Download Biology Notes Ballough Part 2 Blue= Ballough`s lecture words, or my

Biology Notes
Ballough Part 2
Blue= Ballough’s lecture words, or my own summarizations
Green= Wiki copy and paste, or BOOK!
Understanding Muscle Contraction
Structure and Function of Skeletal Muscle
 Muscles move skeletal parts by contracting
 Muscles always contract actively; they can extend only passively
 Ability to move body part in opposite direction requires that muscles be
attached to the skeleton in antagonistic pairs
 Each fiber is a single cell, with many nuclei (results from cell fusion);
consists of bundles of smaller myofibrils arranged longitudinally. Two kinds
of myofilaments are found in each myofibril, Thin and Thick*
*Thick filaments are staggered arrays of myosin molecules
*Thin Filaments: anchored to each side of the Z lines, series of bristles, consists of 2
strands of actin and one strand of regulatory protein coiled around one another.
Sarcomere= Unit of organization of skeletal muscle (“Unit of contraction”). Skeletal
muscle is also striated muscle because the regular arrangement of the myofilaments
and creates a pattern of light and dark bands. Each repeating unit is a sarcomere.
Comprised of two z lines and the myofibril in between.
Sarcolemma: plasma membrane surrounding skeletal muscle to depolarize
In a muscle fiber at rest, thick and thin filaments do not overlap completely, and
the area near the edge of the sarcomere where there are only thin filaments is called
the I band. The A band is the broad region that corresponds to the length of the thick
filaments.
Best way to remember this is to look at the diagram and look for where thin and
thick filaments exist:
Z lines are the borders of the sarcomere; aligned with adjacent myofibrils.
I bands are areas near the edge of the sarcomere containing only thin filaments
A bands are regions where thick and thin filaments overlap and correspond to the
length of the thick filaments (has both thick and thin)
H zones are areas in the center of the A bands containing only thick filaments
Muscle contraction occurs when the thin filaments slide along the thick, bringing
adjacent Z lines toward one another. In other words, the sarcomere becomes
shorter in length.
T-Tubule:
- Runs transversely (perpendicularly) along the axis of the fiber
If this (points to diagram) is the cell body, which is like the initial segment?
The Transverse tubules are equal to the initial segment.
What kind of fluid would you find in the T-Tubule?
Interstitial fluid (extracellular fluid),
It’s how the action potential dives down and triggers the release of
calcium throughout the fiber, and the release of Ca occurs predominantly from
the terminal cisternea, of the sarcoplasmic reticulum (are like swollen ends). In
skeletal and cardiac muscle, the T-tubules are adjacent to the terminal sacs
(terminal cisternea) of the fiber’s sarcoplasmic reticulum.
Fibers are so thick that surface to area volume ratio’s are so small, that the signal
from the exterior cannot penetrate to the interior, that’s why Transverse tubules
exist.
He mentions this briefly, and is also found in wiki, might be helpful for understanding:
Upon release of that calcium from the sarcoplasmic reticulum, you can see that it’s
kind of overlapping with the sarcomere in special places. Particularly overlaps where
the actin and myosin overlap. Calcium is released there, like a symmetrical alignment.
In skeletal muscle, the T-Tubule is surrounded by a pair of terminal cisternea in
an arrangement called a triad, a.k.a “the region of overlap. It is physiologically
important that the t-tubules are so positioned, as there location allows for close
excitation-contraction coupling. That is, the wave of depolarization that spreads down
the t-tubule’s allows for opening of the calcium release channels in the sarcoplasmic
reticulum immediately adjacent to the actin thin filaments (which cause that
contraction via the sliding filament mechanism.)
The Molecular Mechanism of Muscle Contraction
– Muscle contraction reduces the length of each sarcomere
– Sliding filament model = Mechanism of muscle contraction. Thin filaments
ratchet across thick filaments to pull the Z lines together and shorten the
sarcomere. Myosin molecules on thick filaments attach to actin on the thin
filament to form a cross bridge. It then bends inward, pulling the thin
filament toward the center of the sarcomere, breaks the cross bridge, and
forms a new cross bridge further down.
**Neither thin or thick filaments change in length when the sarcomere shortens;
instead they just slide longitudinally past each other producing an overlap. As a result,
both the I bands and H zones shrink.
Troponin: smaller proteins associated with the whole sarcomere. The main one’s
are actin and myosin.
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Energy for conformational changes in myosin heads comes from hydrolysis
of ATP (myosin heads is an ATPase).
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Skeletal muscles contract when stimulated by lower motor neurons (via
acetylcholine)
(Basically, acetylcholine being released by a lower motor neuron is what
is initiating contraction of the skeletal muscles)
In a muscle rest, myosin-binding sites on the actin are blocked by the
regulatory protein strand (tropomyosin) in the thin filament. Attached to
tropomyosin is a troponin complex.
Story time: Imagine you have a log, if I wanna roll that log, essentially the
log roller and the lumberjack is troponin and the log is tropomyosin, and
when they roll that log over it reveals all of these binding sites on the
ground (ants, bugs w.e) and the ground in that case is actin.
Infoldings in the muscle cell plasma membrane (transverse tubules) carry
the resulting graded depolarization deep into the muscle cell
The Sarcoplasmic reticulum membrane becomes depolarized and releases its
store of C2+
The calcium ions bind to troponin causing conformational (shape) change
that moves tropomyosin and exposes the binding sites on actin; myosin
heads attach and muscle contract
Story: Calcium when it’s present and binding to troponin, and
the log is out of the way, myosin will grab the actin, and bind ATP. For
the myosin to detatch, it requires ATP but you aren’t using it’s energy at
that point. Ultimately shorten’s the sarcomere
The contraction is terminated as calcium is pumped out of the cytoplasm,
back into the sarcoplasmic reticulum, by calcium pumps (calcium ATPase); as
the calcium concentration falls, the tropomyosin-troponin complex again
blocks the binding sites.
Creatin Phosphate indirectly provide most of the energy
My stupid way of explaining the role of calcium and regulatory proteins:
If you have a band of actin (thin filament), underneath a smaller band of
tropomyosin, it looks like the tropomyosin is wrapped around it like a candy cane.
Tropomyosin is more like the red stripe and actin is the base (which is white). On
that red stripe, are sprinkles called (troponin) and holes in those sprinkles are
called Ca2+ binding sites. When at rest, the tropomyosin block binding sites, and in
this case those binding sites are like holes on the white part of the cane.
Now imagine that red band of candy moving, like a barber shop sign, as it
moves it exposes the holes, (myosin binding sites). That is when the muscle is
essentially contracting. For that muscle to contract, the calcium ions bind to another
set of regulatory proteins, the troponin (sprinkles), which controls the position of
tropomyosin on the thin filament. Calcium binding re-arranges the tropomyosintroponin complex, exposing the myosin binding (holes on the white candy cane)
sites on the thin filament.
**The stimulus leading to that contraction…is action potential in a motor
neuron. The synaptic terminal of that neuron releases ACH, depolarizing that muscle
fiber and causing it to produce an action potential. That action potential spreads
deep into the interior of the muscle fiber along the inflodings of the plasma
membrane called transverse (t)tubules. The T tubules make close contact with the
sarcoplasmic reticulum. Basically the SR houses the Ca2+ at rest, and makes a lot of
it, like a storehouse. When there is an action potential, Ca2+ channels open in the SR
allowing it to enter the cytosol. That’s where the binding occurs to the troponin
complex, triggering the contraction.
Summarized steps of action:
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ACH is released by synaptic terminal, moves across the synaptic cleft
and binds to receptor proteins on the muscle fibers plasma
membrane, triggering an action potential in the muscle fiber
Action potential moves down membrane and down the T tubules
AP hits the sarcoplasmic reticulum, and triggers it to release Ca2+
Calcium ions float down and bind to troponin, causing that
conformational change, (Changes shape), removing blocking action of
tropomyosin; and exposes those myosin-binding sites
Myosin cross-bridges alternately attach to actin and detach, pulling
actin filaments toward the center of the sarcomere; ATP powers
sliding of the filaments
Cytosolic ca2+ is removed by active transport into the SR after action
potential ends
Tropomyosin blockage of myosin binding sites are restored;
contraction ends, and muscle fibers relax
Fast and Slow Muscle Fibers
Duration of muscle contraction is controlled by how long the calcium
concentration in the cytoplasm remains elevated.
Slow fibers have longer-lasting twitches because they have less sarcoplasmic
reticulum thus, CA2+ remains in the cytoplasm longer. Slow fibers have many
mitochondria, a rich blood supply, and the oxygen-storing protein myoglobin. Used
to maintain posture since they can sustain long contractions.
Slowly fatiguing red fibers (dark turkey meat + more blood), has plenty of time to
rely on oxygen, postural muscles
Fast fibers have short duration twitches and are used in fast muscles for rapid,
powerful contractions
Contain rapidly fatiguing white fibers (white turkey meat). Energy is derived from
glycolysis. Production of Lactic acid is sent out of the cells and used by the slow twitch
muscles.
Stored ATP: Very short source
– ATP required for contractile events
– ATP only energy source that can be used directly for contractile activity.
– ATP also needed to run calcium pumps (to pump Ca2+ into SR).
– Muscle stores only enough for 4-6 sec of activity
– ATP generated by 3 pathways
1. Interaction of ADP with creatine phosphate
2. Anerobic glycolysis
3. Aerobic respiration (Krebs cycle [citric acid cycle] and oxidative
phosphorylation [cytochrome chain]).
Another source: Creatin Phosphate
– Unique high energy molecule stored in muscle
– Used to regenerate ATP (phosphorylate ADP) after 6 sec of activity.
– Creatine phosphate + ADP = Creatine + ATP
– Muscle stores much creatine phosphate
When your not really utilizing your muscles and want to store some of the high
energy, you put it onto the creatine, and the re-phosphorylate the ATP.
Other Kinds of Muscles
Do cardiac muscles have sarcomeres?
Yes, if they didn't it wouldn't be striated, the arrangement of myosin is what
gives it the sarcomere appearance, it does the same thing but doesn't rely entirely
of intracellular calcium. About 20% of the calcium for cardiac contractions come
from the outside, not from the sarcoplasmic reticulum.
The majority for the calcium used for smooth muscle contraction comes
from the outside. Smooth muscle contraction? We studied that, peristalsis? Inner
circular, outer longitudinal layer, stuff like that.
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Smooth muscles lack striation and contain less myosin; the myosin is not
associated with specific actin strands
That doesn't mean that smooth muscle lack actin or myosin, it has
both. It's just that myosin isn't locked in place. It's a lot less myosin. What
smooth muscle can do is really stretch (think uterus), and still generate
contraction. Not as strong as skeletal and cardiac muscle though. But that
smooth muscle can generate force at various lengths. Knowing this, the
following should make sense to you:
Does not have a transverse tubule system or a well developed sarcoplasmic
reticulum; calcium ions must enter the cytoplasm through the plasma
membrane ===> “The majority for the calcium used for smooth muscle
contraction comes from the outside”
Contractions are relatively slow but there is greater range of control.
Generates less tension but can contract over a great range of lengths
Found mainly in the digestive tract organs, uterus, walls of blood vessels