CH. 9-A

1. Produce movement: responsible for all locomotion and

manipulation. Example: walking, digesting, pumping blood

2. Maintain posture and body position

3. Stabilize joints

4. Generate heat as they contract

Skeletal muscle is an organ made up of different tissues with three features: nerve and blood supply, connective tissue sheaths, and attachments

Each muscle receives a nerve, artery, and veins

-Consciously controlled skeletal muscle has nerves supplying every fiber to control activity

Contracting muscle fibers require huge amounts of oxygen and nutrients

-Also need waste products removed quickly

-Epimysium: dense irregular connective tissue surrounding entire muscle; may blend with fascia. Perimysium: fibrous connective tissue surrounding fascicles (groups of muscle fibers). Endomysium: fine areolar connective tissue surrounding each muscle fiber

Attachments can be direct or indirect. Direct (fleshy): epimysium fused to periosteum of bone or perichondrium of cartilage. Indirect: connective tissue wrappings extend beyond muscle as ropelike tendon or sheetlike aponeurosis

Long, cylindrical cells that contain multiple nuclei. Sarcolemma: muscle fiber plasma membrane. Sarcoplasm: muscle fiber cytoplasm

-Contains many glycosomes for glycogen storage, as well as

myoglobin for O2 storage

Myofibrils, Sarcoplasmic reticulum, T tubules

Densely packed, rodlike elements. Single muscle fiber can contain 1000s. Accounts for ~80% of muscle cell volume

Features: Striations, Sarcomeres, Myofilaments, Molecular composition of myofilaments

H zone: lighter region in middle of dark A band (Highlight!)

-M line: line of protein (myomesin) that bisects H zone vertically ( Middle!)

I bands: lighter regions. Italics – just looks lighter and dainty

-Z disc (line): coin-shaped sheet of proteins on midline of light I band (ZIG ZAGs!)

Smallest contractile unit (functional unit) of muscle fiber. Contains A band with half of an I band at each end (Consists of area between Z discs). Individual sarcomeres align end to end along myofibril, like boxcars of train

Actin myofilaments: thin filaments. Extend across I band and partway in A band. Anchored to Z discs. Myosin myofilaments: thick filaments. Extend length of A band. Connected at M line

-Sarcomere cross section shows hexagonal arrangement of one thick filament surrounded by six thin filaments

Heavy chains intertwine to form myosin tail. Light chains form myosin globular head

-During contraction, heads link thick and thin filaments together, forming cross bridges

-Myosins are offset from each other, resulting in staggered array of heads

at different points along thick filament

G actin subunits bears active sites for myosin head attachment during contraction (G actin subunits link together to form long, fibrous F actin (filamentous)). Two F actin strands twist together to form a thin filament

-Tropomyosin and troponin: regulatory proteins bound to actin

Elastic filament: composed of protein titin (Holds thick filaments in place; helps recoil after stretch; resists excessive stretching). Dystrophin: Links thin filaments to proteins of sarcolemma. Nebulin, myomesin, C proteins bind filaments or sarcomeres together (Maintain alignment of sarcomere)

Network of smooth endoplasmic reticulum tubules surrounding each myofibril. Most run longitudinally. Terminal cisterns form perpendicular cross channels at the A–I band junction. SR functions in regulation of intracellular Ca2+ levels. Stores and releases Ca2+

Tubules penetrate cell’s interior at each A–I band junction between terminal cisterns

-Triad: area formed from terminal cistern of one sarcomere, T tubule, and terminal

cistern of neighboring sarcomere

SR cistern membranes = integral membrane proteins --protrude into intermembrane space. SR integral proteins control opening of calcium channels in SR cisterns

-When electrical impulse passes by, T tubule proteins change shape, -> SR proteins to change shape ->release of calcium into cytoplasm

The activation of cross bridges to generate force. Shortening occurs when tension generated by cross bridges on thin filaments exceeds forces opposing shortening. Contraction ends when cross bridges become inactive

S.F.M.C: Neither thick nor thin filaments change length, just overlap more

-When nervous system stimulates muscle fiber, myosin heads are allowed to bind to actin, forming cross bridges, which cause sliding (contraction) process to begin

-Causes shortening of muscle fiber

• Z discs are pulled toward M line

• I bands shorten

• Z discs become closer

• H zones disappear

• A bands move closer to each other

Neurons and muscle cells are excitable cells capable of action potentials (Excitable cells are capable of changing resting membrane potential voltages)

-AP crosses from neuron to muscle cell via the neurotransmitter acetylcholine (ACh)

Two classes of ion channels: Chemically gated ion channels – opened by chemical messengers such as neurotransmitters (Ex: ACh receptors on muscle cells)

-Voltage-gated ion channels – open or close in response to voltage changes in membrane potential

Each axon divides into many branches as it enters muscle

-Axon branches end on muscle fiber, forming neuromuscular junction or motor end plate (Each muscle fiber has one neuromuscular junction with one motor neuron)

Stored within axon terminals are membrane-bound synaptic vesicles (Synaptic vesicles contain neurotransmitter acetylcholine (ACh))

-Infoldings of sarcolemma, called junctional folds, contain millions of ACh receptors

-NMJ consists of axon terminals, synaptic cleft, and junctional folds

1. Events at neuromuscular junction

2. Muscle fiber excitation

3. Excitation-contraction coupling

4. Cross bridge cycling

3. Calcium entry causes release of ACh neurotransmitter into synpatic cleft 4. ACh diffuses across to ACh receptors (Na+ chemical gates) on sarcolemma 5. ACh binding to receptors, opens gates, allowing Na+ to enter resulting in end plate potential 6. Acetylcholinesterase degrades ACh

Resting sarcolemma is polarized, meaning a voltage exists across membrane (Inside of cell is negative compared to outside). Action potential is caused by changes in electrical charges

Occurs in three steps

1. Generation of end plate potential

2. Depolarization

3. Repolarization

->Causes chemically gated ion channels (ligands) on sarcolemma to open. Na+ diffuses into muscle fiber (Some K+ diffuses outward, but not much). Because Na+ diffuses in, interior of sarcolemma becomes less negative (more positive). Results in local depolarization called end plate potential

Large influx of Na+ through channels into cell triggers AP that is unstoppable and will lead to muscle fiber contraction. AP spreads across sarcolemma from one voltage-gated Na+ channel to next one in adjacent areas, causing that area to depolarize

Refractory period: muscle fiber cannot be stimulated for a specific amount of time, until repolarization is complete. Ionic conditions of resting state are restored by Na+-K+ pump (Na+ that came into cell is pumped back out, and K+ that flowed outside is pumped back

into cell)

Example: myasthenia gravis: disease characterized by drooping upper eyelids, difficulty swallowing and talking, and generalized muscle weakness. Involves shortage of Ach receptors because person’s ACh receptors are attacked by own antibodies. Suggests this is an autoimmune disease

AP is propagated along sarcolemma and down into T tubules, where voltage-sensitive proteins in tubules stimulate Ca2+ release from SR (Ca2+ release leads to contraction). AP is brief and ends before contraction is seen

At low intracellular Ca2+ concentration: Tropomyosin blocks active sites on actin. Myosin heads cannot attach to actin. Muscle fiber remains relaxed

-Voltage-sensitive proteins in T tubules change shape,

causing sarcoplasmic reticulum (SR) to release Ca2+ to

cytosol

Myosin heads is then allowed to bind to actin, forming cross bridge. Cycling is initiated, -> sarcomere shortening & muscle contraction. When nervous stimulation ceases, Ca2+ is pumped back into SR, & contraction ends

3. Cross bridge detachment: ATP attaches to myosin head, causing cross bridge to detach

4. Cocking of myosin head: energy from hydrolysis of ATP “cocks” myosin head into high-energy state (This energy will be used for power stroke in next cross bridge cycle)

cycle stops b/t steps 2 & 3

ATP is also needed for cross bridge detachment (Results in myosin head staying bound to actin, causing constant state of contraction)

-Muscles stay contracted until muscle proteins break down, causing myosin to release