cross bridge.
sarcoplasmic reticulum
stores calcium
surrounds myofibrils and has tubules and terminal cisterns (flattended sacs).
terminal cisterns are going to flank T-tubules creating a triad to allow for rapid communication
sliding filament theory
when myosin moves in a power stroke, it walks along actin and pulls on actin and thick and thin filaments slide past one another to grigger skeletal muscle tension. filaments do not change in length, there is a greater degree of overlap between filaments. The I bands get shorter, but A bands (corresponf to length of thick filament) do not change in length. H zone has disappeared.
T-Tubules
T-tubules are intrusions of sarcolemma and allow for changes in membrane potential to reach deep down into the cell. changes in membrane potential (voltage) triggers release of Ca+ from SR. the triad allows for rapid comminication between TT and SR.
electrical signal (action potential) on TT triggers release of Ca+ and then triggers a muscle contraction
tropomyosin and troponin
tropomyosin: rod shaped protein that wraps around tyhin filaments. at rest, it blocks actin binding sites which prevents a cross bridges.
troponin: bound to tropomyosin, complex of 3 polypeptides. binds calcium. calcium is the trigger for muscle contraction. when it binds to troponin, troponin pulls tropomyosin out of the way to expose myosin binding sites of actin.
Why is skeletal muscle striated?
orientation of thick and thin filaments give rise to striations. dark sections correspond to overlap, light sections correspond to no overlap
power stroke
actin binding sites allow for myosin to bind to actin, forming a cross bridge. takes NRG to reach up and bind to actin, so the ATP binding site is neceessary to fuel the movement of myosin. have polarity in their arrangment, myosin heads are only on the outside, not at the center because there is no actin at the center for myson to bind to.
myosin will reach up and bind actin and also hydrolyzes ATP and changes confirmation to pull actin- known as a power stroke, generating tension in muscle
general steps of the power stroke
- the active site on actin is exposed as Ca2+ binds troponin.
- the myosin head forms a cross bridge with actin.
- during the power stroke, the myosin head bends, and ADP and phosphate are released.
- a new molecule of ATP attaches to the myosin head, causing the cross-bridge to detach.
- ATP hydrolyzes to ADP and phosphate, which returns the myosin to the ready position.
events at the neuromuscular junction
the point of chemical communication
motor neurons controlled by somatic nervous system
single somatic motor neuron can interact with many skeletal muscle cells.
motor unit
a motoneuron and all of its associated muscle fibers
the basic functional units of skeletal muscle
neuromuscular junction- on test
passes action potential from motor neuron to skeletal muscle cell.
action potential is a change in charge across membrane. voltage gated calcium channels open when an action potential arrives.
calcium will then flood the axon terminal.
when ca levels rise in axon terminal, synaptic vesicles fuse with membrane and release of a neurotransmitter (ACh) by exocytosis.
ACh tells muscle fiber to generate another action potential by binding to receptors on the sarcolemma after diffusing across the synaptic cleft.
the skeletal muscle sarcolemma region at the junction is called the motor end plate. has folds for more surface area for recepting.
when ACh binds to to chemically gated ion channels on motor end plate, it allows for sodium to enter and potassium leaves. more sodium enters than potassium leaves. inside is now more positive, outside is negative. (end plate potential) beginnings of an action potential on that muscle fiber.
end plate potential is local, but leads to an action potential in entire skeletal muscle cell
when AChesterase degrades Ach, sarcolemma
muscle fiber excitation
end plate potential leads to action potential on adjacent sarcolemma that carries along sarcolemma
excitation contraction coupling
action potential on sarcolemma spreads along sarcolemma, action potential dives deep down into the muscle cell and triggers the release of calcium.
sarcolemma has T-tubules thast allow action potential to dive deep down. T-tubules are flanked by two terminal cisterns (triad) and very close to sarcoplasmic reticulum that allows for quick diffusion. when action potential arrives at t tubules, it triggers the release of ca from the sarcoplasmic reticulum. voltage sensitive t tubule protein changes conformation. when it changes conformation, it kicks open calcium channels on the sarcoplasmic reticulum, and ca floods the sarcoplasm. ca is trigger for muscle contraction. ca binds to troponin when it enters sarcoplasm and causes a change in conformation and pushes tropomyosin out of the way, exposing actin binding sites so myosin can reach up and bind to actin and forms a cross bridge.
cross bridge cycling
how myosin reaches up to form a cross bridge with actin
- starting with where mysoin is bound to actin: high energy or cocked position because it has already bound ATP, hydrolyzed it, (now ADP because phosphate group is broken off) and mysosin has the energy to enter high energy or cocken position.
- mysosin releases ADP and phosphate, and changes conformation and enters low energy or bent conformation once it has released ADP and phosphate. mysosin is still bound to actin, so it pulls on actin (power stroke- tension is developed). this increases degree of overlap between thick and thin filaments.
- myosin detaches from actin when ATP binds to myosin (cross bridge detaches). ATP is then hydrolyzed and phosphate group is broken off, giving mysosin energy to bind actin again.
cycle continues until calcium returns to SR, because then actin binding site is no longer exposed, so cross bridge cycling occurs only as ca is present.
what causes relaxation?
action potential is no longer present, and ca will be pumped back into the SR by the SR.
Requires ATP- once Ca is back into SR, tropomyosin again covers the actin active sites.
sarcoplasmic reticulum
specialized smooth ER
Where is ATP required in muscle contraction?
for myosin detachment, and for pumping ca back into the SR.
filaments at rest
thin filaments: when ca is not present, tropomyosin blocks attachment points on actin
thick: ATP bonds to myposin heads, hyrdolyzing it, and waits for ca to be released so it can bind to actin right away.
Rigor mortis
since ATP is required for myosin detachment, cross bridges cannot detach right away
energy consideration
ATP is produced by oxidation reduction rxns in which e- are lost from food fuels and transfered to ADP and to form ATP.
glucose is broken down by pulling off e- through rxns. lost e- are passed off and ATP forms ADP
direct phosphorylation
muscle has a high NRG molecules called creatine phosphate
creatine phosphate helps generate ATP immediately when muscle needs to contract (exercise), by transferring a phosphate to ADP to generate ATP and creatine
first way you generate ATP, but has short duration
muscle stores 2-3 times more creatine phosphate than ATP, because ATP could be used nonspecifically, as it cannot be reserved on its own to fuel this proccess. so it is stored is CP so it can be reserved.
creatine kinase- catalyzes rxn
glucose oxidation rxn
either gaining O or losing a H. e- are lost
main focus is losing e- when H+ is pulled off
products: ATP, CO2, and H2O
glycolysis
2nd process to occur, fuels for 30-40 seconds
anaerobic pathway, starts with glucose (6 C) and ends with 2 pyruvates (3 C each) + 2ATP net gain generated, and H+ are lost and held onto by NAD+ which turns to NADH, so +2NADH
occurs in the cytosol of muscle cells, begins with glucose from bloodstream or glycogen.
fast, but produces only 2 ATP
if O2 is present, pyruvic acid enters citric acid cycle (areobic cellular respiration) where it is oxidized more to create more ATP.
if O2 is not present, pyruvic acid is converted to lactic acid so NAD+ can be regenrerated and another round of glycolysis can occur.
substrate level phosphorylation
pulling P off another molecule in order to produce ATP
aerobic cellular respiration
produces majority of ATP needed to fuel muscle contraction
occurs in the mitochondria
produces ATP, water and CO2
transitional phase:
occurs in matrix of mitochondria, pyruvate is in the matrix and converted into acetyl coenzyme A (CoA). go from a 3 C molecule to a 2 C molecule (decarboxylation- remove C as CO2)
H is also lost, and is transfered to NAD to form NADH.
generated CO2, NADH, and CoA
trying to prepare pyruvate into the appropriate form to enter TCA cycle
Citric acid cycle (TCA cycle, Krebs cycle): CoA (2 C)combines with oxaloacetic acid (4C) to form citric acid (6 C). CoA is released to again react with another pyruvic acid.
citric acid is converted to many intermediary molecules, last one is oxaloacitate. called pick up molecule because it always picks up CoA to get it into the TCA cycle.
Go back to slide: “As ONE citric acid is produced,”
4 oxidation events (pull of H four times), 2 decarboxylations (two carbons come off as CO2), and 1 ATP (for each pyruvic acid, substrate level phosphorylation)
3 NADH, and 1 FADH2
e- transport chain: final stage
takes place in mitochondria. enzyme called ATP synthase on cristae of mitochondria produces ATP by oxidative phosphorylation
at the end of ETC, e- are passed to O, which forms water.
O is final e- acceptor
net yield about 30 ATP (cost 2 to transport)
more efficient
oxidative phosphorylation
e- are transferred from NADH and FADH (e- stroing molecules) to a series of protein complexes in inner mitochondrial membrane. as they are passing the e-, they harness the NRG of the e- to drive the transport of H from the matrix to the intermembrane space.
now a H+ gradient. inner membrane is not permeable to H, so ATP synthase uses NRG from H flow through it. It hooks ADP and phosphate together to make ATP (chemiosmosis)
produces 28 ATP
chemiosmosis
the only way for H+ ions to get back into the mitochondrial matrix from the intermembrane space is via ATP synthase. ATP synthase will harness the chemical energy associated with the proton gradient to drive the conversion of ADP + Pi to ATP. This is known as chemiosmosis. Eventually, electrons passed from complex to complex are passed to oxygen to form a water molecule. Thus, oxygen is known as the final electron acceptor.
Why will you die without oxygen?
e- will stop being passed with no O as the final acceptor in the ETC, and no H gradient exists, so you will not be able to produce ATP
3 types of skeletal muscle cells/fibers
most muscles have all 3 types of fibers but proportions vary, genetically determined but can be developed with training.
slow oxidative, fast oxidative, fast glycolytic
slow oxidative
slow contraction and myosin ATPase activity,
aerobic
myoglobin content is high
glycogen stores are low
recruitment order is first
rate of fatigue is slow
best for endurance
red (capillaries)
fast oxidative
fast oxidative,
aerobic, some aerobic glycolysis
high myoglobin content
intermediate glycogen stores
rate of recruitment is second
rate of fatigue is intermediate
best for sprinting and moderate walking
red to pink (capillaries)
fast glycolytic
fast contraction,
fast ATPase activity
anaerobic glycolysis
low myoglobin content
high glycogen stores
recruitment order is third
rate of fatigue is fast
best for short term intense movement, ex. weight lifting hitting a baseball
white (capillaries)
myoglobin
binds oxygen, helps to keep O2 levels high in slow and fast oxidative muscle fibers, final e- acceptor
fast twitch
generate muscle tension faster than ST, generate high peak muscle force than ST
asynchronous summation/recruitment
motor units to a given muscle are used sequentially, tension may remain the same in muscle, but at any given moments, different motor units are responsible for generating tensions
skeletal muscles rotate so they won’t get fatigued
used in muscle tone and posture (always partially contracted because of gravity)
treppe
if the stimulus remains the same, the tension generated with each subsequent stimulus, the tension will increase.
force will be increased each time an action potential arrives at a muscle
because ca is still left over in the cytoplasm, so some cross bridges remain so more force in generated. heat also makes myosin ATPase work more efficiently, so cross bridges form faster and create more tension
why you want to warm up to start generating heat
muscle fatigue
inability for muscles contract even though muscle is being stimulated
NOT due to lack of ATP
fatigue is due to ionic imbalances that result from using ATP alter excitation-contraction coupling in moderate exercise
EPOC (excess post exercise oxygen consumption)
oxygen debt
the amount of additional oxygen that must be inhaled following exercise to restore body to pre-exercise conditions
used to: convert lactic acid back to pyretic acid (prevents drastic pH changes so enzymes will function)
replenish glycogen
restore creatine phosphate and ATP reserves
replace oxygen stores on myoglobin for cellular respiration
liver also converts lactic acid in the bloodstream to glucose or glycogen
EPOC begins as soon as exercise stops
better conditioned you are, less EPOC
because of increased capillary supply
increased mitochondria
increased efficiency if cardiovascular system
isotonic vs isometric contractions
force = tension in (g)
isotonic contraction: if tension produced by muscle exceeds load, muscle will contract and change length
isometric contraction: if tension produced by muscle does not exceed load, muscle will not change in length
muscle is still contracting, but not changing length so mechanical load won’t move
concentric and eccentric isotonic contractions
concentric: muscle is shortening
eccentric: muscle in lengthening
DOMS (delayed onset muscle soreness)
NOT due to lactic acid build up, but micro trauma or small tears
most evident in eccentric muscle contractions because lengthening a muscle is more likely to produce a small tear
satellite cells
repairs skeletal muscle, myoblast-like cells are stem cells in muscle, help repair injured muscle cells
smooth muscle characteristics
lines walls of hollow organs or structures (airways, digestive tract, urinary tract). exception is the heart
cells are usually arranged into sheets
cells are smaller than skeletal muscles, spindle shaped, and uninucleate
no obvious striations because myofilament organization is not as precise (lattice like), distinct from sarcomere pattern in skeletal muscle.
no polarity in arrangement of myosin heads all along thick filaments, allows smooth muscle to generate the same amount of tension to to be generated as skeletal muscle despite being smaller.
Intermediate filaments are in smooth muscle to provide support to cells and help resist tension.
Gap junctions (communicating junctions) are present to pass action potentials from one cell to the next, and allows for all of smooth muscle to contract as a unit. If one cell in a sheet is stimulated, it will spread to all in the sheet.
No T-tubules present.
Have caveolae are pouch like infoldings of the sarcolemma with ca channels inside them. this allows for ca to enter the cell from extracellular fluid and sarcoplasmic reticulum to trigger muscle contraction.
Much less extensive SR because the ca comes in through the ca channels at the caveolae.
no triads.
have tropomyosin, but no troponin, instead we have calmodulin regulatory protein which binds ca in smooth muscle.
longitudinal layer: oriented along long axis of organ
causes entire layer to shorten- propels substances
circular layer: oriented around the circumference
changes diameter of lumen, causes constriction
endomysium is the only CT sheet in smooth muscle
How does ca trigger smooth muscle contractions?
when ca enters the cytosol, it enters either from ca channels at the caveolae or the from the scant SR.
ca then binds to calmodulin (exists separately from tropomyosin) once in the cell, which activates calmodulin.
activated calmodulin activates an enzyme called myosin light chain kinase (MLCK).
kinases phosphorylate things, meaning they add a phosphate group to other structures.
Activated MLCK will phosphorylate myosin heads and catalyzes the transfer of a phosphate to myosin heads.
the myosin heads (activates myosin ATPases) are then activated so they can hydrolyze ATP and enter high energy or cocked position.
once in ready position, myosin can form a cross bridge with actin.
Tropomyosin never has to move because it never blocks actin sites (acts as a stabilizer), and myosin heads are not always ready for a contraction, it needs ca to go through the process and have ATPases activated to be ready to contract.
Smooth Muscle NRG Requirements
take little ATP to contract smooth muscle, it takes 30 times longer to contract and relax compared to skeletal muscle because of sluggish myosin ATPases.
contractions can be sustained for longer (endurance activity for smooth muscle)
uses aerobic cellular respiration so it is fatigue resistant.
Smooth muscle mechanisms
autonomic motor neurons (ANS) innervate and stimulate smooth muscle to contract.
ANS neurons release neurotransmitters in a structure called varicosities (expanded regions of ANS neurons). These can release neurotransmitters in the general vicinity of a smooth muscle sheet (diffuse junction). neurotransmitters diffuse to a sheet of smooth muscle (not a precise). this allows fro contraction as a unit.
2 different neurotransmitters in smooth muscle, ACh and norepinephrine. NT can be excitatory or inhibitory.
effect of NT is dependent on the receptors on the specific tissue.
Ex. in bronchioles, ACh is excitatory (contracts) and norepinephrine inhibits (relaxation).
smooth muscle can also contract in response to hormones or local chemical factors.
Ex. is reproductive hormons contracting uterus, or CO2 on bronchioles.
special features of smooth muscle
smooth muscle exhibits muscle tone or sustained muscle contractions
stress relaxation response, so when SM is stretched, it contracts quickly then relaxed. Ex. when the bladder fills with urine and stretched, it quickly contracts (to tell how much urine is present) and relaxes.
spontaneously generates action potentials (pacemaker cells) Ex. smooth muscle in the digestive tract contracts every 2 hours to move food along.
two types of smooth muscle
unitary smooth muscle
-pacemaker cells
-ANS regulates activity
- responds to chemical stimuli
-has gap junctions
ex. digestive system
multiunit smooth muscle (behaves more like skeletal muscle)
- only contracts if stimulated by ANS
-junctions are more precise/discrete (no gap junctions)
ex. bronchioles, iris, blood vessels
characteristics of smooth muscle contraction
smooth muscle contractions are slow because myosin ATPases are sluggish (take more time to hydrolyze ATP), but very powerful because it can contract as a unit and because there is no polarity in myosin arrangement, meaning myosin heads are oriented all along thick filaments so many cross bridges can be formed.
contractions are synchronized because of the gap junctions so it can contract as a unit.
ca is still a trigger for ca, but regulatory mechanism is very different.
smooth muscle relaxes when ca is pumped out of the cytosol back into SR.
excitability
responsiveness
contractibility
ability to shorten when stimulated
extensibility
Ability to extend or stretch, stretch beyond resting length
elasticity
Recoil and resume resting length
oxidation
is the gain of oxygen or the loss of hydrogen. Either way electrons are lost.
