Hphy 322

Front 1

Transport Proteins

Back 1

large proteins lay within membrane, and allow substances to pass through

Front 2

Simple
 diffusion

Back 2

directly through membrane (if lipid soluble; like oxygen) or through watery channel in large protein for small molecules (no interaction with the protein occurs).

Front 3

Facilitated diffusion

Back 3

requires interaction (chemical binding) with a carrier protein (i.e. glucose and amino acids enter cell via facilitated diffusion)

Front 4

Active Transport

Back 4

ion movement against the electrochemical gradient that requires energy (energy can come from ATP, or from the potential energy released as an ion moves down its gradient).

Front 5

Selective permeability

Back 5

some channels only allow certain molecules to move through, such as sodium and potassium channels which are ion specific.

Front 6

Voltage gated

Back 6

channel opens or closes depending on the electrical charge across the cell membrane

Front 7

Chemical (ligand) gated

Back 7

channel opens or closes depending on the presence of the ligand in the receptor

Front 8

Nernst equation

Back 8

movement of ions across a membrane is effected by the concentration gradient (ions will tend to flow down their concentration gradient) and the electrical gradient (if the ion has a charge, it will move toward side of the cell membrane with the opposite charge). The Nernst equation calculates the necessary local voltage (membrane potential) on the inside the cell membrane, that would OPPOSE the driving force of a specific concentration gradient (chemical gradient) and thus prevent movement of that particular ion at one moment in time. The calculation is based on the concentration of the ion inside and outside the cell and the sign (- vs +) is based on whether the membrane potential inside the cell would be positive or negative

Front 9

EMF

Back 9

electromotive force;voltage

EMF = +/- 61log C1/C2
or
Eion = 61/z x log [ionout]/[ionin];
in this case z is the charge of the ion (-1 or +1)

Front 10

Pressure

Back 10

can affect the movement of ions across a membrane

Front 11

Osmosis

Back 11

movement of water across a cell membrane due to a concentration difference of water

Front 12

Osmotic pressure

Back 12

It is the number of particles, not the mass of the particles, which determines the osmotic pressure (unit is osmole)

Front 13

Describe how the sodium-potassium ATPase pump works, and why it is important to the cell. Also describe how the sodium concentration gradient (maintained by the sodium-potassium pump) can then be used in co-transport and counter transport:

sodium-potassium ATPase pump

Back 13

uses active transport through a carrier protein to move sodium ions out of the cell and potassium ions into the cell AGAINST their electrochemical gradients

Front 14

Describe why the sodium-potassium ATPase pump is important to the cell. Also describe how the sodium concentration gradient is maintained by the sodium-potassium pump

Back 14

the sodium potassium pump is important to the maintenance of the negative electrical voltage inside the cell and of the sodium and potassium electrochemical gradients, and therefore to the ability for a cell to produce an action potential. Without this pump, the ions would eventually leak across the membrane (down their concentration gradients) until there was no electrochemical gradient left (and the cell could no longer produce an action potential).

Front 15

Describe how the sodium-potassium ATPase pump works, and why it is important to the cell. Also describe how the sodium concentration gradient (maintained by the sodium-potassium pump) can then be used in co-transport and counter transport:

co-transport and counter-transport

Back 15

When ions (like sodium) are pumped into a high concentration gradient, they now hold potential energy to use when diffusing back into the cell. In co-transport, the sodium ions can pull another substance into the cell (i.e. glucose and amino acids) and in counter-transport, the carrier protein can bind to sodium on the outside and another substance on the inside of the cell and use the potential energy from the sodium concentration gradient to drive the conformational change in the protein that allows the sodium to diffuse into the cell, while the other substance is moved out (i.e. hydrogen and calcium).

Front 16

Diffusion potential

Back 16

aka equilibrium potential or Nernst potential
is the electrical gradient (described by the local voltaged on the inside of the cell membrane) that balances the chemical gradient of a particular ion at a given chemical concentration gradient.

Front 17

The diffusion potential of sodium alone

Back 17

approximately +61 mV
Sodium is a positive ion that has a much higher concentration just outside the cell membrane as opposed to just inside the cell membrane. Since like charges are repelled, a positive electrical charge on the inside of the cell membrane would repel the positive sodium ions on the outside of the cell, or "balance" sodium's positive charge on the outside of the cell membrane.

Front 18

The diffusion potential of potassium alone

Back 18

approximately -94
Potassium is a positively charged ion with a higher concentration on the inside of the cell membrane and, therefore, a negative charge on the inside of the cell membrane would attract potassium ions and produce an electrical force that would balance the driving force of the potassium's concentration gradient (the force of the concentration gradient is encouraging the ion to the outside of the membrane while the equal and opposite force of the electrical gradient is encouraging the ion to the inside of the membrane).

Front 19

Goldman equation

Back 19

Calculates the membrane potential where there is more than one permeable ion under consideration. The ion CONCENTRATION, ion CHARGE and ion PERMEABILITY of multiple ions are included in this equation

Front 20

How does the voltage gated sodium channel produce an action potential

Back 20

2 gates; activation gate on ouside of the cell and inactivation gate on inside of the cell. Both the activation and inactivation gate are triggered at the same membrane potential (~-70 to -50mV), but the conformational change that causes the inactivation gate to close is a "slower" process (clower...but still occurs within 10,000ths of a second). At rest, the activation gate is closed and the inactivation gate is open. At threshold for that cell, the activation gate opens wide causing Na+ influx (500 to 5000x increase in permeability). In a few 10,000ths of a second, the inactivation gate closes, stopping the influx. The activation gate closes next (although flow has already stopped), and eventually the inactivation gate opens again (requires the membrane potential to return to resting membrane potential).

Front 21

How does the voltage gated potassium channel produce an action potential

Back 21

1 gate; at resting potential it is closed. As membrane potential moves closer to zero, the gate opens causing K+ efflux. The voltage required to open the K+ gate is the same as Na+, but the K+ gate conformation change is slightly slower. Actual gate opening happens around the same time as Na+ inactivation gate closure; combining efforts to repolarize the cell membrane. K+ gates don't close until the voltage returns to resting values, which leads to a short period of hyperpolarization and a relative refractory period in which the stimulus must be stronger for the next action potential.

Front 22

Polarization

Back 22

resting membrane potential is somewhere between -70 to -90 mV (the value depends on the size of the neuron, and on the source

Front 23

Describe the nerve impulse (or propagation of the action potential) & the all-or- none principle. Be sure to include the terms “threshold” and “subthreshold potential”.

Back 23

the nerve impulse is the change in voltage that occurs when Na+ channels open & there is an influx of positive ions (which effects the large nerve fiber from 1-3 mm on either side of the initial stimulus), causing propagation of the action potential in both directions along the length of the nerve. The all-or-none-principle indicates that once the stimulus has past the threshold (typically 15-30 mV less negative than resting potential), and an action potential has occurred, it should propagate along the entire length of the nerve fiber (assuming conditions are right). If the local potential is subthreshold, an action potential will not occur.

Front 24

What is a motor unit?

Back 24

A motor unit is an alpha (α) motor neuron (also called motoneuron or nerve fiber) and all of the muscle fibers it innervates. There are typically multiple
α-motor neurons housed in any given peripheral nerve (such as the median nerve) leading to a muscle.

Front 25

How does stimulus intensity affect motor unit recruitment (the number of motor units activated)?

Back 25

The greater the stimulus the more motor units recruited.

Front 26

In what order are motor units recruited, what is the name of this principle, and
what is the cause of this phenomenon?

Back 26

Motor units are recruited from smallest to largest, which is called the Size Principle. Smaller motor units are recruited first because they are innervated by the smallest motoneurons, which are the most “excitable” and thus produce actions potentials first (before larger motoneurons).

Front 27

What is the role of calcium at the neuromuscular junction (as well as other synaptic junctions elsewhere in the body... the neuromuscular junction is just one example)?

Back 27

When an action potential reaches the end of the neuron at the neuromuscular junction (presynaptic neuron), voltage-gated channels open, which allow calcium ions to enter into the cell. This attracts acetylcholine vesicles to the presynaptic neural membrane, which release acetylcholine into the synaptic cleft.

Front 28

What happens when acetylcholine attaches to the channels on the post- synaptic muscle fiber membrane (as well as other postsynaptic neurons in the body; muscle is just one example)? Which ions can pass through, which cannot, and which particular ion has the greatest number of particles move across the postsynaptic membrane?

Back 28

A chemically-gated channel opens when 2 acetylcholine molecules bind to the receptor. Sodium, potassium and calcium can pass through, but negative ions such as chloride cannot due to a negative charge at the exterior opening of the channel. The ion that moves across the membrane the most is sodium, which enters the cell through this channel when it is opened by acetylcholine. The result is that the membrane potential becomes more positive and an action potential is initiated.

Front 29

What are two ways the system could be manipulated (ie: think poisoned) that would result in a local (graded) potential at the postsynaptic membrane that was too small to reach threshold or cause an action potential?

Back 29

If something was competing with Acetylcholine (ACh) for the receptor, fewer channels would open, less sodium would flow into the cell, and the graded potential would be smaller (e.g.: curare, or poison from a plant in South American natives used on the tip of an arrow or dart to hunt wild game).
If something caused less ACh to be released from the presynaptic membrane, less binding would occur, less sodium, lower graded potential (e.g.: botulism from botulinum bacteria).

Front 30

Describe chemical and electrical synapses, how they are different, and which are more abundant.

Back 30

Chemical synapses are far more abundant. They involve secretion of a neurotransmitter from the first neuronal membrane (presynaptic neuron) that then acts on the adjacent nerve membrane (once the neurotransmitter has bound to the receptor) to excite, inhibit or otherwise modify the membrane permeability of the second neuron (postsynaptic neuron).
Electrical synapses connect at gap junctions and involve ion movement from one neuron to the next (examples include smooth muscle and cardiac muscle contraction).

Front 31

Explain “one-way conductance” utilizing the terms presynaptic and postsynaptic.

Back 31

Signals in neurons with chemical synapses only travel in one direction, the presynaptic neuron causes an effect in the postsynaptic neuron (never in the other direction).

Front 32

Describe anion & cation channels found in the postsynaptic membrane and the most common ion to travel through each.

Back 32

Cation channels allow positive ions through, mostly to allow sodium to enter the cell (but also potassium and calcium). The channel is lined with negative charges, which attract positive ions but repel negative ions. When positive sodium ions enter the cell, the membrane becomes more positive and an action potential can occur if the stimulus is greater than the threshold for activation (in other words, the neuron is excited).
Anion channels allow negative ions through (mostly chloride). The channel is large enough for chloride to pass through, but not large enough for hydrated sodium, potassium or calcium ions. When negative ions enter the postsynaptic neuron, the membrane is hyperpolarized, and the neuron is inhibited.

Front 33

Axodendritic

Back 33

axon synapses with another neuron’s dendrite.

Front 34

Axoaxonal

Back 34

axon synapses with another neuron’s axon.

Front 35

Axosomatic

Back 35

axon synapses with another neuron’s cell body (soma).

Front 36

Explain what “excitatory postsynaptic potentials” (EPSP) and “inhibitory postsynaptic potentials “(IPSP) are.

Back 36

EPSPs occur when either sodium channels are opened (positive ions move into the neuron), or chloride and/or potassium channels are closed (negative ions do not come into the neuron, and positive ions do not leave the neuron) in the postsynaptic membrane. These scenarios all cause the postsynaptic membrane potential to become more positive or “excitable” (more likely an action potential will occur). The EPSP is the change in the membrane potential (in the positive direction) following an excitatory stimulus.

IPSPs occur when either chloride channels are opened (negative ions enter neuron), or potassium channels are opened (positive ions leave the neuron) in the postsynaptic membrane. Both scenarios cause the postsynaptic membrane potential to become more negative or “inhibited” (less likely an action potential will occur). The IPSP is the change in membrane potential (in the negative direction) following an inhibitory stimulus.

Front 37

Define “presynaptic inhibition”

Back 37

Presynaptic inhibition occurs when an inhibitory substance is released onto the presynaptic axon terminal (axoaxonal synapse) before it has a chance to communicate with the next neuron. Typically, it involves release of GABA, which opens anion (chloride) channels, which hyperpolarize the neuron membrane, and neutralize the action potential.

Front 38

What is the typical concentration difference of chloride across the neuron membrane, and why?

Back 38

Chloride is typically in a higher concentration outside the cell compared to inside (similar to sodium). The reasons for this likely include
a) the fact that the cell membrane is somewhat permeable to chloride,
b) because there may be a weak chloride pump, and
c) because the negative resting membrane potential repels the negative chloride ions (notice how close the Nernst potential for Choride is to the actual resting potential; meaning that the electrical gradient of the cell is opposing the concentration gradient of the ion).

Front 39

How does a “second messenger activator” respond differently than an ion channel when a neurotransmitter binds to the receptor? What are the four functions that a “second messenger” can serve, depending on the type of neuron?

Back 39

When a neurotransmitter binds to the postsynaptic ion channel receptor, the ion channel is opened (since it was a ligand-gated channel). Depending on the type of ion that can flow through the channel (i.e: if it is an anion or cation channel), the membrane potential may be changed in the positive or negative direction, depolarizing or hyperpolarizing the neuron membrane).
When a neurotransmitter binds to the postsynaptic receptor for a G-protein second messenger activator, the activated α component of the G-protein will detach from the receptor protein, as well as from the β and γ G-proteins. This activated α
component can now cause one of the following to occur:
1. activate the opening of ion channels,
2. activate cAMP or cGMP,
3. activate intracellular enzymes,
4. activate gene transcription (producing new proteins for metabolism or structure).

Front 40

Explain the basic mechanism of the G protein coupled receptor system. Include what happens to the Gα when its associated receptor is activated.
Briefly describe how this system affects
1. adenylyl/adenylate cyclase, and
2. phospholipase C, and what these enzymes do when they are activated.

Back 40

In the inactive state of the receptor and G-protein complex, the α component is bound to GDP. When the receptor has been activated (ligand/neurotransmitter has bound to receptor) the GDP is replaced with GTP. The Gα GTP complex is then
released from the rest of the G protein complex and floats freely in the cytosol.
When it comes into contact with adenylate cyclase, the complex activates adenylate cyclase, causing it to produce cAMP from ATP. The cAMP is then used within the cell for various functions, depending on the cell type.
Other neurotransmitters cause the Gα GTP complex to activate phospholipase C, which helps breakdown phospholipids in the cell membrane (specifically PIP2: phosphatidylinositol biphosphate) into IP3 (inositol triphosphate) and DAG (diacylglycerol). These second messengers then can affect calcium ions (ie: IP3 releases calcium from mitochondria & endoplasmic reticulum), or protein kinase C (DAG activates protein kinase C which phosphorylates proteins). The release of
calcium ions, as well as the phosphorylation of proteins, causes further responses within the cell.

Front 41

Sarcolemma

Back 41

membrane around muscle cell; includes both plasma membrane and connective tissue outer layer which is continuous with the muscle’s tendon.

Front 42

Sarcoplasm

Back 42

intracellular fluid (fluid within the muscle cell).

Front 43

Sarcoplasmic reticulum

Back 43

similar to endoplasmic reticulum, but in the muscle cell. Stores intracellular calcium in muscle cells (releases calcium and re-sequesters the calcium at the appropriate times during the muscle contraction cycle).

Front 44

Mitochondria

Back 44

many found within muscle cells and produces ATP to be used in muscle contraction.

Front 45

T-tubules

Back 45

extension of the sarcolemma deep within the muscle cell (an invagination). Allows for action potential to be transmitted into the depths of the muscle cell TO THE LOCATION OF the voltage gated calcium channels throughout cell.

Front 46

Terminal cisternae

Back 46

The part of the sarcoplasmic reticulum that is in contact with the T-tubules; releases calcium when there is an action potential, & re-sequesters calcium at rest.

Front 47

Triad (of the reticulum)

Back 47

Two terminal cisternae surrounding one T-tubule is called a Triad.

Front 48

Muscle

Back 48

gross anatomy (ie: biceps, quadriceps), contains bundles of muscle fascicles.

Front 49

Muscle fasciculus (fascicle)

Back 49

contains bundles of muscle fibers.

Front 50

Muscle fiber (muscle cell)

Back 50

contains bundles of MYOFIBRILS; one muscle fiber = one
muscle cell. Runs the entire length of the muscle.

Front 51

Myofibril

Back 51

contains bundles of myofilaments (actin and myosin) arranged in sarcomeres.

Front 52

Myofilaments

Back 52

actin & myosin filaments, which are contractile protein molecules that combine to form the basic machinery of muscle contraction.

Front 53

Actin (F & G)

Back 53

F-actin is the double-stranded elongated portion of the actin filament. G-actin is the molecule on the F-actin that creates the binding site for the myosin head.

Front 54

Myosin (heavy & light chains)

Back 54

Two myosin heavy chains create the tail of the myosin complex, and each chain extends to create one of the heads of the myosin. In addition, the heads of the myosin complex each have two light chains attached to the heavy chain portion. The head of the myosin has a binding site for ATP, and acts as an enzyme for the breakdown of ATP into ADP and Pi. The head also has a binding site for G-action. Many myosin tails combine together to create the myosin filament visualized in the sarcomere.

Front 55

Titin

Back 55

is a very strong, and very elastic molecule that attaches the MYOSIN filament to the Z-disk in the sarcomere.

Front 56

Troponin complex (I, T & C)

Back 56

Troponin attaches to the G-actin molecule. Troponin I binds to actin, troponin T binds to tropomyosin, and troponin C binds to calcium.

Front 57

Tropomyosin

Back 57

is believed to be another elongated protein strand that is wrapped around the F-actin double-strand. It is thought that tropomyosin covers the active G- actin bind site, blocking the myosin head from binding there. When troponin C is bound to calcium, the troponin is thought to have a conformational change that pulls the tropomyosin away from the G-actin binding site, allowing the myosin heads to bind to the G-actin.

Front 58

A band

Back 58

for “anisotrophic to polarized light” called “DARK BANDS”
refers to the area of the sarcomere in which the myosin filaments are located, as well as a portion of the actin filaments that overlap the myosin filaments.
(note: anisotrophic means that the appearance varies with the angle it is viewed at).

Front 59

I band

Back 59

for “isotrophic to polarized light” (Wikipedia, Oct. 2011); also called “LIGHT BANDS”; refers to the area of the sarcomere in which only actin filaments are located (but no myosin).
(note: isotrophic means that the appearance is the same from all angles).

Front 60

H band (or H zone)

Back 60

“from the German "Heller", bright: (Wikipedia, Oct. 2011); center portion of the myosin filaments INCLUDING M line structural elements; DOES NOT overlap actin at rest.

Front 61

M line (or M band)

Back 61

“from the German "Mittel", middle of the sarcomere” (Wikipedia, Oct. 2011); structural proteins (i.e.: myomesin) hold myosin in place.

Front 62

Z disc (or Z line, or Z band)

Back 62

“from the German "Zwischenscheibe", the band in between the I bands” (Wikipedia, Oct. 2011). This is where the ends of the actin filaments are attached, as well as the end of the titin strands (that secure the myosin filaments to the Z line).

Front 63

how is the neuromuscular junction is excited by an action potential

Back 63

When the action potential reaches the presynaptic axon terminal of the motor neuron, it opens calcium channels in the presynaptic membrane. Calcium enters the presynaptic axon terminal causing acetylcholine vessels to bind to membrane and release their contents into the synaptic cleft. Acetylcholine binds to LOCAL NICOTINIC CHOLINERGIC RECEPTORS on the post-synaptic muscle cell membrane (at the neuromuscular junction), causing the muscle membrane to depolarize. The local depolarization opens voltage-gated sodium channels, and elicits an action potential to be spread along the sarcolemma, and down the T-tubules, of the entire muscle fiber.

Front 64

how an action potential causes changes in the muscle cell

Back 64

Where two Terminal Cisternae run along side of one T-tubule (triad) the depolarization activates voltage sensitive DHP (dihydropyridine) receptors on the T-tubule, which in turn connect to (and open) ryanodine calcium channels in the sarcoplasmic reticulum, allowing calcium to flow from the SR into the sarcoplasm and come in contact with Troponin C in the myofibrils.

Front 65

how the contents of the muscle cell react to those changes and produce a muscle contraction.

Back 65

When calcium is bound with Troponin C, Tropomyosin is pulled away from the active binding sites on the actin myofilaments, and the “cocked” myosin head (which is equipped with ADP + Pi) is able to bind with actin. As the ADP + Pi is released from the myosin head, the ratcheting of the head occurs pulling the actin filament toward the M line of the sarcomere. ATP is then able to bind to the myosin head, allowing the head to be released from the actin binding site. As the ATP is broken
down by the ATPase on the myosin head (into ADP + Pi), the myosin head changes its orientation and returns to the “cocked” or perpendicular position (with ADP + Pi still attached).
This cycle continues as long as ATP and calcium are present in the intracellular fluid. Calcium is only present if there are action potentials constantly being produced in the motor neuron and releasing acetylcholine in the neuromuscular junction. When the action potentials cease, DHP is no longer activated, so the ryanodine calcium channels close. The Ca2+ATPase pumps constantly pump calcium back into the SR.

Front 66

Length-tension curve for one sarcomere

Back 66

“optimum” overlap of actin and myosin filaments creates maximum force (tension) production. If the filaments are overlapping too much (sarcomere is too short) or not enough (sarcomere is too long), force (tension) drops off.

Front 67

Length-tension curve for whole muscle

Back 67

this can be more confusing, since there are both “passive” and “active” tissues intertwined together in the whole muscle. The blue line is describing the length-tension relationship for only the “passive”, non-contractile, connective tissues found in the whole muscle. The connective tissue that surrounds the bundles of myofilaments, myofibers, fascicles etc. come together at the ends of the muscle to form a tendon. The longer the whole muscle gets, the more force (tension) is created in these non-contractile connective tissues as they stretch. The red line includes both the passive and “active” (contractile) parts of the whole muscle, so it is a combination of both the blue line in Figure 6-10 and the line in Figure 6-9. Therefore, from 1⁄2 normal length to normal length, it is the contractile (active) elements that create the force (tension). From normal length to 2x normal length, the contractile (active) forces are decreasing, but the force due to the passive elements are increasing, producing the dip and then second rise in tension for the whole muscle.

Front 68

Draw the “load-velocity” curve for skeletal muscle. Label the extremes of the curve with a few words to describe the speed of contraction and the load (force opposing contraction) at those two extremes.

Back 68

Hopefully, this graph was more intuitive, since you have likely experienced this phenomenon yourself. At the left side of Figure 6-11 on p. 77 the velocity is maximum when the load is zero. In other words, you can contract your
muscle very fast when you have nothing heavy opposing it. On the right side of the curve the maximum force that the muscle can oppose is represented and, at this point, the speed of contraction is zero (meaning there is no shortening of the muscle, even though cross-bridges are cycling, the actin just isn’t going anywhere due to the heavy load opposing it).

Front 69

Use words or images to describe some of the basic differences between fast & slow muscle fibers

Back 69

our body contains muscle fibers with different twitch speeds. Slow fibers are typically well suited for endurance instead of speed, since they are able to participate in energy production using oxygen (which can supply ATP for a much longer time than systems that do not use oxygen). Therefore, they have plenty of mitochondria (which produce ATP using oxygen), capillaries (to bring oxygen to the muscle) and myoglobin (which stores oxygen), and are called “red muscle” due to the myoglobin’s affect on the muscle’s appearance. The fibers themselves are often small and innervated by the smaller motor neurons.
In contrast, fast fibers are suited for power, not endurance. They are larger fibers (producing strong contractions), with less dependence on “oxidative” metabolism, and greater dependence on making ATP quickly, but for a shorter period of time. Less need for oxygen means fewer capillaries, fewer mitochondria and fewer myoglobin, and therefore a “white” appearance.

Front 70

Describe the “Size Principle” as it relates to multiple muscle fiber summation, and include how frequency of action potentials sent by the CNS affects the EPSPs in the alpha motor neurons, and ultimately determines which motor units are activated.

Back 70

When only a small amount of force is required, the central nervous system (CNS) sends a weak signal in the form of less frequent action potentials, down the spinal cord to the motor neurons in the anterior horn of the spinal cord (causing some, but not a lot, of EPSPs at the motor neuron cell bodies). The smaller neurons, which innervate smaller motor units (meaning that one neuron innervates fewer muscle fibers) produce a small amount of force when stimulated.
If the CNS sends a stronger message in the form of more frequent action potentials (causing more EPSPs in the motor neuron cell bodies) the larger motor neurons, innervating larger motor units, will begin to also be stimulated, producing much more force.
The CNS can control the amount of force with small increments when a small amount of force is needed because a weaker signal will stimulate only smaller motor units incrementally. Once the larger motor units join in, the force produced during contraction increases in larger increments.

Front 71

Define isometric and isotonic muscle contractions.

Back 71

Isometric contraction occurs when the actin and myosin cross-bridges are engaged & cycling, but the entire muscle is not changing in length. You might imagine yourself contracting your muscles to push an immoveable object (like a wall). You can feel your muscle contracting, but the joint angles are not changing.
Isotonic contraction occurs when the actin and myosin cross-bridges are actively changing the length of the entire muscle. When I pick up a book, the joint angles at my elbow are changing and my biceps muscle as a whole is changing length as the cross-bridge cycling occurs.

Front 72

Define muscle hypertrophy, and describe how physiologists currently think muscle hypertrophy occurs.

Back 72

Physiologists currently believe that muscle hypertrophy (or an increase in the size of the whole muscle) occurs due to an increase in the number of actin and myosin filaments found in each muscle cell. There is some evidence for a very small amount of “hyperplasia” that might also occur, which is the increase in the number of muscle cells. Therefore, this suggests that (for the most part) you are born with the number of muscle cells that you will have as an adult, but that you can increase the number of actin and myosin molecules that each muscle cell will have based on the stimulus that muscle receives over time (ie: weight training).

Front 73

Types of Sensory Receptors:

Back 73

1. Mechanoreceptors: detect mechanical changes such as compression or stretch.
2. Thermoreceptors: detect changes in temperature.
3. Nociceptors: detect mechanical or chemical changes that are related to tissue damage (pain).
4. Electromagnetic: detect changes in light.
5. Chemoreceptors: detect changes in chemical environment.

Front 74

Rigor Mortis

Back 74

Joint stiffness and muscular rigidity of dead body.
Begins 10 minutes to several hours post mortem. Can last up to 4 days depending on temperature and other conditions.
Caused by leakage of Ca2+ ions into cell and ATP depletion.
Maximum stiffness ∼ 12-24 h post mortem, then muscles start to decompose.

Front 75

What is responsible for the increase in tension (of a whole muscle) when the length of the muscle is increased from normal res2ng length to 2x normal length?

a) Increased overlap of actin & myosin filaments.
b) Stretching of the passive connective tissues.
c) Increased force produced by cross-bridges.
d) All of the above.
e) Only A and C.

Back 75

b) Stretching of the passive connective tissues.

Front 76

Which of the following are true about the maximum load the muscle can oppose during contraction?

a) Occurs at the maximum velocity of contraction.
b) Occurs during an isotonic contrac2on.
c) Occurs at the minimum velocity of contraction.
d) Only A and B.
e) Only B and C.

Back 76

c) Occurs at the minimum velocity of contraction.

Front 77

Concentric Isotonic Contraction

Back 77

strength of actin-myosin binding exceeds load
(sarcomeres can shorten).

Front 78

Eccentric isotonic contraction

Back 78

strength of actin-myosin binding does not exceed load
(sarcomeres are lengthening).

Front 79

Maximal isometric contraction

Back 79

strength of actin-myosin cross-bridges does not
exceed load, therefore no movement

Front 80

Submaximal isometric contraction

Back 80

agonist and antagonist muscles both contract to maintain joint position, therefore no movement

Front 81

Actin: Thin Filament, 2 types

Back 81

F actin: long strands (fibrous)

G actin: binding sites (globular)

Front 82

Myosin: Think Filaments

Back 82

heavy chains (tail) and light chains (heads)
-myosin head forms cross bridge with G-actin

Front 83

Which of the following blocks the myosin head from binding with G-actin at rest?

a) Tropomyosin
b) Troponin I
c) Troponin T
d) Troponin C
e) None of the above

Back 83

a) Tropomyosin

Front 84

Troponin: 3 polypeptides

Back 84

– TnI – binds to actin
– TnT – binds to tropomyosin
– TnC – binds to Ca2+

Front 85

Titin (3)

Back 85

– Largest protein known; elastic!
– Stabilizes position of myosin filaments
– Provides passive tension in muscles

Front 86

Nebulin

Back 86

– Inelastic
giant protein
– ALIGNMENT of actin

Front 87

What happens to the bands/zones in the sarcomere during contraction of a skeletal muscle cell? !

a. Z-lines move closer together, and sarcomeres shorten
b. I bands shorten
c. A bands stay the same length, but H zones shorten
d. All of the above
e. Only A and B

Back 87

d. All of the above

Front 88

How does shortening of the sarcomere occur?

Back 88

Myosin “walks down” an actin fiber towards Z-line
Myosin = motor protein: chemical energy →
mechanical energy
of motion (power stroke)

Front 89

What is necessary for sequenOal power strokes (muscle contracOon) to occur?

a) Action potential from motor neuron
b) Calcium release from SR
c) Available ATP
d) All of the above
e) Only A and B

Back 89

d) All of the above

Front 90

Which of the following occur when ATP is broken down into ADP + Pi at the myosin head?

a) Myosin head is released from actin binding site.
b) Myosin head moves to “cocked” (90 degree) posiOon.
c) Power stroke occurs.
d) Tropomyosin is pulled away from actin
binding site.
e) None of the above.

Back 90

b) Myosin head moves to "cocked" position

Front 91

When the muscle is at rest, where is there a high concentraIon of calcium?

a) In the sarcoplasm.
b) In the sarcoplasmic reIculum.
c) In the axon terminal of motor neuron.
d) All of the above
e) Only B and C

Back 91

b) In the sarcoplasmic reticulum

Front 92

Which of the following is in contact with extracellular fluid?

a) Sarcoplasmic reIculum
b) Sarcolemma
c) T-tubule
d) All of the above
e) Only B and C

Back 92

e) Only B and C

Front 93

Myofibrils

Back 93

Sarcomeres connected end to end, contractile units
(makes up ~ 80% of muscle cell)

Front 94

Myofilaments

Back 94

– Actin (thin filament)
– Myosin (thick filament)

Front 95

Which of the following includes the enIre length of the myosin filament within a sarcomere?

a) H band
b) M line
c) Z disc
d) I band
e) None of the above

Back 95

E is correct
(A band)

Front 96

Depolarization

Back 96

Na+ activation gates open; influx of positively charged Na+ ions; changes the initially polarized state (negative voltage inside the cell membrane) to depolarized (positive voltage inside cell membrane; or at least less negative that resting....tends to overshoot zero and end as a positive voltage).

Front 97

Hyperpolarization

Back 97

K+ gates are "slow" to close, causing the membrane potential to be even more negative that the resting state following an action potential

Front 98

Repolarization

Back 98

immediately after the Na+ inactivation gate close and K+ gates open; Na+ ions stop influx, plus efflux of K+ positive charged ions; repolarizes cell membrane (makes it negative again).

Front 99

What are the 2nd messengers?

Back 99

cAMP, IP3, DAG

Front 100

Name an enzyme activated by a 2nd messenger

Back 100

Protein Kinase A or C

OR Ca2+ channels of smooth muscle

Front 101

Name all the G proteins (that we have discussed) whose activation promotes muscle contractility in the particular type of muscle cell associated with it (ie: Gsα, Giα, Gqα...)?

Back 101

Giα and Gqα

Front 102

Which myofilament is attached directly to the Z-line (Z-disks)?

Back 102

Actin (0 pt for titin or I-Band since they are not the names of myofilaments)

Front 103

Which myofilament can impact the speed of cross bridge cycling through its different
isoforms?

Back 103

Myosin

Front 104

When the frequency of action potentials in a muscle reaches the point in which
contraction is not limited by calcium availability, it is referred to as

Back 104

Tetany (1/2 pt for maximal contraction, and summation or temporal summation) _____