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Balliet SysPhys musc
NYCC System physiology Balliet Muscle Ch. 6 & 7
Question | Answer |
---|---|
major determinant of whole body activity | muscle |
determines the basal and active state metabolic rates | muscle MASS |
determines relative utilization of glucose and fatty acids as fuels | muscle |
predominant muscle type in body | skeletal |
three muscle types | skeletal, cardiac, smooth |
both of these muscle types are striated but which has mitochondria and nuclei centrally located | cardiac (skeletal mito and nuclei are out by the endplates and scarcoplasmic reticulum) |
function of skeletal muscle | locomotin, heat, protein and gluconeogen reserve, MAIN DETERMINATE OF METABOLIC RATE |
functional unit of muscle | sarcomere |
long multinucleated cells made of myofibrils are called | myofibers |
sarcomere goes from __line to __line. | z-line to z-line |
A band | (anisotropic) Actin and Myosin |
I band | (isotropic) Actin only |
H band | (zone) Myosin |
vowels have actin, consonants have myosin, and they are all in a band together | I is Actin, H is Myosin and they are both in A band together. |
M line is an assembly of | Myosin |
Z line is where | Actin is ANCHORED |
M line is for Myosin and Z line is where Actin is ? | Anchored |
sarcomere boundaries | Z-line to Z-line |
Nebulin is an accessory protein that extends from z-discs and attaches to | actin (thin) |
accessory protein that connects myosin to z-disk | Titin |
where is the sarcoplasmic reticulum and why? | outside of cell because Ca+ needs to go out of cell because you can't violate the concentration gradient rule |
extensions of the cell membrane that conduct electrical signals to center of myofibril | T-tubules |
accessory proteins for myosin and actin | Nebulin (keeps actin straight) and Titin (bungees down myosin) |
name for skeletal mm cell membrane | sarcolemma |
name for skeletal mm cell cytoplasm | sarcoplasm |
name for skeletal mm. cell endoplasmic reticulum | sarcoplasmic reticulum |
extracellular space outside of myofibril that stores Ca++ | sarcoplasmic reticulum |
Why does Ca++ have to be stored outside of the cell? | because you can't violate the concentration gradient rule that Ca++ has to be stored outside - it is an EXTRACELLULAR ION |
why is anything in a T-tubule considered to be OUTside of a cell? | because a T-tubule can propagate an action potential - it conducts electrical signals to the center of the myofibril. It is not inside the cell membrane or it couldn't conduct electricity/action potential. T-tubules are the messengers. |
During sarcomere/myofilament contraction, ____ must come in second, since it is extracellular. | Ca++ |
describe A-band, I-band and H-band during contraction | A (actin & myosin) stays the same, I (actin only) shortens, H (myosin only) practically disappears! |
what is the involvement of A-bands, H-bands, I-bands, M-lines and Z-lines called? | Sliding Filament model |
Myosin composition | composed of 2 Heavy chains and 4 Light chains |
where is the globular head on myosin chains? | at the 2 identical heavy chains |
where are the 4 light chains on myosin | 2 lights are attached to each heavy head |
what makes up the globular head of myosin? | 2 light chains and a little bit of 1 heavy chain |
Where is ATP on myosin? | globular head (2 lights and 1 heavy chain) |
which filament controls skeletal muscle contraction? | myosin (thick heavy muscle myosin) |
which filament controls smooth muscle contraction? | actin (thin smooth squeeze actin) |
How is the body of myosin formed? | tails bundle together -twist |
Part of the body of myosin (from tails) forms the arms. The heads are made of? | 2 light chains and one heavy chain |
myosin arm and head is called | crossbridge |
myosin head and actin binding site | crossbridge formation |
Where is ATP? | on myosin head light chain |
Where is ATPase? | on myosin head light chain, next to ATP and actin-binding site |
gives energy to make and then break crossbridge formation | ATPase on myosin head |
_________ _______ contains ATPase | myosin head |
Describe the components of Actin in skeletal muscle | F-actin, Tropomyosin, Troponin |
The binding site for myosin is on the actin molecule - it is a _______________ monomer. | G-actin |
F-actin is 8nm in diameter (tiny!). What is it composed of? | G-actin monomers with one molecule of ADP each |
Where is F-actin anchored? | at the Z-disk -via binding proteins |
covers the binding sites for myosin when in its relaxed state | Tropomyosin (the mother) |
lines the grooves of the actin filament | tropomyosin |
stabilizes and stiffens the actin filament | tropomyosin |
covers the binding sites for myosin | tropomyosin (the mother) |
has a binding site for Ca++ in skeletal muscle | troponin (the pool boy) |
the pool boy distracts the mother so his best friend Myosin can get into bind on F-actin's sites | Pool boy is Troponin, mother is TropoMyosin |
attaches tropoMyosin to actin | troponin |
has 3 complexes of protein, each with a strong affinity for either actin, tropomyosin, or calcium | troponin |
describe the protein complexes of troponin (the pool boy) | Troponin-I: actin binding, Troponin-T: tropoMyosin binding, Troponin-C: Ca++ binding |
Need 2 ATP that breakdown to ____&_____. When these latter two are released, what happens? | ATP to ADP & Phosphate. When ADP & Phosphate are released, the POWER STROKE happens and the muscle CONTRACTS. Then another ATP binds to release the myosin head from the actin binding site. |
What prevents actin and myosin from interacting? | tropoMYosin (the mother covering her daughter F-actin's binding sites by way of the devious pool boy Troponin) |
In the presence of ________ and _______, pure actin and myosin bind instantly | Mg+ and ATP |
appearance of skeletal, smooth and cardiac muscle | striated, smooth, striated |
fiber arrangement of skeletal, smooth and cardiac muscle | sarcomeres, oblique bundles, sarcomeres |
how are smooth muscle fibers arranged | oblique bundles |
attached to bones; a few sphincters close off hollow organs | skeletal muscle |
forms the walls of hollow organs and tubes; some sphincters | smooth muscle |
heart muscle | cardiac muscle |
multinucleate; large, cylindrical fibers | skeletal |
uninucleate; small, spindle-shaped fibers | smooth |
uninucleate; shorter branching fibers | cardiac |
Has T-tubules and sarcoplasmic reticulum | skeletal and smooth muscle |
no t-tubules; sarcoplasmic reticulum reduced or absent | smooth muscle |
which kind of muscle does not have t-tubules? | smooth |
fiber proteins of smooth muscle | actin, myosin, tropoMYosin |
fiber proteins of skeletal muscle | actin, myosin, tropomyosin, troponin (same as cardiac) |
fiber proteins of cardiac muscle | actin, myosin, tropomyosin, troponin (same as skeletal) |
control of skeletal muscles | Ca++ and troponin, fibers independent of one another |
control of smooth muscle | Ca++ and calmodulin (CaM), fibers electrically joined via GAP junctions (like cardiac) |
control of cardiac muscle | Ca++ and troponin, fibers electrically linked via GAP junctions (like smooth) |
are skeletal muscle fibers independently controlled or electrically linked via GAP junctions? | independent skeletal |
contraction speed of each of the 3 types of muscle, from fastest to slowest: | skeletal is fastest, cardiac is intermediate, smooth is slowwwwww |
smooth is sloooooowwwwwww | slowest contraction speed |
is the contraction force of a single skeletal fiber twitch graded or not graded? | not |
THe contraction force of both smooth and cardiac single muscle fibers is | GRADED (builds up, is not an all or none) |
Skeletal muscle contraction requires ____ from a _______ neuron. | Ach, motor |
Acetylcholine from a motor neuron is required for | the initiation of a skeletal muscle contraction. |
What is required for the initiation of smooth muscle contraction? | Stretch! Chemical signals. Can be autorhythmic. |
What is required for the initiation of contraction of cardiac muscle? | nothing - they are autorhythmic! |
neural control of skeletal muscle? | somatic motor neuron (from ventral horn) |
neural control of smooth muscle? | autonomic neurons |
neural control of cardiac muscle? | autonomic neurons |
What is the hormonal influence of skeletal muscles? | nothing. |
Do hormones and paracrines influence smooth muscle? | yes, many |
What hormones influence the heart? | Epinephrine! |
muscles generate ________, _________ & heat. | motion, force and heat |
Cardiac and smooth muscles are controlled by (3) | autonomic innervation, paracrines, hormones |
autorhythmic muscles | some smooth and all cardiac - means they contract spontaneously |
allow action potentials to move rapidly into the interior of the muscle fiber (skeletal and cardiac) and release calcium from the sarcoplasmic reticulum | t-tubules |
from where does Ca++ get released in skeletal muscles? | sarcoplasmic reticulum |
what holds the thin actin filaments in position? | Nebulin |
what holds the thick myosin filaments in position? | Titin |
Myosin binds to actin, creating _________ formations between the thick and thin filaments. | crossbridge |
One sarcomere is composed of two | z-disks and the filaments between them |
A sarcomere (between two Z-disks), is divided into what bands? | I, A, H, M |
I-band | actin/thin filaments only |
A-band | both actin and myosin overlap area |
A-band is the area of overlap between actin and myosin. It runs the length of the ________ filament. | thick/myosin |
zone occupied by thick/myosin filaments only | H-zone |
attachment site for myosin | M-line |
attachment site for actin | z-disk |
largest protein in the body | Titin, bungee-ing myosin back into place |
regulatory skeletal muscle proteins | tropomyosin and troponin |
giant accessory proteins for skeletal muscle (skm) | titin and nebulin |
motor protein with the ability to create movement in skm. | Myosin |
allows myosin heads to swivel around their point of attachment | hinge |
in skm, 250 myosin molecules join to form a | thick filament |
a protein that makes up the thin filaments of skm fibers | Actin [actum: to do] |
One actin molecule is a _________ protein | globular protein called G-protein |
Many actin molecules polymerize to form chains or filaments called | F-actin. |
In skm, 2 _______polymers twist together like a double strand of beads, creating the thin filaments of the myofibril | F-actin (made of polymerized G-actin proteins) |
Each G-actin molecule has a ________-binding site. | myosin |
Each myosin head has one ______-binding site and one binding site for _____. | actin, ATP |
Forms when the myosin heads of thick filaments bind to actin in the thin filaments | crossbridges |
2 states of crossbridges: | low force (relaxed muscles) and high force (contracting) |
sarkos | flesh (sarcomere is flesh + unit) |
zwischen | the German word for "between," hence z-disks are the ends of a sarcomere and have all the filaments between them |
isotropic | the lightest band is the I-band, reflecting light uniformly/isotropically, hence I-band for actin. |
runs through the middle of each I-band of actin | z-disk, so each half of an I-band belongs to a different sarcomere |
darkest of the sarcomere's bands and encompasses the entire length of a thick filament. At the outer edges of this band, myosin and actin overlap. | A-band (has both). The center is occupied by only myosin |
anisotropic | A-band has both myosin and actin so proteins in this region scatter light unevenly/anisotropically (not isotropically) |
helles | the German word for clear |
central region of the A-band that contains only myosin and is clearly present. | H-band (helles is Ger. word for clear- you can clearly see myosin) |
the band represents proteins that form the attachment site for thick filaments, equivalent to the z-disk for thin filaments | M-line [M is for 'mittel' in Ger. which means middle - so myosin is attached to the M line which divides each A-band in half/down the mittel) |
A single _______ molecule stretches from z-disk to the neighboring M-line and is the largest known protein. | Titin |
Imagine one of these molecules as an 8-ft long piece very thick rope used to tie a ship to the wharf while a single actin molecule would be about the length and weight of an eyelash. | Titin (myosin's accessory protein) |
it's elasticity returns muscles to their resting length and it stabilizes contractile filaments of skm. | Titin |
an inelastic giant protein that lies alongside actin and attaches to the Z-disk, helping align actin in the sarcomere. | Nebulin |
what makes up a 'triad' of skm? | One t-tubule and its flanking 2 terminal cisternae for Ca++ storage. |
the membranes of t-tubules are continuous with | the muscle fiber membrane (sarcolemma) which makes the t-tubules continuous with the extracellular fluid |
t-tubules are continuous with both | sarcolemma and extracellular fluid |
rapidly move action potentials from the cell surface to the interior of a skm fiber. Without them, the only way an action potential would get to the center of the fiber is by diffusion of a + chg. through the cytosol and that would be very slow for a skm | t-tubule |
what two things are in the cytosol between the myofibrils and provide reserve energy and ATP | glycogen (reserve E), mitochondria (ATP) |
how do mitochondria provide ATP for muscle contraction? | oxidative phosphorylation of mainly glucose |
the force created by a contracting muscle | muscle tension |
the creation of a contraction (tension in a muscle) requires E from ____ | ATP |
the release of tension created by a contraction | relaxation |
events at the neuromuscular junction convert an _____ signal from a __________ motor neuron into an electrical signal in the muscle fiber. | Ach, somatic motor neuron |
the process in which muscle action potentials initiate calcium signals that in turn activate a contraction-relaxation cycle | Excitation-Contraction coupling (E-C coupling) |
E-C coupling | muscle action potentials initiate Ca++ signals that in turn make a contraction-relaxation cycle |
How is E-C coupling explained at the molecular level? | sliding filament theory of contraction |
In muscles, one contraction-relaxation cycle is called a muscle ________. | twitch |
band which stays the same length during muscle contraction | A-band |
how can a muscle create force without creating movement? | the sliding fl theory because tension generated in a muscle is directly proportional to the number of high-force crossbridges between actin and myosin |
tension in a muscle is directly proportional to the number of high-force _____________ between actin and myosin. | crossbridges (# = tension) |
provides the force that pushes the actin filament during contraction | rotation of myosin crossbridges |
What initiates the power stroke that causes myosin crossbridges to swivel and push actin ropes towards the center of the sarcomere? | Ca++ signal!!!! |
At the end of its power strokes, each myosin head releases actin then | swivels back and binds to a new actin molecule, ready to start another contraction cycle. |
Do all the myosin heads release at once? | no, the fibers would slide back to their start |
In the power stroke, what causes myosin heads to swivel? | Myosin converts the chemical bond energy of ATP into the mechanical E of crossbridge motion. |
Myosin is an _______, so it hydrolyzes ATP into ADP and Pi. | ATPase |
What is stored in the angle between the myosin head and arm, keeping it "cocked" and ready to rotate during the power stroke? | the potential energy released when myosin hydrolyzed ATP into ADP + Pi. (Myosin IS an ATPase) |
How does a Ca++ signal turn a muscle contraction on? | troponin |
tropos | 'to turn' |
what controls tropoMyosin position? | troponin |
In resting skeletal m., what partially covers actin's myosin-binding sites? | tropoMyosin in its blocking or 'off' position |
Can weak, low-force binding of myosin to actin still take place if tropoMyosin is blocking actin? | yes, but cannot complete power stroke (like the safety on a gun) |
What has to happen to tropoMyosin before contraction of skm can occur | must be shifted to 'on' position that uncovers the actin myosin-binding site |
What regulates the on/off position of tropoMyosin? | troponin |
When contraction of skm begins in response to Ca++ signal, what binds reversibly to Ca++? | troponin-C |
What pulls tropoMyosin completely away from actin's myosin-binding site? | Calcium/troponin-C complex |
The "on' position of tropoMyosin allows | myosin heads to form strong, high-force crossbridge formations and carry out a power stroke, moving the actin filament |
Contractile cycles repeat as long as the | binding sites on actin are uncovered (tropoMyosin is in it's "on" position and Ca++ is bound to troponin-C) |
What must happen for relaxation skm to occur? | Ca++ concentrations in the cytosol must go down |
By law of mass action, when levels of Ca++ decrease in the cytosol, Ca++ unbinds from | troponin-C |
In the absence of Ca++, troponin allows | tropoMyosin to return to the 'off' position and cover actin's myosin-binding sites. |
How does the skm return to its original length? | during the brief relaxation phase, when actin and myosin are unbound, the filaments in the sarcomere slide back with the help of Titin (myosin) and elastic tissues |
In the rigor state, the myosin head is bound to G-actin molecules of actin but there is no | nucleotide (ADP or ATP) |
Rigor state is brief. Then, | ATP binds and myosin detaches. |
what decreases the actin-binding affinity of myosin? | ATP binding to it - myosin will release actin when ATP binds to its head |
After ATP has bound to myosin and myosin detaches from actin, what provides the E for myosin head to rotate and reattach to actin? | ATP hydrolysis! Myosin head closes around ATP, busts it into ADP and phosphate, and both ADP and Pi stay bound to myosin as the E released by the ATP hydrolysis rotates the head until it forms a new 90 deg. angle to the filament. |
In the cocked, post-hydrolyzed ATP position of having ADP and a Pi attached to its head, myosin swivels with the released E and ? | attaches to a new actin molecule 1-3 molecules away from where it started. |
Now that myosin is on a new actin molecule, the newly formed crossbridge is weak and low force because? | tropoMyosin is partially blocking the binding site. |
In the rotated, cocked position, myosin has stored ___________ energy. | potential |
Most resting muscle fibers are in a state of cocked, prepared readiness, waiting for a ? | Ca++ signal |
the power stroke is also called | crossbridge tilting |
When does the actual power stroke begin? | Ca++ signal comes in, binds to troponin-C and this pulls tropomyosin off binding sites on actin. THe strong, high-force bond happens when myosin releases it's phosphate. The release of the Pi allows the myosin head to swivel toward the M-line. |
When myosin releases its Pi in the power stroke, what happens to the actin filament? | The myosin head swings towards the M-line with the release of the Pi, dragging actin along with it. |
Why is the power stroke also called crossbridge tilting? | myosin head and hinge region was at 90 deg. but now at 45 deg. |
At the beginning of the power stroke, myosin releases | Pi |
At the end of the power stroke, myosin releases | ADP. |
With ADP release at the end of the power stroke, myosin is again tightly bound to actin in the _______ state. | rigor state |
What will break the rigor state of myosin to actin and begin the E-C coupling again? | the binding of a new ATP to myosin |
combination of elec. and mechanical events in a muscle fiber | E-C coupling (excitation-contraction coupling) |
how many major events of E-C coupling? | 4 |
1st E-C coupling event | Ach is released from the somatic motor neuron |
2nd E-C coupling event | Ach initiates an action potential in the muscle fiber |
3rd E-C coupling event | The muscle action potential triggers Ca++ release from the sarcoplasmic reticulum |
in E-C coupling, from where is Ca++ released in the 3rd major event? | sarcoplasmic reticulum |
4th E-C coupling event | Ca++ combines with troponin-C and initiates contraction |
When Ach released from somatic motor neuron binds to Ach receptor-channels on motor end plate of muscle fiber, the Ach receptor channels open to let in? | Na+ and K+ come in and cross the membrane |
When Na+ and K+ come in after the Ach receptor channels open in the motor end plate of a muscle fiber, Na+ influx _______ K+ efflux because the electrochemical driving force is greater for ___+. | Na+ influx exceeds K+ because the driving force is greater for Na+ (more Na+ is going to come in than K+ going out at first) |
Why does the membrane depolarize when Ach causes Ach channel receptors to open? | Because the channel receptors let in Na+ and let K+ out, but more Na+ comes in than K+ goes out so membrane voltage goes from negative (resting) to positive (influenced by Na+ influx) and and end-plate action potential results! |
EPP | End Plate Potential created when more Na+ influxes vs. K+ effluxing out of cell, cell depolarizes (goes positive) and end plate potential fires. |
do EPP's always reach threshold and fire? | normally |
At EPP, once more Na+ is coming in than K+ going out and the cell depolarizes, what happens to the action potential? | it is conducted across the muscle fiber into the t-tubules by the sequential opening of voltage-gated Na+ channels |
What is like a domino effect in a muscle action potential? | after EPP, the ap travels to the t-tubules via the sequential or domino-effect of voltage gated Na+ channels flipping open BOOM BOOM BOOM ONE AFTER THE OTHER DOWN INTO THE T-TUBULE, PROPAGATING THE A.P. ACROSS THE MEMBRANE |
Once the a.p. gets down in the t-tubule via domino-effect of opening Na+ channels, what does it run into? | L-type calcium channel receptor called dihydorpyridine (DHP) receptor! |
The a.p. goes down the t-tubule on the backs of opening Na+ channels, runs into the DHP receptor. What happens to the DHP receptor when the a.p. slams into it? | It changes conformation and yanks the ryanodine receptor cap off the sarcoplasmic reticulum storage bin. Ca++ comes pouring out into the cytosol, flowing down towards an area of lesser concentration from the SR sardine can it's been holed up in. |
The a.p. slams into a DHP in the t-tubule. The DHP changes shape, yanking RyR cap off the sarcoplasmic reticulum storage bin and Ca++ streams into the cytosol. Guess where it heads? | To the area of lesser concentration - this would be the troponin-C receptors on the F-actin. You know what happens next! myosin hydrolyzes ATP to ADP & Pi, waits in the cocked position. Ca++ in, binds to troponin-C, tropomyosin shifts, then POWER STROKE! |
Free cytolosolic Ca++ levels in a resting muscle are normally low but the release of Ca++ from SR when DHP yanks RyR cap off means Ca++ levels increase 100x with the _______________ | action potential |
How does the muscle fiber end the contraction? | the Sarcoplasmic Reticulum pumps Ca+ back into it's lumen with a Ca+/ATPase. |
Ca+/ATPase pump used to? | pump cytosolic Ca++ back into the SR and stop muscle fiber contraction. |
As the SR uses the Ca+/ATPase pump to get Ca++ back into it's storage bin (SR lumen), the levels of Ca++ in the cell drop. What happens? | Ca++ releases from troponin-C, which then allows tropoMyosin to slide back into blocking actin's myosin-binding site. Crossbridges release and the muscle fiber relaxes. |
The signal for muscle contraction is | Ca++ |
Why isn't the action potential the signal for muscle contraction? | Because Ca++ is required so Ca++ is the SIGNAL |
the signal for muscle contraction is | Ca++ |
Ca++ is an almost universal __________ messenger. | second |
The somatic motor neuron a.p. is followed by the skeletal muscle a.p., which is followed by a __________. | contraction |
A single contraction-relaxation cycle in a skeletal muscle fiber is called a | twitch! |
the delay representing the time for E-C coupling to take place when the muscle a.p. and the muscle tension develops. | latent period |
what it takes to evoke a single twitch in a muscle fiber | a single action potential |
where does muscle ATP come from? | creatine kinase transferring Pi to ADP= ATP and fatty acids via beta-oxidation (requires Oxygen and makes acetyl-CoA) |
experimental evidence suggests that muscle fatigue is the result of | excitation-contraction failure in the muscle fiber, rather than in the neurons or neuromuscular transmission. |
A new theory that sarcoplasmic Ca++ causes __________ | fatigue. |
What preceeds physiological fatigue? | psychological fatigue (and acidosis) |
______-twitch fibers pump Ca++ back into their Sarcoplasmic Reticulum more rapidly than _______-twitch fibers do. | fast, slow. So fast twitch fibers have quicker twitches! |
The tension a muscle fiber can generate is directly proportional to the number of _________ formed between the thick and thin filaments. | crossbridges |
In a muscle fiber, the tension developed during the twitch is a direct reflection of the ________ of the individual sarcomeres BEFORE contraction begins. | length |
Each sarcomere contracts with optimal force if it is at optimum ________ before the contraction begins. | length (neither too long or too short) |
Why is a very long sarcomere length unable to contract very well? | because of so little overlap between the actin and myosin - not many crossbridges can form |
sarcomere length is really a reflection of the __________ between thick and thin filaments. | OVERLAP = sarcomere length |
optimum force is generated in a twitch when the optimum number of overlaps between actin and myosin occurs in the sarcomere. If it's too short, what happens? | overlap prevents crossbridge formation and the thick filaments run into the z-disks |
The development of single-twitch tension in a muscle fiber depends on | filament overlap and sarcomere length |
Force of contraction increases with ________ of muscle twitches. | SUMMATION |
Not only does the optimum sarcomere length determine single-twitch tension, the force can be increased by raising the _________ at which muscle a.p.'s stimulate the fiber. | frequency/rate |
When a muscle fiber does not have time to relax between stimuli, a more forceful contraction results. What is this called? | summation |
If action potentials continue to stimulate a fiber repeatedly at short intervals (high frequency), what happens? | no more relaxation but maximum stimulation called TETANUS |
The basic unit of contraction in an intact skeletal muscle | motor unit |
the group of muscle fibers that function together and the somatic motor neuron that fires an action potential | motor unit |
Although one somatic motor neuron innervates multiple fibers, each muscle fiber is innervated by | one single neuron. |
fine motor skill muscle motor units | motor unit contains only 3-5 muscle fibers, so small response allows fine gradations of movement |
gross motor action muscle motor unit | each motor unit may contain hundreds or 1000's of muscle fibers. |
All muscle biers in a single motor unit are of the same ______ type. | fiber (fast-twitch motor units and slow-twitch motor units) |
In skeletal muscle, each motor unit contracts in an _____________manner. | all-or-none manner. |
contraction that moves a load | isotonic contraction |
contraction that creates force without movement | isometric contraction |
extension of a muscle when lengthening with a weight but still letting down slowly | eccentric contraction (dumbell 'uncurl' part of a curl) |
Once the elastic elements in a muscle have been stretched and the force generated by the sarcomeres equals the load, the muscle _________ and an ________ contraction results. | shortens, isotonic {'teinein' means 'stretch' so think of tonic as a stretch receptor that finally says GO!] |
what kinds of muscle are most important for maintaining homeostasis | cardiac and smooth |
Smooth muscle is noticeably different from skeletal muscle in the way it develops ________. | tension (smooth m. relax and contract are much slower and uses less E and can maintain contraction for a long time) |
Think of skeletal muscle as weasel and smooth muscle as an anaconda. Cardiac muscle is a hamster in a wheel. | Okay, you come up with something. |
Where is smooth muscle found? | 6 types: vascular (blood vessel walls), GI, urinary, respiratory (airway passages), reproductive, ocular |
contractile fibers of this kind of muscle are arranged in oblique bundles and may run in several directions | smooth |
what controls smooth muscle contractions | hormones, paracrines, neurotransmitters (ie, Ach and NE) |
Normal skeletal muscle responds to an action potential with a twitch, but smooth muscles may | hyperpolarize, depolarize, depolarize without firing. Contract after an a.p., after a SUB-threshold graded potential, or WITHOUT ANY CHANGE IN MEMBRANE POTENTIAL AT ALL! |
Skeletal muscles contract when Ach is released from a somatic motor neuron, and relax when stimulus stops, but smooth muscles must act as integrating centers. Why? | because multiple neurotransmitters, hormones, paracrines can all hit it at once, inhibiting and causing contraction. Smooth muscle has to integrate overlapping regulatory pathways and respond correctly. |
composed of small, spindle shaped cells with a single nucleus | smooth muscle |
when a neurotransmitter is controlling a smooth muscle, how does it get to the receptor? | no specialized receptor regions on smooth muscle (like motor end plates)! The nt simply diffuses across the cell surface until it finds a receptor. |
single-unit smooth muscle (unitary) is so called because | the individual muscle cells contract AS A SINGLE UNIT |
What is another name for single-unit smooth muscle? | Visceral smooth muscle because it forms walls of viscera like blood vessels and intestines. |
All the fibers of single-unit/visceral smooth muscle are electrically connected to each other. How does the signal spread? | GAP junctions |
Why aren't there any reserve units left to be recruited (as skeletal muscle does) to increase a contraction force in a smooth muscle? | Because ALL fibers contract EVERY TIME together (nobody left out)in smooth muscle |
What determines the force of contraction in smooth muscle? | the amt of Ca++ |
The amount of ____ determines the FORCE of contraction in smooth muscle. | Ca++ = Force of contraction in smooth muscle |
Multi-unit smooth muscle cells consist of cells that are not linked ____________-- | electronically |
Because multi-unit smooth muscle cells are not linked electronically like single-unit cells (get it? these fire as a single unit), each individual multi-unit cell must be closely assoc. with | an axon terminal or variscosity and stimulated independently |
What is the advantage of multi-unit arrangement of smooth muscle cells? | allows fine control of contractions through selective activation (they don't all contract at once like the gut muscles) |
Where is multi-unit smooth muscle found? | Iris and ciliary body of eye, vas deferens, uterus just prior to labor and delivery |
Which has longer actin and myosin filaments, smooth or skeletal? | smooth, and the myosin in smooth is different! |
How is smooth muscle myosin different? | the myosin ATPase activity is much SLOWER, decreasing the rate of crossbridge cycling and lengthening the contraction phase. |
In addition to smooth muscle myosin ATPase having a much slower activity than in skeletal muscle, a small protein chain plays a regulatory role in controlling contraction and relaxation. What is it? | Myosin light chain (gets phosphorilyzed by MLC kinase) |
Actin is _____ plentiful than myosin in smooth muscle. | more! Actin to myosin ratio is 10-15 to 1 |
Smooth muscle has tropoMyosin, like skeletal, but does not have | troponin |
Smooth muscle doesn't have __________ | troponin |
Smooth muscle doesn't have troponin and its sarcoplasmic reticulum is _____ in number. | weak |
How is Ca++ released from the SR in smooth muscle? | IP3 receptor channel (Inositol triphosphate is a second messenger created in the phospholipase-C pathway) |
Instead of DHP and Ryn using Ca++, smooth muscle's sarcoplasmic reticulum uses | IP3 as a second messenger |
What supplements the Ca++ storage function of smooth muscle SR since there is so little SR? | CALVEOLAE |
small vesicles that cluster close to the membrane of smooth muscle and help with the Ca++ storage function since smooth contains so little SR | calveolae |
is smooth muscle arranged in sarcomeres? | no -ergo, no distinct banding patterns |
Actin and myosin are arranged in long bundles that extend diagonally around the cell periphery, forming a lattice around the central ________ in smooth muscle cell. | nucleus |
the oblique arrangement of contractile elements of smooth muscle beneath the cell membrane causes the fibers to become _______ when they contract. | globular (rather than simply shortening like skeletal fibers) |
The long actin filaments of smooth muscle attach to ___________ of protein in the cytoplasm | dense bodies |
In smooth muscle, because there are fewer myosin, the entire myosin filament is covered with | globular heads (skeletal myosin filaments don't have heads along the M-line) |
What is the advantage of the continuous line of myosin heads in smooth muscle? | allows actin to slide along the myosin for longer distances |
Since actin can slide along the myosin for longer distances due to myosin being completely covered with globular heads, what can smooth muscle do? | be stretched more while still maintaining absolute tension (ie, the bladder won't give) |
The dense bodies that anchor smooth muscle actin are analogous to what structure in the sarcomere? | Z-disk |
What is similar about the signal to contract in both skeletal and smooth muscle? | Both use Ca++ |
Where does the Ca++ signal come from in skeletal muscle? | Sarcoplasmic reticulum after Ryn channel receptor opens due to DHP and is ALWAYS preceeded by an action potential |
Where does Ca++ signal to contract come from in skeletal muscle? | weak SR but more from extracellular fluid and an action potential is NOT required for Ca++ release. |
Is an action potential required for Ca++ release in skeletal muscle? Smooth? | Yes in skeletal, NO in smooth |
In skeletal muscle the Ca++ acts upon _________ to initiate contraction | troponin-C |
In smooth muscle, there is no troponin-C so what happens to Ca++ signal? | initates a cascade that ends with the phosphorylation of myosin |
4th step of smooth mm contraction: | Phosphorylation of myosin enhances myosin. ATPase activity results in contraction. |
3rd step in smooth mm contraction: | Ca++ binding to calmodulin is first step in cascade that ends in phosphorylation of myosin |
2nd step in smooth mm contraction: | Ca++ binds to Calmodulin, a binding protein found in the cytosol |
1st step in smooth mm contraction: | Increase in cytosolic Ca++ initiates contraction. Ca++ is released from the sarcoplasmic reticulum and also enters from the extracellular fluid (calveolae) |
Smooth muscle contraction begins when | cytosolic Ca++ increase |
what makes cytosolic Ca++ concentrations increase in smooth muscle | extracellular fluid Ca++ entry and release of Ca++ from SR |
What happens to cytosolic Ca++ in smooth muscle after it enters from extracell fluid and from SR? | It binds to calmodulin (CaM) |
CaM | calmodulin - the thing to which Ca++ binds in smooth muscle when it initially enters the smooth muscle cell |
Why does Ca++ bind to CaM in smooth muscle cell? Why not troponin-C? | It is obeying the law of mass action (concentration gradient). There is NO troponin-C, but just like Ca++ goes to t-C in skeletal because it is in an area of less concentration, so the same it goes to Calmodulin in smooth muscle cell. |
Once Ca++ has bound to calmodulin in smooth muscle, what happens? | The Ca++/Calmodulin complex then activates an enzyme called MYOSIN LIGHT CHAIN KINASE |
what do kinases do? | add phosphates to things |
MLCK | Myosin Light Chain Kinase |
What binds to MLCK in the smooth muscle? | Ca++/Calmodulin complex |
What does MLCK do inside the smooth muscle cell once Ca++/calmodulin has bound to it? | enhances ATPase activity by phosphorylating light protein chains (remember: myosin heads contain 4 light protein chains attached to an ATP) |
MLCK phosphorylates? | light protein chains near the myosin heads in smooth muscle (remember: there are A LOT of heads on the myosin in smooth muscle so it makes sense that there'd be someone to help phosphorylate with the ATPase - a buddy) |
When myosin ________ activity is high in smooth muscle cell, actin binding and crossbridge cycling increase tension in the muscle | ATPase |
What happens when ATPase activity (and MLCK, too) is high in the smooth muscle cell? | actin binding and crossbridge cycling creates TENSION in the muscle |
As a result of myosin ATPase activity intensifying and subsequent actin binding and crossbridging, smooth muscle contraction is primarily controlled by? | MYOSIN-linked regulatory processes, rather than troponin or tropoMyosin |
phosphorylates light chains in myosin heads and increases myosin ATPase activity | Myosin LIght Chain Kinase |
In skeletal muscle relaxation, what happens? | Ca++ is pumped back into the SR by Ca++/ATPase pumps and as Ca++ levels drop, Ca++ dissociates from troponin-C, tropoMyosin returns to "off" and myosin detaches when a new ATP arrives. Extra Ca++ is pumped out of cell by Ca+/Na+ ANTIPORTER. |
In smooth muscle relaxation, what happens? | Ca++ is pumped back into SR by Ca/ATPase pump and out of cell by Ca/Na antiporter, same as skeletal. Ca++ dissociates from CaM. No Ca/CaM, MLCK shuts down. |
Not only does the dissociation of Ca++/Calmodulin cause MLCK to inactivate, but the myosin light chain is ____________ by the enzyme? | dephosphorylated by myosin phosphatase |
what does a phosphatase do? | takes the phosphates off of things (de-phosphorylates) |
myosin phosphatase | dephosphorylates the light chains on the plentiful myosin heads in smooth muscle (counteracts the added phosphorylation activity of MLCK from earlier when contraction was happening) |
what is working with MLCK? | myosin ATPase |
what works to restore the balance of DEphosphorylated myosin heads when smooth muscle cell needs to relax? | myosin phosphatASE (comes in when Ca+/CaM dissociates from MLCK because Ca++ is being pumped back into SR by Ca++/ATPase and Ca++/Na+ antiporter to outside) |
the removal of myosin's phosphate group decreases ______________ activity so the smooth muscle can relax | myosin phosphatase |
Does the dephosphorylation of myosin by myosin phosphatase and the inactivation of MLCK (after Ca/CaM dissociates) mean that smooth muscle will automatically relax? | NO! Nothing is all or none with smooth muscle, remember? Dephosphorylated myosin might stay attached to actin for a period called the LATCH STATE. |
this condition maintains tension in smooth muscle fiber without consuming ATP | the LATCH STATE -when myosin is dephos'd but still stays attached to actin |
the significant factor that allows smooth muscle to sustain a contraction without fatiguing | the LATCH STATE (dephosphorylated myosin stays attached to actin) |
Smooth muscle Ca++ comes from: | SR and extracellular fluid |
Variable amts of Ca++ enter a smooth muscle fiber cytosol, creating __________________ whose force varies according to the strength of the Ca++ signal. | graded contractions |
What determines the strength of contraction in smooth muscle? | the strength of the Ca++ signal! (graded contractions) |
The smooth muscle's intracellular Ca++ store | sarcoplasmic reticulum |
SR Ca++ release is mediated by | IP3 activated receptor channel, which opens in response to signal transduction pathways that produce IP3 |
How is SR Ca++ release mediated in skeletal muscle? | by ryanodine receptor that opens when an action potential slams into DHP receptor |
How does a smooth muscle cell monitor and replenish its internal Ca++ (SR) store? | store-operated Ca++ channels allow more Ca++ into the cell from the extracellular fluid |
How does smooth muscle know when to let in extra Ca++ from outside (extracellular)? | membrane channels whose openings are sensitive to stretch, depolarization or chemical signals |
blood vessel smooth muscle cells contain _______________ that open when pressure or other force distorts the cell membrane | STRETCH-ACTIVATED Ca++ channels in blood vessels |
When contraction originates from a property of the muscle itself, as in stretch-activated Ca++ receptors in blood vessels allowing Ca++ in, the muscle is said to be | myogenic |
myogenic | able to originate a contraction without a chemical signal, as in blood vessels with stretch-activated Ca++ channels that contract to maintain a constant tone |
Eventually during a sustained stretch-activated Ca++ influx, the Ca++ channels will... | close and the Ca++ will be pumped out of the cell so the muscle can RELAX |
small invaginations of the sarcolemma of smooth muscle that concentrate Ca++ | caveolae |