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42 Cards in this Set

  • Front
  • Back
1) Fiber/Myocyte/Myofiber
2) Cell Membrane + Endomysium
3) Cytoplasm
4) Smooth ER
1) Cell
2) Sarcolemma
3) Sarcoplasm
4) Sarcoplasmic Reticulum
Myofibrils are long cylindrical bundles of myofilaments; these are contractile elements of each muscle fiber
Skeletal Muscle - CT sheaths' function and the 3 types
-Each skeletal muscle has several CT Sheaths containing blood vessels and nerves; the sheaths help to transmit the force of contraction between the fibers.
1) Epimysium - outermost sheath of dense CT
2) Perimysium - thin collagenous septa coming from epimysium that divide muscle fibers into groups called Fascicles
3) Endomysium - delicate network of reticular fibers and basal lamina which invests each muscle fiber within the fascicles
Embyonic Formation of skeletal muscle fibers
-develop embyonically from mesenchymal cells that differentiate into Myoblasts
-these fuse together to form MULTINUCLEATED Myotubes
-myotubes then designated as immature myofibers
-myofibers secrete an External Lamina around themselves, forming the Endomysium.
Satellite Cells form what and how, what happens to them w/ increase in exercise
-They have the potential to undergo mitosis and to differentiate into Myoblasts following injury to the muscle.
-W/ increase in exercise, satellite cells divide and one of the daughter cells from each division fuses w/ existing muscle fibers, causing a hypertrophic increase in muscle mass. The remaining daughter cells become a Stem Cell Population which allows more regeneration or a further increase in muscle mass. More importantly, there is an increase in protein synthesis which increases the number of myofibrils, thereby increasing muscle mass
Striated muscle fibers - why do they appear striated (3)
A Band - dark-staining band (contains H band and M line)
I Band - light-staining band
Z Line - dark line which bisects each I band - connects to adjacent sarcomere

Striated muscle fibers contain myofibrils (arrangements of myosin and actin) that exhibit alternating light and dark bands. B/c the myofibrils are all in a similar state of contraction, the fiber as a whole appears striated
Sarcomere - basic unit of what, equals what distance, makes up what, when does its length change, when do the bands change
-Is the basic unit of contraction and equals the distance from one Z line to the next Z line.
-Myofibrils are made up of a continuous chain of sarcomeres
-The lengths of sarcomeres change during contraction and relaxation
-The I Band (and the sarcomere) shortens during contraction and lengthens during relaxation
-The A Band always remains the same length

Within each sarcomere, 2 types of myofilaments exist:
1) Thin Filaments
2) Thick Filaments
Thin Filaments - present in what band, composed of what proteins (3) and their descriptions
-Only filaments present in the I band
-Composed of the protein Actin (in its filamentous form F-Actin, which is actually 2 chains of G actin), Tropomyosin, and Troponin

G-Actin is a globular protein which can polymerize to form long chains. Each thin filament is actually composed of 2 polymerized chains of G actin which are twisted in a helical configuration; this is F-Actin

Tropomyosin is a long rop-like protein which runs the length of each thin filament

Troponin is composed of 3 globular subunits that are bound at specific sites along the tropomyosin molecule
Thick Filaments - present in what band, composed of what protein

*Thin to Thick Filaments Ratio
-present in the A band of the sarcomere
-composed primarily of the protein Myosin II
Myosin II has a head and tail region. The heads have binding sites for Actin and for ATP; they have ATPase activity

*In striated muscle, 6 thin filaments surround each Thick filament in the region of the A Band WHERE THIN AND THICK FILAMENTS OVERLAP
Accessory Proteins
Other proteins within the sarcomere act to maintain the relative position of the myofilaments and regulate the length of polymerized filaments.
Accessory Proteins for Thin Filaments (3)
-The Z-line anchors the ends of thin filaments of the adjacent sarcomeres

1)Alpha-Actinin - bundles thin filaments together and anchors them to Z lines
2)Nebulin - Maintains regular geometric arrangement of thin filaments, ataches them to z line
3) Tropomodulin - caps the Free End of each thin filament to regulate the length of the thin filaments
Accessory Proteins for Thick Filaments (3)
Firmly attached to the M line; also attached to Z line.

1) Titin - maintains central position of the A band by attaching the thick filaments to the z line.
2) Myomesin
3) C Protein
How do the myofibrils resist
stress and stay in register
with each other?
There is a meshwork of
proteins around each
myofibril at the level
of the Z line, including
Desmin, which is linked to
the basal lamina.
Actin filaments are linked to
basal lamina by Dystrophin
via the dystroglycan complex.
A defiiency in dystrophin
results in Duchenne
muscular dystrophy
What happens in a Belgian Blue cattle?
Mutation produces an INEFFECTIVE
form of Myostatin,
a muscle growth inhibitor

In a mouse model of muscular dystrophy, antibodies directed against myostatin allowed increased muscle growth and better muscle function
Sliding Filament Theory (SFT) - what two things are necessary for contraction to occur and how do they aid contraction?
ATP and Calcium Ions (released from sarcoplasmic reticulum)

Myosin cannot interact with actin when a muscle is at rest b/c TROPOMYOSIN BLOCKS THE BINDING SITE ON ACTIN. When calcium is present, it binds to troponin and causes a CONFIGURATIONAL CHANGE, dislodging tropomyosin and exposing the actin-myosin binding site
First 3 steps of SFT
1) Myosin heads then bind tightly to the exposed actin binding site. This is the RIGOR CONFIGURATION

2) The myosin head region also has a binding site for ATP. ATP binds and induces conformational changes that result in DETACHMENT of the myosin heads from the actin binding sites.
3) ATPase Enzyme activity is resident within the myosin heads. ATP is hydrolyzed and the myosin head bends toward the Z line
Last 2 Steps of SFT
4) Myosin heads again bind to the thin filament. When Pi is released, the bindin of actin to myosin becomes even tighter, resulting in CROSSBRIDGES. The myosin heads return to the original unbent position, causing them to swing and pull the thin filaments toward the center of the sarcomere (this is the POWER STROKE). Thin filaments are pulled past thick filaments, Z lines come closer together, shortening of I band and consequently shortening sarcomere. ADP molecule drops off

5) Myosin heads again bind to actin myosin binding sites. If calcium is still bound to troponin, the cycle will start over and contraction wil continue; new crossbridges form and muscle will continue to shorten.

*when a muscle contracts, it is the result of HUNDREDS OF CYCLES of crossbridges formed and broken in a coordinated manner, causing entire length of muscle to shorten. Also, again the myofilaments do not shorten but the sarcomere does.
How is contraction controlled in skeletal muscle
By nerve impulses to the muscle fibers via MOTOR END PLATES, which are specialized synaptic areas on the sarcolemma. One axon can innervate 1 or more muscle fibers (A MOTOR UNIT).
Where is each motor endplate located, what else is in this area, what neurotransmitter is present within the endplates
-Located in a hollow in the sarcolemms called the PRIMARY SYNAPTIC CLEFT
-In this cleft, the sarcolemma is further folded into smaller ridges called the SECONDAY SYNAPTIC CLEFTS (aka JUNCTIONAL FOLDS).
-Acetylcholine present within endplates
Depolarization during nerve impulse and disease associated with acetylcholine
Neurotransmitter is acetylcholine;
binds to receptors on sarcolemma once it is released into synaptic cleft after action potential depolarizes nerve-->increased Na+ permeability

Acetylcholinesterase in sarcolemma breaks down acetylcholine when action potential is finished

Myesthenia gravis - autoimmune disease in which acetylcholine recepotrs are destroyed resulting in progressive muscle weakness
Pathway of depolarization signal after the influx of Na
The depolarization signal is carried to the myofibrils by the TRANSVERSE (T) TUBULES, which are present at every A-I Juntion.

Depolarization signal then goes to TRIADS, which are formed by the T tubule and the terminal cisternae of the SARCOPLASMIC RETICULUM at the A-I junction in skeletal muscle
How do the T Tubules and Terminal Cisternae communicate?
How is calcium finally released?
What binding protein is found here in terms of calcium and how does calcium's reuptake occur?
-Communicate via Junctional Chennel Complexes that sense the voltage change and stimulate the release of Ca++ from the terminal cisternae.

The binding protein Calsequestrin binds Ca++ to the sarcoplasmic reticulum until it is depolarized and CA++ is released allowing contraction to occur.
Re-uptake of Ca++ into the sarcoplasmic reticulum occurs with Ca++ ATPase/ACtive transport mechanisms.
What 2 types of modified muscle fibers(spindle cells) do Muscle Spindles have?
Role of gamma motor neurons in muscle spindle
1) Nuclear Bag Fibers
2) Nuclear Chain Fibers

Gamma motor neurons innervate the spindle cells to regulate the sensitivity of the muscle spindles
3 Types of skeletal muscle fibers
1) Red Fibers
2) White Fibers
3) Intermediate Fibers
Red Fibers - what kind of twitch, found where, get energy from where, general description
(type I - slow twitch)
- numerous capillaries,
-mitochondria (oxidative
phosphorylation supplies ATP)
- lots of myoglobin, mitochondrial
cytochromes (red color)
- slow sustained contraction
(limbs, back musculature)

Myoglobin serves as reserve supply of oxygen
White Fibers - what kind of twitch, found where, get energy from where, general description
(type IIb - fast twitch: fatigue prone)
- fewer capillaries and mitochondria
(anaerobic glycolysis supplies ATP )
- low myoglobin content
- rapid, forceful contraction; quick to
fatigue; precise movements ( bc of neuromuscular junctions)
(extraocular muscles, digits)
Intermediate Fibers - what kind of twitch, general description
Type IIa - Fast Twitch, Fatigue Resistant
Characteristics are intermediate between red and whtie fibers
General Info on Cardial Muscle
Forms bulk of heart wall; Involuntary contraction
Cardiac fibers surrounded by endomysium only; no perimysium or epimysium
Branching fibers each have
1-2 centrally located nuclei
Intercalated Discs - facilitate formation of what, and its formation's 2 subunits
-Intercalated discs facilitate the formation of a FUNCTIONAL SYNCYTIUM
a) Desmosomes and Fascia Adherens (analogous to zonula adherens) maintain strong cell to cell cohesion
b) Gap junctions are areas of low electrical resistance that allow rapid spread of impulses from one cell to the next.
Difference between where T Tubules invaginate in skeletal muscle vs. cardiac muscle
Altho mechanism of contraction is exactly the same as in skeletal muscle, the T Tubules invaginate at the Z LINES and not the A-I JUNTION AS IN SKELETAL MUSCLE.

Also, there ARE NO TERMINAL CISTERNAE of the sarcoplasmic reticulum and therefore NO TRIADS in cardiac muscle.
Instead of motor endplates, cardiac muscle uses what for depolarization
The Purkinje Fiber System conducts depolarization and spreads through the myocardium, gap junctions in the intercalated discs allow it to spread randomly from fiber to fiber.
-Purkinje Myocytes have less obvious intercalated discs and there are large gap junctions at the ends and sides of cells.
Conduct impulses 4X as fast as normal cardiac fibers
Myocytes in atria contain what cells and what do these cells do?
Myocytes in atria, called MYOCARDIAL ENDOCRINE CELLS, contain Atrial Natriuretic Polypeptides: Cause vasodilation,
diuresis --> Lowered blood pressure & decreased blood volume
General info on Smooth Muscle
No sarcomeres – not striated bc actin and myosin filaments are much less formally arranged.
Present in walls of hollow organs (gut, reproductive, urinary tract) and blood vessels as well as in eye, skin, exocrine glands.
Centrally located nucleus
Diameter: 3 – 8 mm
Length: 15 – 200 mm (Longer in pregnant uterus)
Slow, sustained involuntary contraction
What shape are smooth muscle fibers
Are FUSIFORM (spindle-shaped) with 1 centrally located, cigar shaped nucleus. Packed very tightly together
Innervation of Multiunit Smooth Muscles
are richly innervated (unlike smooth muscle fibers which have a poor nerve supply) and are capable of precise contractions, as in iris of the eye.
-Axons pass NeAR the smooth msucle cells (EN PASSANT) but DO NOT HAVE MOTOR END PLATES as in skeletal muscle
How is contraction stimulated in smooth muscle? (3)
By atuonomic nerve impulses (blood vessels), hormonal stimulation (uterus) or stretch (GI)
Contraction in terms of thin filaments in smooth muscle- what are they made up of, attached to sarcolemma how? troponin or tropomyosin present?
Thin filaments (F actin + tropomyosin) are distributed as a network of small, irregular bundles; NO Troponin
- attached to sarcolemma by dense bodies (a-actinin)

- Dense bodies also in sarcoplasm (equal to Z lines)
Contraction in terms of thick filaments in smooth muscle - polarity, role of Ca++, compare to SFT
Thick filaments not well preserved – myosin II that is present in smooth muscle is folded until the REGULATORY MYOSIN LIGHT CHAIN is phosphorylated (different type).

Thick filaments are side-polar, not bipolar as in straited muscle. Myosin molecules are oriented in one direction on one side
of the filament,
and in the opposite direction on the other side of the filament


Altho TROPONIN is LACKING in smooth muscle fibers, calcium availability is absolutely necessary for contraction to occur.

Phosphorylation of the myosin light chain via myosin light chain
kinase is necessary for contraction – mediated by Ca++
Since no troponin, what binds calcium instead in smooth muscle? where is calcium stored or moved to?
Smooth muscle has no troponin/T Tubule – Calmodulin binds calcium instead. The calcium/calmodulin complex activates MYOSIN LIGHT CHAIN KINASE which then phosphorylates the regulatory myosin light chain.

Calcium may be stored in the vesicles (called Caveolae) or may diffuse into the fibers
Hydrolysis of ATP in smooth muscle
ATP is hydrolyzed at 10% the rate of skeletal muscle, allowing slow, sustained contractions - use little energy
Stimulation of Smooth Muscle Contraction/Contraction Mechanisms (4)
1) Neural stimulation: Multiunit smooth muscle is richly innervated by autonomic nerves (axons pass close to cells but don’t contact them)

- 1:1 axon:fiber relationship (iris)

- neurotransmitters diffuse through 10 – 20 nm gap between axon and smooth muscle fibers (no neuromuscular junctions) and act on voltage-gated Ca++ channels

2) Chemical stimuli (e.g. vasopressin, angiotensin II) act on SM membrane receptors to activate 2nd messenger systems --> contraction

3) Hormones can also affect smooth muscle via ligand-gated Ca++ channels (e.g. uterus)
- contraction (Estrogens, Oxytocin)
- relaxation (Progesterone)

4) Stretching of smooth muscle can initiate contraction
(gastrointestinal tract)
What allow spread of excitation from one fiber to the next and what does this result in?

Regeneration of smooth muscle after injury?
Gap Junctions between smooth muscle fibers in gut allow the spread of excitation through the muscle mass, resulting in Contraction Bands (during peristalsis in GI)

*smooth muscle is capable of regenerating after injury via mitosis and pericytes around blood vessels differentiate into vascular smooth muscle