Week 6 Flashcards
define tendon, insertion, and origin
Tendon: connective tissue between bone and muscle
Insertion: the more movable bony attachment of the muscle
Origin: less movable bony attachment of the muscle
The muscle contracts and places tension on the tendon, which causes the insertion to pull towards its origin
define flexor and extensor muscles and agonist and antagonistic muscles, how do they relate
flexor muscles decrease the angle of a joint
extensor muscles increase the angle of their attached bones at the joint
agonist muscles are the prime mover of any skeletal movement, e.g. in flexion the flexor is the agonist
antagonist muscles act on the same joint as agonist muscles to produce the opposite actions, e.g. an extensor is an antagonist to a flexor
describe the structure of skeletal muscles (not within the cells, just the larger tissue structure)
The epimysium is the dense connective tissue that extends from the tendons around the muscle in a sheath. Connective tissue from this outer sheath extends into the body of the muscle, subdividing it into fascicles (the stringy meat stuff). Each of these fascicles is surrounded by its own connective tissue sheath called the perimysium.
The fascicle is composed of many muscle fibers (cells) that are surrounded by sarcolemma (plasma membrane) and enveloped in a thin layer called endomysium.
how are muscle cells unique from other body cells
they are multinucleate - have multiple nuclei - because they are a syncytial structure
review the process of a motor end plate potential
Each motor neuron stimulates muscle fiber to contract via Acetylcholine at the neuromuscular junction/synapse. ACh stimulates the motor end plate which is rich in nicotinic ACh receptors and voltage gated Na+ channels. ACh binds the receptor and opens ligand gated channels. Na+ and K+ diffuse but Na+ is the dominant effect and results in depolarization (end plate potential) and subsequent contraction.
define motor unit
a somatic motor neuron together with all of the muscle fibers that it innervates (can be a few to thousands)
Describe the two mechanisms that cause muscle contraction to be graded and why are small gradations important?
- motor units are stimulated asynchronously at greater frequency so there is summation of contractions
- larger motor units are recruited with more muscle fibers per motor neuron to increase contraction force.
fine neural control over the strength of muscle contraction is optimal when there are many small motor units involved (example the eyes have a lower innervation ratio where one neuron has a few muscle fibers). Larger motor units are used in powerful but less fine control like in a calf muscle. this would be accomplished by a higher ratio of muscle fibers to a single neuron’s control and by recruiting larger units
*describe the subunits of a muscle fiber (cell)
myofibrils: densely packed inside the cell packed in register (aligned vertically) so striations appear continuous.
myofilaments: contained in myofibrils. Thick filaments (made of myosin) compose A bands and thin filaments (made of actin) compose I bands. The thick filaments give the A band a dark appearance
sarcomeres: the repeating subunit patterns of the myofilaments including A bands, I bands, H bands, Z lines, and M lines
*describe the bands of a muscle cell. what makes each band light/dark? what holds the bands in place?
I bands of the myofibril are the lighter areas from the edge of one stack of thick (dark) filaments to the edge of the next stack of thick (dark) filaments. They are light due to only containing thin (actin) filaments. The thin filaments extend partway into the A bands (where dark, thick, myosin filaments are) making the edges of the A bands darker than the center. The central, lighter, region of the A band is an H band where only thick filaments are present (no thin filaments overlap).
At the center of each I band is a Z line/disc that anchors the thin filaments in place. At the center of each A band (also the center of the H band) there is a M line which anchor the thick filaments in place.
What is Titin? what does it do
Titin (the largest protein in human body) is present in myofibrils with a springlike portion running through the thick and thin filaments and storing energy. Titin contributes to contraction (pulls things towards its center) by its elastic recoil and force produced by unfolded domains becoming refolded. These two processes supplement the greater force produced by the myosin cross bridges.
**what happens to the band as muscle contracts?
Muscle contraction decreases the length of the muscle by shortening of its fibers. Myofibrils shorten because distance from Z disc to Z disc (sarcomere) shortens, however the A bands do NOT shorten but just move closer together. The I bands (which are the light spaces containing only thin filaments) do decrease in length and the H bands (containing only thick filaments) do decrease in length. This is not because any filament changes length! The filaments just SLIDE together and produce increased amounts of overlap area between thin and thick - hence the A band stays the same length as the H and I shorten.
*describe the process of myosin heads attaching and moving actin to produce sliding of the filaments
- myosin ATPase action splits ATP into ADP and Pi, the Pi binds and phosphorylates the myosin head changing to the cocked position (ready to contract) - still at rest!
- Pi is released and the dephosphorylated myosin binds actin and produces a powder stroke, pulling thin filaments toward the center of the A band
- after the power stroke the myosin head releases ADP and is in a tightly bound “rigor state” (think of rigor mortis, which occurs because of absence of ATP)
- a new ATP binds and allows myosin to break the bond with actin. cycle can then continue as long as nothing blocks myosin from binding
NOTE: splitting of ATP required BEFORE cross bridge can attach and attachment of new ATP needed to RELEASE the cross bridge from actin
Each cross bridge power stroke contracts muscle by less than 1%, so how is it possible to contract the muscle up to 60%?
contraction cycles are repeated many times as the cross bridges detach after a stroke and then reset and stroke again. Power strokes are NOT in synchrony because they would lose grip on the actin if they all let go at the same time. Instead some are engaged in a stroke at all times and the greater the muscle’s load, the more cross bridges are engaged
*What regulates the attachment of cross bridges to actin? (2 proteins)
Tropomyosin lies between the G-actin (globular subunits) monomers and troponin is attached to to the tropomyosin. Tropinin is composed of three subunits: Tropinin I which inhibits binding of cross bridges to actin, Troponin T which binds to tropomyosin, and Troponin C which binds Ca2+. Together, tropomyosin and troponin physically block the cross bridges from bonding actin and only move out of the way when Ca2+ is present
who discovered the importance of Ca2+ in muscle?
Sydney Ringer. found that hearts would beat if there was Ca2+ present
What is the result of Ca2+ bonding to troponin
tropomyosin blocks cross bridge attachment when Ca2+ is very low in the sarcoplasm. When Ca2+ increases, it attaches to troponin C and causes a conformation change that moves tropomyosin out of the way, allowing the cocked myosin to bind and power stroke (contracting filaments). Contractions can continue as long as Ca2+ is bonded to troponin C
what produces muscle relaxation? does relaxation require energy expenditure
The ACTIVE transport (consumes ATP!) of Ca2+ out of the sarcoplasm into the sarcoplasmic reticulum. Most of the Ca2+ is stored in terminal cisternae of the sarcoplasmic reticulum.
where does Ca2+ come from during contraction to increase concentration in the sarcoplasm? how does it move to the sarcoplasm?
Ca2+ stored in the terminal cisternae of the sarcoplasmic reticulum is released by passive diffusion through calcium release channels (called ryanodine receptors!). A tiny amount of Ca2+ from the sarcolemma moves to the sarcoplasm, but it is really the reticulum that increases Ca2+ concentration to allow contraction
What structure allows an action potential to directly affect Ca2+ concentration and therefore contraction? How does it does this? What is the term for this coupled reaction?
Transverse tubules (T tubules) narrowly separate the terminal cisternae (where Ca2+ is stored) and are continuous with the sarcolemma, therefore they are able to conduct action potentials into the interior of the fiber. When an end plate potential occurs (via ACh causing electrical activation) it causes voltage gated channels to open on the sarcolemma and the transverse tubules, specifically it opens Dihydropyridine (DHP) receptors which are voltage-gated calcium channels. This receptor has a DIRECT molecular coupling to the ryanodine RyR1 receptors in the sarcoplasmic reticulum, so DHP directly opens RyR1 and releases Ca2+ into the sarcoplasm, stimulating contraction.
this process is termed Excitation-Contraction Coupling
what is defective in hypokalemic periodic paralysis? what is the effect? what is it often misdiagnosed as?
Dihydropyridine receptors are non-functional. Therefore, depolarizations are not sensed and RyR1 receptors in sarcoplasmic reticulum are not activated and muscle contraction doesn’t occur = paralysis. Hypokalemic because low K+ concentration causes faster repolarization, and doesn’t sustain calcium conductance, so severity of the condition can be reduced by maintaining high K+. This is often misdiagnosed as conversion disorder
Describe the major excitation-contraction coupling mechanism in the heart
The heart (and also skeletal muscles, but less so) uses a Ca2+ induced Ca2+ release mechanism. The sarcoplasmic reticulum contains RyR2 ryanodine receptors which open in response to a small rise in the Ca2+ concentration. The initial rise in Ca2+ is caused by opening of T-tubule dihydropyridine (DHP) receptors opening in response to an action potential.
What are the two ryanodine receptors? how are they different?
RyR1: part of the electromechanical release mechanism because it is physically (mechanically) coupled to the voltage gated calcium channel (dihydropyridine receptor).
RyR2: part of the Ca2+ induced Ca2+ release mechanism because it is NOT mechanically coupled to dihydropyridine receptor but instead opens in response to the Ca2+ increase produced by opening of the DHP channels. This is the primary mechanism of the heart, but is present in skeletal muscles as well.
Both are present on the sarcoplasmic reticulum and open to allow Ca2+ to flow into the sarcoplasm and trigger muscle contraction
how is muscle relaxation acheived
action potentials cease and calcium channels close so Ca2+ doesn’t flow out of the terminal cisternae anymore. Ca2+ is then moved back into the sarcoplasm via Sarcoplasmic/Endoplasmic Reticulum Ca2+ ATPase pups (SERCA pumps) that actively transports (consumes ATP). This stops the Ca2+ binding troponin and tropomyosin resumes its position to block the myosin heads
how are muscle contractions studied? name of the device and its product
a physiograph measures muscle contraction by electrical current and records it in a chart called a myogram
define twitch
muscle is stimulated with a single electric shock and quickly contracts and relaxes. all of the contraction events (action potential to calcium release) occur during the latent period.
define summation and graded contractions
summation: if a second electrical shock is delivered before the muscle has fully relaxed from a first twitch, the second twitch piggybacks on the first they make a larger impulse
graded contractions: increasing the stimulus voltage increases the frequency of action potentials (leading to summation) and the number of recruited muscle fibers, allowing variations of strength of contractions to be produced
define incomplete and complete tetanus
when stimulation occurs very frequently there is a decrease in the relaxation time between twitches as strength of the contraction increases in amplitude. This is called incomplete tetany. Then, once a “fusion frequency” occurs there is no visible relaxation between twitches and a smooth, sustained contraction called complete tetanus occurs
what is the major factor in producing graded contractions of a whole muscle in vivo? there are two mechanisms that cause graded contractions, but one is the predominant effect
Recruitment. Additional and larger motor units are activated to produce stronger muscle contractions. Frequency of action potentials is also a factor, but recruitment is the major cause. For a larger contraction (like lifting a 30 pound weight vs a 5 pound weight) there are more large motor units activated.
how is smooth sustained contraction (complete tetany) achieved in vivo when production of super high frequency action potentials are rare?
Asynchronous activation of motor units. Different units fire at slightly different times so the whole muscle is continually contracted in complete tetany
