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Physiology (MPP 3202) > Ch. 12 Muscles > Flashcards

Ch. 12 Muscles Flashcards

1
Q

How are skeletal muscles connected to bones?

A

Skeletal muscles are connected to the bones they move by tough tendons, composed of closely-packed, parallel arrays of [mostly] collagen protein.

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2
Q

Is skeletal muscle under voluntary or involuntary control?

A

For the most part, contraction is voluntary, i.e. under conscious control.

Contraction of skeletal muscle depends upon stimulation by motor neurons—this is very different from cardiac and smooth muscle, both of which are capable of spontaneous contraction, and are under autonomic control.

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3
Q

Muscle cell vs Muscle fiber vs Myofiber

A

muscle cell = muscle fiber = myofiber

*different terminology, same thing

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4
Q

Fasciculus

A

A “fasciculus” is a bundle of individual muscle (myo) fibers (i.e. muscle cells).

Each myofiber extends the full length of the muscle of which it is part—i.e. all the way from its origin to its insertion. So, these are long cells, and this anatomic feature is UNIQUE to skeletal muscle—IOW, cardiac and smooth muscle cells are very short, and do NOT extend the full length of their respective tissues.

Another key feature of skeletal muscle fibers is that they are NOT electrically connected—in other words, each individual muscle cell must be stimulated by a nerve signal. This is very different from cardiac and the major type of smooth muscle.

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5
Q

Muscle Fiber

A

Contains bundles of contractile elements (myofibrils), each of which is surrounded by cytoplasm (sarcoplasm).

Make sure you understand the distinction between a myofiber (a muscle cell) and a myofibril (bundles of contractile proteins within a myofiber).

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6
Q

Are skeletal muscle cells multi-nucleated? If so, why?

A

Yes

They develop (i.e. via fusion of progenitor myoblasts), skeletal muscle cells each have multiple nuclei

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7
Q

Sarcoplasm

A

In muscle cells it is similar to the cytoplasm of other cell types, except that it has numerous “glycosomes,” which are storage granules containing glycogen. This glycogen is a ready source of glucose for use during intense muscular activity, e.g. during exercise.

Has high content of the oxygen-binding protein, myoglobin. This protein can actually “store” oxygen for use during periods of systemic hypoxia (oxygen deficit).

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8
Q

Sarcoplasmic Reticulum (SR)

A

Plays a major role in excitation-contraction coupling, in that it is the myofiber’s storage repository for calcium, in response to a signal from a motor neuron, it releases calcium into the sarcoplasm for muscle contraction, then takes that calcium back up during relaxation.

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9
Q

Z discs (lines)

A

Center of each I band

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10
Q

A bands

A

Thick filament + thin filament overlap; thick filament = MYOSIN

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11
Q

I bands

A

Only thin filaments; primarily ACTIN

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12
Q

Sarcomere

A

basic cellular unit of contraction

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13
Q

M lines

A

Center of each A band; help hold down/anchor thick filaments

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14
Q

Titin

A

Contributes to elastic recoil during relaxation
–runs from Z disc to M line

Titin acts as a “spring”

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15
Q

In muscular contraction…

A

Thin filaments slide along thick filaments

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16
Q

Sliding Filament Mechanism

A

When a muscle contracts, sarcomeres shorten

–Z lines move closer together

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17
Q

List the 4 steps of the Sliding Filament Mechanism.

A
  1. A bands do not shorten, but move closer together
  2. I bands shorten, but thin filaments do not
  3. Thin filaments slide toward H band
  4. H band shortens or disappears
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18
Q

H band

A

Located in the middle of the Z disc/line

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19
Q

Thick Filaments

A

Aggregates of myosin, long fibrous “tail” connected to globular “head”
–heads are hinged, sticking out

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20
Q

Thin Filaments

A

Composed of a double helixes of polymerized actin molecules

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21
Q

What are the regulatory proteins that run along F-actin helices?

A

Tropomyosin and Troponin

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22
Q

Actin Monomer

A

G-actin (blue spheres)

G = “globular”

Each has a myosin-recognition site to which an actin-binding site on the globular myosin head can bind. Under resting conditions, this site is obscured - covered up - by the tropomyosin, such that myosin cannot bind

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23
Q

Actin Polymer

A

F-actin (joined spheres)

F = “filamentous”

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24
Q

The globular head of the myosin binds ____ and splits off its terminal phosphate.

A

ATP

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25
Q

What are the 3 key features of the globular head of myosin which are critical for the mechanism of contraction?

A
  1. The tip of the head has the actin-binding site
  2. A second domain on the side of the head has an ATP-binding site, directly linked to a third domain, which has ATPase enzymatic activity
  3. The head is connected to the “tail” by a fourth domain which is a hinge, around which the entire head can pivot
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26
Q

Pivoting of the globular head is triggered by ____ ____.

A

ATP hydrolysis

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27
Q

In the resent state, myosin binding sites on actin are blocked by ____.

A

Tropomyosin

–this prevents cross bridge formation

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28
Q

What happens when calcium (Ca2+) binds to troponin?

A

Tropomyosin moves away from the myosin-binding site

This induces a conformational change in its configuration that is large enough for it to pull away from actin. As it does so, since it is firmly connected to tropomyosin, when the troponin moves away, it drags the tropomyosin away with it, thus exposing the myosin-binding site on the actin

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29
Q

What happens if Ca2+ is not present?

A

Myosin-actin interactions (crossbridges) cannot form, and no contraction is possible.

30
Q

What happens after Power Stroke?

A

ADP is released and a new ATP binds. This makes myosin release actin—and the cycle begins again, continuing until the sarcomere has shortened

31
Q

Where does Ca2+ come from?

A 
Sarcoplasmic reticulum (SR)
--major reservoir for Ca2+ storage and release
32
Q

List the 5 sequence of events at a single cross bridge (starting at end of previous contraction)

A
  1. The myosin head is bound to the binding site on actin.
  2. ATP binds to the myosin head—this triggers release from the actin (i.e. the crossbridge is dissolved)
  3. ATP is hydrolyzed to ADP—this energizes the myosin head, and it engages with the binding site on actin
  4. Release of inorganic phosphate (Pi) causes the myosin head to move, which drags the bound actin along with it.
  5. A new ATP molecule binds to the myosin head and the cycle starts again.
33
Q

Hydrolysis of bound ATP allows what?

A

Binding of head to actin and “energizes” the head (like cocking a trigger)

34
Q

Release of Pi pulls the trigger producing?

A

Powerstroke, which pulls thin filament towards the center

35
Q

Describe the SR and Ca2+ at rest, stimulation, and at the end of contraction.

A

SR is modified e.r. that stores Ca2+ when muscle is at rest

Upon stimulation, Ca2+ diffuses out of calcium release channels (ryanodine receptors)

At end of contraction, Ca2+ actively pumped back into the SR.

36
Q

What is the relevance of the extensive SR w/in a single muscle fiber?

A

This ensures that all the bundles of myofibrils can be potentially be exposed to a flood of calcium.

37
Q

What is the relevance of the proximity of the SR to the transverse (T) tubules?

A

Ensures that an action potential traveling down the tubule is quickly transduced into a signal for calcium release.

38
Q

T-Tubules

A

Extensions of cell membrane (sarcolemma) that associate w/ ends (terminal cistern) of sarcoplasmic reticulum.

39
Q

How do nerves signal to muscle?

A

Each skeletal muscle fiber requires separate stimulation by a signal from a motor neuron

The neurotransmitter released from a motor neuron is acetylcholine (ACh). When it binds to its receptor, it triggers opening of a Na+ channel (ligand-gated sodium channel). Na+ floods in, depolarizing the membrane—that local change in voltage next triggers opening of so-called voltage-gated Na+ channels, they in turn let more Na+ in and that changing voltage is propagated along the membrane (sarcolemma) and passes down into the T-tubules.

40
Q

What is the neurotransmitter released in signaling?

A

ACh
–depolarizes end-plate region of the muscle fiber

Depolarization initiates A.P. in the muscle fiber –> contraction

41
Q

Excitation-Contraction Coupling in Skeletal Muscle

A

Refers to the conversion of a nerve signal (“excitation”) into a muscle contraction. The molecule that “couples” these two processes is Ca2+.

As that propagating action potential proceeds down the T-tubule, it activates dihydropyridine (DHP) receptors (aka voltage-gated calcium channels). The ryanodine recptors are calcium release channels. When the DHP receptors are activated by an action potential, they change their conformation and that in turn, open the ryanodine receptors, allowing calcium to flow out of the s.r. into the sarcoplasm, and flood the contractile apparatus with calcium.

In a nut shell: A.P.’s conducted along T-tubules –> voltage-gated Ca2+ channels –> open Ca2+ release channels in SR –> Ca2+ stimulates contraction
–in skeletal muscle, ALL Ca2+ comes from SR!!!

42
Q

Muscle Relaxation

A

Action potentials stop; no further calcium release from s.r.

Active pumping of Ca2+ back into s.r. via SERCA pump
–(Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase; requires ATP)

43
Q

ATP is required for both inhibition and termination of contraction. Describe the 3 steps of this.

A
  1. Unbinding of myosin head from actin at the end of a contraction cycle
  2. Energization (activation) of myosin head
  3. Pumping of Ca2+ out of sarcoplasm back into s.r.
44
Q

Muscle Contraction Steps (7)

A
  1. Acetylcholine from motor neuron
  2. End plate potentials
  3. Action potentials (propagated down T-tubules)
  4. T-tubule V-gated calcium channels (DHPR) activated
  5. Opening of calcium release channels (ryanodine receptor) in s.r.
  6. Calcium released, binds to troponin.
  7. Contraction
45
Q

Muscle Relaxation Steps (5)

A
  1. Action potentials cease.
  2. Calcium release channels close
  3. Ca2+-ATPase pumps (SERCA) move Ca2+ back into SR
  4. No more Ca2+ bound to troponin C
  5. Tropomyosin blocks myosin binding sites on actin
46
Q

Contraction [of muscles] –> Tension

A

Can be studied in vitro where one end of the muscle is fixed and the other is movable

Electrical stimulations are applied, and contractions recorded and displayed as currents

47
Q

Isometric Contraction

A

If tension never overcomes the weight of the load, still generates heat

Muscle length stays same even though tension increases (no external work performed = no load movement)

48
Q

Isotonic Contraction

A

If tension is greater than load, muscle shortens, allowing it to perform the external work (e.g. moving the load)

49
Q

Force vs Velocity (F vs V) Curve

A

For muscles to contract: F(muscles) greater than F(load)

As F(load) increases –> V(shortening) decreases

50
Q

Muscle Twitch and Summation

A

Single action potential generated by a motor neuron stimulates an all-or-none twitch of a muscle fiber
–single muscle twitch generated

Latent period:
–time between stimulus and contraction (Ca2+ release –> binding to troponin –> cross bridge formation)

If second stimulus occurs before the muscle completely relaxes from first twitch, second twitch will summate the first one.

Reason: Ca2+ from first twitch has not all been taken back up by SR, so it adds to the total Ca2+ released by second stimulation

51
Q

Tetany

A

As the frequency of stimulations increases, it will increase the tension up to a peak plateau, beyond which the muscle is able to respond any further
–muscle stuck in a contraction

52
Q

Length-Tension Relationship

A

Maximum tension generated when muscle is 100-120% of its resting length – above that range and tension decreases (due to fewer interactions between myosin and actin) – below that range and tension decreases (due to fiber getting shorter and thicker, generating increased fluid pressure, increased distance between actin and myosin)

Under normal conditions this optimum state is maintained by NEURAL REFLEXES

53
Q

Whole Muscle

A

Individual muscle fibers respond in an all-or-none fashion. Yet our muscles are capable of smooth, graded movements, allowing variations in effort and fine motor control

54
Q

Motor Unit

A

One motor neuron + all the muscle fibers it innervates. A muscle may have many motor units of different types

  • -(“a family”)
  • -one neuron does NOT innervate the entire muscle
  • -this is how all-or-none twitches of single muscle fibers are integrated into smooth, graded movements of a whole muscle
  • -strength of contraction = number of motor units recruited
55
Q

Single Motor Unit

A

Single motor neuron makes synaptic contract w/ a number of muscle fibers - this is the basic unit of motor organization

The number varies from one muscle to another and from one motor neuron to another
–e.g. a single motor neuron may contact 10-20 muscles fibers or more than 1,000

However a single muscle fiber normally receives synaptic input from only one motor neuron

When a motor neuron fires, all the muscle cells in that neuron’s motor unit will contract together - fundamental unit of contraction of the whole muscle is not the contraction of a single muscle fiber, but the contraction produced by all the muscle cells in a motor unit

56
Q

Gradation in the overall strength with which a particular muscle contracts is under control of what system?

A

Nervous system

57
Q

Increasing motor units activated…

A

By variation in total number of motor neurons activated (and hence, the total number of motor units contracting)
–as increasing number of motor units activated –> increasing strength of contraction

58
Q

As action potential frequency increases…

A

By variation in the frequency of action potentials in the motor neuron of a single motor unit
–as increasing rate of firing w/in a motor unit –> increasing strength of contraction [up to the point of tetany]

59
Q

Fine Muscle Control

A

Fine muscle control requires smaller motor units (fewer muscle fibers per motor neuron)

  • -eye muscles: ~20 muscle fibers/motor unit
  • -larger, stronger muscles have have 1,000s of myofibers/motor units

Thus, control vs strength are tradeoffs

60
Q

Muscle Strength (i.e. strength of contraction) is determined by?

A
  1. Frequency of stimulation
  2. Thickness of each muscle fiber (e.g. via strength training - protein synthesis of contractile/regulatory components for new myofibrils)
  3. Initial length of fiber at rest
  4. Number of fibers recruited to contract (concept of the motor unit)
    - -more units required to lift arm quickly versus lifting it slowly
61
Q

Twitch Muscles

A

Time delay between muscle fibers action potential and peak muscle tension varies across muscle fibers

62
Q

Slow-Twitch Fibers

A

Steady contractions, e.g. for standing upright (postural muscles) - rich capillary supply, more mitochondria (high oxidative capacity), more myoglobin (aka red fibers)

  • -more active aerobically
  • -use these primarily w/ low/moderate exercise
  • -longer lasting
63
Q

Fast-Twitch Fibers

A

Rapid contraction (e.g. running, jumping); fastest are ocular muscles (control eye movements) - fatigue faster, fewer capillaries, fewer mitochondria (lower oxidative capacity), less myoglobin (aka white fibers), have more glycogen stores

  • -more active anaerobically
  • -much faster return to baseline
64
Q

Where does ATP for contraction come from?

A

Energy Stores:

  1. Ready reserve (phosphagens)
    - -pools in muscle cells, constantly replenished
    - -store phosphate in creatine forming phosphocreatine
    - -only lasts a few seconds
  2. Long-term
    - -glycogen, triacylglycerol, protein
    - -lasts minutes to months
65
Q

Muscle At Rest

A

ATP from metabolism + creatine – (add kinase) –> ADP + phosphocreatine

66
Q

Working Muscles

A

Phosphocreatine + ADP — (add kinase) –> creatine + ATP

67
Q

Phosphocreatine

A

Resting muscle stores energy from ATP in the high-energy bonds of phosphocreatine. Working muscle then uses that stored energy.

68
Q

ATP is needed for?

A

Myosin ATPase (contraction

Ca2+-ATPase (relaxation)

Na+-K+-ATPase (restores ions that cross cell membrane during action potential to their original compartments)

69
Q

Sources of energy for muscle during exercise?

A

Sources of energy for muscle contraction depends on:

  1. duration
  2. intensity or effort
70
Q

Effects of Duration

A
  1. Use up phosphagen supplies (if greater than 10 seconds)
  2. Glycolysis (substrate-level ATP generation from small glucose pools, glycogen)
  3. Longer-term stores (start w/ glycogen, shift to fatty acids - hours)
71
Q

“Crossover” effect from fat to CHO during exercise

A

Lactate threshold (exercise intensity at which the blood concentration of lactate and/or arctic acid begins to exponentially increase):

  • going at a higher intensity:
  • -switches to using glucose –> too much = less glucose for the brain
  • -going at a lower intensity for longer period: using fat stores
72
Q

Which fuel creates the most energy?

A

FA oxidation: 20.4
Glucose oxidation: 30.0
Glucose fermentation: 60.0
P-creatine/ATP hydrolysis: 96-360

Physiology (MPP 3202) (32 decks)

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