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CBIO 2200 EXAM 4

Terms in this set (57)

skeletal muscle
structure: see photo

location: muscles attached to skeleton

function: contract and cause movement; stop movement; prevent excess movement of the bones and joints, maintaining skeletal stability and preventing skeletal structure damage or deformation; located throughout the body at the openings of internal tracts to control the movement of various substances; protect internal organs; maintenance of homeostasis in the body by generating heat

properties: tissues include the skeletal muscle fibers, blood vessels, nerve fibers, and connective tissue. Each skeletal muscle has three layers of connective tissue that enclose it and provide structure to the muscle as a whole, and also compartmentalize the muscle fibers within the muscle; striated; multinucleate; Nuclei pushed off to the side; Cells run the length of the muscle; voluntary
smooth muscle
structure: see photo

location: present in the walls of hollow organs like urinary bladder and in the walls of passageways, such as the arteries and veins of the circulatory system, and the tracts of the respiratory, urinary, and reproductive systems

function: change the size of the iris and alter the shape of the lens; causes hair to stand erect in response to cold temperature or fear; move substances through body

properties: no striations; spindle-shaped ( and have a single nucleus; they produce their own connective tissue, endomysium. Although they do not have striations and sarcomeres, smooth muscle fibers do have actin and myosin contractile proteins, and thick and thin filaments. These thin filaments are anchored by dense bodies; involuntary; organized in sheet
cardiac muscle
structure: see photo

location: only found in the heart

function: pump blood into the vessels of the circulatory system.

properties: striated and organized into sarcomeres; shorter than skeletal muscle fibers and usually contain only one nucleus, which is located in the central region of the cell. Cardiac muscle fibers also possess many mitochondria and myoglobin, as ATP is produced primarily through aerobic metabolism. Cardiac muscle fibers cells also are extensively branched and are connected to one another at their ends by intercalated discs.
muscle fiber
a single muscle cells
multinucleated

an elongated contractile cell that forms the muscles of the body
sarcolemma
plasma membrane of muscle fibers
sarcoplasm
cytoplasm of muscle fibers
t-tubules
projection of the sarcolemma into the interior of the cell
Facilitate the uniform contraction of the muscle by allowing the action potential to spread through the muscle cell more rapidly.
For the action potential to reach the membrane of the SR, there are periodic invaginations in the sarcolemma
myofibrils
contains actin and myosin

Microscopic protein filaments that make up muscle cells.

100s and 1000s found inside one muscle fiber
sarcoplasmic reticulum
specialized smooth endoplasmic reticulum, which stores, releases, and retrieves calcium ions (Ca++)

The smooth ER of a muscle cell, enlarged and specialized to act as a Ca2+ reservoir. The SR winds around each myofibril in the muscle cell.
sarcomere
longitudinally, repeating functional unit of skeletal muscle, with all of the contractile and associated proteins involved in contraction
thin filaments
thin strands of actin and its troponin-tropomyosin complex projecting from the Z-discs toward the center of the sarcomere
thick filaments
the thick myosin strands and their multiple heads projecting from the center of the sarcomere toward, but not all to way to, the Z-discs
actin
protein that makes up most of the thin myofilaments in a sarcomere muscle fiber
myosin
protein that makes up most of the thick cylindrical myofilament within a sarcomere muscle fiber
tropomyosin
Tropomyosin is a protein that winds around the chains of the actin filament and covers the myosin-binding sites to prevent actin from binding to myosin.
To initiate muscle contraction, tropomyosin has to expose the myosin-binding site on an actin filament to allow cross-bridge formation between the actin and myosin microfilaments.
troponin
regulatory protein that binds to actin, tropomyosin, and calcium
calcium attaches to troponin, which causes it to change shape, exposing binding sites for myosin (active sites) on the actin filaments.
Ca++ to bind to troponin so that tropomyosin can slide away from the binding sites on the actin strands.
sarcomere structure
z disc to z disc
myosin attached to z disc by titin
actin attached directly to z disc
i band - only thin filaments shortens during contraction
a band - myosin is and actin isn't there (only thick)
h zone - shortens in length during contraction
sliding filament mechanism
sliding can only occur when myosin-binding sites on the actin filaments are exposed by a series of steps that begins with Ca++ entry into the sarcoplasm.

Tropomyosin is a protein that winds around the chains of the actin filament and covers the myosin-binding sites to prevent actin from binding to myosin. Tropomyosin binds to troponin to form a troponin-tropomyosin complex. The troponin-tropomyosin complex prevents the myosin "heads" from binding to the active sites on the actin microfilaments. Troponin also has a binding site for Ca++ ions.

tropomyosin has to expose the myosin-binding site on an actin filament to allow cross-bridge formation between the actin and myosin microfilaments. The first step in the process of contraction is for Ca++ to bind to troponin so that tropomyosin can slide away from the binding sites on the actin strands. This allows the myosin heads to bind to these exposed binding sites and form cross-bridges. The thin filaments are then pulled by the myosin heads to slide past the thick filaments toward the center of the sarcomere. But each head can only pull a very short distance before it has reached its limit and must be "re-cocked" before it can pull again, a step that requires ATP.
What would happen if the sarcolemma suddenly became very permeable to Ca2+?
If the sarcolemma of a resting skeletal muscle suddenly became permeable to Ca2+, the cytosolic concentration of Ca2+ would increase, and the muscle would contract. In addition, because the amount of calcium ions in the cytosol must decrease for relaxation to occur, the increased permeability of the sarcolemma to Ca2+ might prevent the muscle from relaxing completely.
muscle cell membrane at rest
The inside of cell will be negative, the cell exterior will be slightly positive
All voltage-gated Na+ and K+ channels are closed (-70)

sodium excess on outside and potassium in excess on outside;
sodium-potassium pump maintains potential
what happens during action potential in a muscle cell
ACh is released from the motor neuron, crosses the synaptic cleft and binds on the motor plate. This binding causes the opening of Na gates allowing Na to flow down its concentration gradient. The inside of the cell is now positive. This triggers the opening of K gates allowing for K to flow out of the cell down its concentration gradient. This process continues like a wave across the cell until resting potential is reached again via no more ACh from the motor neuron.
events inside the muscle cell that lead to contraction
begins with a signal—the neurotransmitter, ACh—from the motor neuron innervating that fiber. The local membrane of the fiber will depolarize as positively charged sodium ions (Na+) enter, triggering an action potential that spreads to the rest of the membrane will depolarize, including the T-tubules. This triggers the release of calcium ions (Ca++) from storage in the sarcoplasmic reticulum (SR). The Ca++ then initiates contraction, which is sustained by ATP (Figure). As long as Ca++ ions remain in the sarcoplasm to bind to troponin, which keeps the actin-binding sites "unshielded," and as long as ATP is available to drive the cross-bridge cycling and the pulling of actin strands by myosin, the muscle fiber will continue to shorten to an anatomical limit.
events inside the muscle cell that lead to relaxation
begins with the motor neuron, which stops releasing its chemical signal, ACh, into the synapse at the NMJ. The muscle fiber will repolarize, which closes the gates in the SR where Ca++ was being released. ATP-driven pumps will move Ca++ out of the sarcoplasm back into the SR. This results in the "reshielding" of the actin-binding sites on the thin filaments. Without the ability to form cross-bridges between the thin and thick filaments, the muscle fiber loses its tension and relaxes.
contractile elements in smooth muscle
actin and myosin
doesn't have t-tubules or connective tissue packing
more thin filaments (actin)
myosin is bundled differently
intermediate filaments
dense bodies
contraction: influenced by hormones
contractile elements in skeletal muscle
actin and myosin
striations: a lot sarcomeres that are tightly packed
contraction: not affected by hormones
ACh from vesicle of presynaptic terminal through muscle contraction
At the NMJ, the axon terminal releases a chemical messenger, or neurotransmitter, called acetylcholine (ACh). The ACh molecules diffuse across a minute space called the synaptic cleft and bind to ACh receptors located within the motor end-plate of the sarcolemma on the other side of the synapse. Once ACh binds, a channel in the ACh receptor opens and positively charged ions can pass through into the muscle fiber, causing it to depolarize, meaning that the membrane potential of the muscle fiber becomes less negative (closer to zero.)

As the membrane depolarizes, another set of ion channels called voltage-gated sodium channels are triggered to open. Sodium ions enter the muscle fiber, and an action potential rapidly spreads (or "fires") along the entire membrane to initiate excitation-contraction coupling.

Immediately following depolarization of the membrane, it repolarizes, re-establishing the negative membrane potential. Meanwhile, the ACh in the synaptic cleft is degraded by the enzyme acetylcholinesterase (AChE) so that the ACh cannot rebind to a receptor and reopen its channel, which would cause unwanted extended muscle excitation and contraction.

Propagation of an action potential along the sarcolemma is the excitation portion of excitation-contraction coupling. Recall that this excitation actually triggers the release of calcium ions (Ca++) from its storage in the cell's SR. For the action potential to reach the membrane of the SR, there are periodic invaginations in the sarcolemma, called T-tubules

The T-tubules carry the action potential into the interior of the cell, which triggers the opening of calcium channels in the membrane of the adjacent SR, causing Ca++ to diffuse out of the SR and into the sarcoplasm. It is the arrival of Ca++ in the sarcoplasm that initiates contraction of the muscle fiber by its contractile units, or sarcomeres.
What happens to ACh when muscle contraction is complete?
broken down and reabsorbed back into system
why does botulinum toxin produce paralysis?
blocking ACh blocks the contraction
what might be expected to reverse the paralysis with botulinum toxin?
formulate toxin removal to allow ACh to be released
muscle twitch
latent phase
contraction phase
relaxation phase
latent phase
during which the action potential is being propagated along the sarcolemma and Ca++ ions are released from the SR. This is the phase during which excitation and contraction are being coupled but contraction has yet to occur.
contraction phase
The Ca++ ions in the sarcoplasm have bound to troponin, tropomyosin has shifted away from actin-binding sites, cross-bridges formed, and sarcomeres are actively shortening to the point of peak tension.
relaxation phase
when tension decreases as contraction stops. Ca++ ions are pumped out of the sarcoplasm into the SR, and cross-bridge cycling stops, returning the muscle fibers to their resting state.
motor unit
A motor neuron and all of the muscle fibers it innervates
contractions in large motor units: - one large motor unit that innervate many muscle fibers for large powerful actions
contractions in small motor units: • In places with fine motor skills there will be more motor units innervating fewer muscle fibers
isotonic contractions
muscle length changes and moves the load, the tension remains relatively constant through the rest of the contractile period; come in two flavors concentric and eccentric
isometric contractions
Muscle contraction in which there is no change in length - muscle tension increased
concentric contractions
Skeletal muscle movement leading to shortening of the agonist muscle.
eccentric contractions
Lengthening of muscle during contraction due to an external force
fast glycolytic fibers
This type of muscle fiber is described as white, has a fast rate of fatigue, fast contraction, is anaerobic, has a low myoglobin content, is last to be recruited for contraction and is associated with fast powerful contractions, such as hitting a baseball
slowest recovery
slow oxidative fibers
This type of muscle fiber is described as red, has a slow rate of fatigue, has slow contraction, is aerobic, has a high myoglobin content, is the first to be recruited for contraction and is associated with endurance type activities

more blood flow
fatigue resistant
high mitochondrial content to supply with energy
fast oxidative fibers
This type of muscle fiber is described as red to pink, has a intermediate rate of fatigue, has fast contraction, is aerobic and anaerobic, has a high myoglobin content, is second to be recruited for contraction and is associated with activities such as walking and sprinting. These fibers "can do either"
muscle contraction
Formation of an active potential and muscle synapses travels down cell and into the middle via sarcomlema invaginations (t-tubules) which influence the sarcoplasmic reticulum to release Ca2+ into the cytosol through voltage gated channels. Ca2+ binds to troponin which shifts tropomyosin away from actin myosin binding sites allowing for myosin-II binding and contraction of the sarcomere through the cocking (uses ATP) and power stroke of the myosin heads
Ca++ in smooth muscle contraction compared to skeletal
activates enzymes, which in turn activate myosin heads.
epimysium
dense, irregular connective tissue which allows a muscle to contract and move powerfully while maintaining its structural integrity. The epimysium also separates muscle from other tissues and organs in the area, allowing the muscle to move independent
fascicle
a bundle of muscle fibers
perimysium
The connective-tissue sheath that forms sheaths for the bundles of muscle fibers
endomysium
each muscle fiber is encased in a thin connective tissue layer of collagen and reticular fibers
contains the extracellular fluid and nutrients to support the muscle fiber. These nutrients are supplied via blood to the muscle tissue.
excitation(-contraction coupling)
Signaling begins when a neuronal action potential travels along the axon of a motor neuron, and then along the individual branches to terminate at the NMJ. At the NMJ, the axon terminal releases a chemical messenger, or neurotransmitter, called acetylcholine (ACh). The ACh molecules diffuse across a minute space called the synaptic cleft and bind to ACh receptors located within the motor end-plate of the sarcolemma on the other side of the synapse. Once ACh binds, a channel in the ACh receptor opens and positively charged ions can pass through into the muscle fiber, causing it to depolarize, meaning that the membrane potential of the muscle fiber becomes less negative (closer to zero.)

As the membrane depolarizes, another set of ion channels called voltage-gated sodium channels are triggered to open. Sodium ions enter the muscle fiber, and an action potential rapidly spreads (or "fires") along the entire membrane to initiate excitation-contraction coupling.

Immediately following depolarization of the membrane, it repolarizes, re-establishing the negative membrane potential. Meanwhile, the ACh in the synaptic cleft is degraded by the enzyme acetylcholinesterase (AChE) so that the ACh cannot rebind to a receptor and reopen its channel, which would cause unwanted extended muscle excitation and contraction
contraction (after excitation)
triggers the release of calcium ions (Ca++) from its storage in the cell's SR. For the action potential to reach the membrane of the SR, there are periodic invaginations in the sarcolemma, called T-tubules

The T-tubules carry the action potential into the interior of the cell, which triggers the opening of calcium channels in the membrane of the adjacent SR, causing Ca++ to diffuse out of the SR and into the sarcoplasm. It is the arrival of Ca++ in the sarcoplasm that initiates contraction of the muscle fiber by its contractile units, or sarcomeres.
What are the opposite roles of voltage-gated sodium channels and voltage-gated potassium channels?
The opening of voltage-gated sodium channels, followed by the influx of Na+, transmits an Action Potential after the membrane has sufficiently depolarized. The delayed opening of potassium channels allows K+ to exit the cell, to repolarize the membrane.
sequence of events in muscle contraction
begins with a signal—the neurotransmitter, ACh—from the motor neuron innervating that fiber. The local membrane of the fiber will depolarize as positively charged sodium ions (Na+) enter, triggering an action potential that spreads to the rest of the membrane will depolarize, including the T-tubules. This triggers the release of calcium ions (Ca++) from storage in the sarcoplasmic reticulum (SR). The Ca++ then initiates contraction, which is sustained by ATP. As long as Ca++ ions remain in the sarcoplasm to bind to troponin, which keeps the actin-binding sites "unshielded," and as long as ATP is available to drive the cross-bridge cycling and the pulling of actin strands by myosin, the muscle fiber will continue to shorten to an anatomical limit.

when signaling from the motor neuron ends, which repolarizes the sarcolemma and T-tubules, and closes the voltage-gated calcium channels in the SR. Ca++ ions are then pumped back into the SR, which causes the tropomyosin to reshield (or re-cover) the binding sites on the actin strands. A muscle also can stop contracting when it runs out of ATP and becomes fatigued
Creatine phosphate
In a resting muscle, excess ATP transfers its energy to creatine, producing ADP and creatine phosphate. This acts as an energy reserve that can be used to quickly create more ATP. When the muscle starts to contract and needs energy, creatine phosphate transfers its phosphate back to ADP to form ATP and creatine. This reaction is catalyzed by the enzyme creatine kinase and occurs very quickly; thus, creatine phosphate-derived ATP powers the first few seconds of muscle contraction. However, creatine phosphate can only provide approximately 15 seconds worth of energy, at which point another energy source has to be used
glycolysis
an anaerobic (non-oxygen-dependent) process that breaks down glucose (sugar) to produce ATP; cannot generate ATP as quickly as creatine phosphate. Thus, the switch to glycolysis results in a slower rate of ATP availability to the muscle. The sugar used in glycolysis can be provided by blood glucose or by metabolizing glycogen that is stored in the muscle. The breakdown of one glucose molecule produces two ATP and two molecules of pyruvic acid, which can be used in aerobic respiration or when oxygen levels are low, converted to lactic acid
lactic acid
If oxygen is available, pyruvic acid is used in aerobic respiration. However, if oxygen is not available, pyruvic acid is converted to _______, which may contribute to muscle fatigue. This conversion allows the recycling of the enzyme NAD+ from NADH, which is needed for glycolysis to continue. This occurs during strenuous exercise when high amounts of energy are needed but oxygen cannot be sufficiently delivered to muscle. Glycolysis itself cannot be sustained for very long (approximately 1 minute of muscle activity), but it is useful in facilitating short bursts of high-intensity output.
Aerobic respiration
the breakdown of glucose or other nutrients in the presence of oxygen (O2) to produce carbon dioxide, water, and ATP. Approximately 95 percent of the ATP required for resting or moderately active muscles is provided by aerobic respiration, which takes place in mitochondria. The inputs for aerobic respiration include glucose circulating in the bloodstream, pyruvic acid, and fatty acids. Aerobic respiration is much more efficient than anaerobic glycolysis, producing approximately 36 ATPs per molecule of glucose versus four from glycolysis. However, aerobic respiration cannot be sustained without a steady supply of O2 to the skeletal muscle and is much slower
wave summation
If the fibers are stimulated while a previous twitch is still occurring, the second twitch will be stronger.
excitation-contraction coupling effects of successive motor neuron signaling is summed, or added together
tetanus
If the stimulus frequency is so high that the relaxation phase disappears completely, contractions become continuous in a process called complete
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