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M2M Unit 4 Vomit > Do you even lift bro? > Flashcards

Do you even lift bro? Flashcards

1
Q

3 classes of muscles

A

skeletal
cardiac
smooth

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2
Q

Functions of intercalated disc in CARDIAC muscle

A
  1. physically ties adjacent cells together = don’t pull apart when contracting
  2. contains jap junctions for transmission of electrical current from one cell to the next (simultaneous contraction)
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3
Q

Sarcomere structure

A

Sarcomere: basic unit of contraction

Oh so fun!

  1. 2 vertical lines: Z lines
  2. actin thin filaments grow out from Z lines
  3. 1 central vertical line between Z’s: M line
  4. Myosin thick filaments grow out from M lines.

Tada!

Now line up a bunch of these bad boys n you git a myofibril

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4
Q

Muscle fiber (myofiber)

  • made from what?
  • what is it?
A

myofilaments –> sarcomere –> myofibril –> MUSCLE FIBER
(–> muscle fascicle –> skeletal muscle)

muscle fiber = single skeletal muscle cell

bundles upon bundles of contractile filaments!

  • long cylindrical cell
  • skeletal muscle cell
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5
Q

Sarcomere structure: how do they serve in skeletal muscle contraction?

A

Actin Thin filaments
-actin with tropomyosin bound,
and troponin bound to end tropomyosin

Myosin Thick filaments
-myosin chains that have big globular heads interact with actin
.

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6
Q

Myofilament

A

polymerized stand made of myosin thick filaments or actin thin filaments (with tropomyosin/troponin)

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7
Q

Myofibril

A

bunch of sarcomeres (bundles of myofilaments) placed end to end

Bunch of myofibrils make a muscle fiber (muscle cell) covered with own network of sarcoplasmic reticulum

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8
Q

How are connections of muscle contractile proteins made to surrounding CT?

A

Complex of proteins that span PM and bind to ECM molecules:

Dystrophin: connects actin to surface membrane
- (links cytoskeleton with ECM)

Titin: links myosin to Z line
- (centering thick filaments)

Nebulin: organizes actin

Alpha-actinin: crosslinks actin fibers

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9
Q

How do connections of muscle contractile proteins contribute to contractile force/movement?

A

Because a shit load of filaments are attached (thanx to contractile protein complex) there is now a passive tension in muscle fibers

-Ie: passive muscle balance when sitting

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10
Q

Where do motor nerve terminals associate with skeletal muscle fibers????

A

Motor nerve terminals (synapses) are located at center of skeletal muscle fiber.

The AP will propagate in both directions from there

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11
Q

What makes up a motor unit?

Why is this important?

A

Each muscle is innervated by group of motor neurons.

Motor unit: single motor neuron + single muscle
Each motor neuron innervates only one muscle (including all muscle fibers in that muscle)

Motor unit contract in unison

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12
Q

What is the distribution of cells innervated by one motor neuron in a muscle?

A

Distribution of innervated cells vary greatly depending on particular neuron, muscle, or even parts of a muscle.

  • Fine movements: have smaller motor units (not many muscle fibers 3…10…)
  • Gross movements: large motor units (hundreds of muscle fibers)
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13
Q

What allows for fine control of muscle movement?

A

During voluntary movement:

  1. Small motor units are recruited first.
  2. Progressively, larger motor units are recruited.
  3. Strength of contraction is increased.

= fine control

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14
Q

Physiological and biochemical basis of skeletal muscle contraction (8 freaking steps)

A
  1. Actin is bound to tropomyosin, which is bound to troponin
  2. Influx of intracellular Ca2+ binds to troponin
  3. Bound troponin changes conformation of tropomyosin
  4. Tropomyosin exposes binding site on actin filaments
  5. The sneaky hoe myosin gives head (binds) to actin and like a “compressed spring” is released during binding
  6. Sarcomere shortens by 10 nm
  7. ATP binds myosin, releasing acting
  8. ATP is hydrolyzed, and again, pre-loads myosin “spring”
  9. Repeat until Ca2+ or ATP supply runs out
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15
Q

What are regulatory proteins in muscle contraction?
Where are they located?
How do they respond to changes in {Ca2+]?

A

Regulatory proteins: Tropomyosin + Troponin

Tropomyosin sits on actin and covers the myosin binding sites
Troponin sits at end of tropomyosin and binds Ca2+

As intracellular free calcium rises –> BAM! It binds, muscle contraction starts.

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16
Q

Starting with AP, describe process of a single contraction/relaxation (a twitch)

A
  1. AP in motor neuron –> propagates
  2. AP causes ACh release at synapse
  3. ACh binds to ACh rcptrs in muscle fiber, opening ion channels in muscle fiber n causing depolarization (muscular AP)
  4. AP propagats down fiber
  5. AP goes down into t-tubules
  6. DHP receptors at ends of t-tubules sense voltage change and open RyR channels in SR
    - -> Releases Ca2+ into muscle cytosol
  7. Ca2+ binds troponin, causing tropomyosin to move off acting, myosin head binds and contract
  8. Ca2+ and ATP drive contraction as long as signal continues and Ca2+ and ATP are present
  9. Ca2+ pumps (using ATP) move Ca2+ back into SR, troponin releases Ca2+, tropomyosin rebinds to actin

Muscle relaxes

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17
Q

the transverse-tubule system (t-system) in skeletal and cardiac muscle

A

You need a way to get membrane surface signal (AP) to center of muscle fiber.

Muscle fiber diameter are too wide so calcium diffusion from surface membrane to center of muscle fiber is too slow that contraction won’t be uniform.

T-Tubules to the rescue! Set of membranes extensively branched inside muscle fiber at regular intervals.
AP will propagate on the surface p membrane into t tubule and carry electrical signals down into depths of muscle fiber.

When AP reaches T tubule, it can trigger release of Ca2+ and cause uniform contraction

Depolarization propagates into t-tubule system –> receptors in SR

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18
Q

Explain excitation-contraction coupling (E-C) in skeletal muscle

A
  • AP propagates down membrane, and continues down t-tubule.
  • As voltage gets to end of t-tubule, it runs into DHP V-G receptor,
  • DHPR binds to RyR channels causing it to open and Ca2+ will flow out into cytoplasm of muscle cell = contraction.
19
Q

Explain excitation-contraction coupling (E-C) in cardiac muscle???

A

Similar to skeletal (uses t-tubule) but:

Difference:
-instead of DHPR channel, you have cardiac Ca2+ release channels that release some Ca2+
- this Ca2+ binds the RyR
(2channels don’t touch eachother like in skeletal m)
- RyR opens releases Ca2+

20
Q

Explain excitation-contraction coupling (E-C) in smoothmuscle

A

Different from skeletal/cardiac: don’t need t-tubules at all

SM is thin and small, Ca2+ released at cell surface can diffuse through whole cell.

Very complex. Don’t bother.

21
Q

What grades skeletal muscle strength?

A
  1. motor neuron recruitment

2. action potential frequency

22
Q

What signals do exercising muscle provide to other cells?

A

Activation of

  1. satellite cells
  2. adipose tissue
23
Q

What is the difference between a myofiber and a myocyte?

A

myofiber = skeletal muscle cell

myocyte = cardiac muscle cell

24
Q

2 major mechanism for how cardiac and smooth muscle tension is graded/regulated

A
  1. cell length (length tension)

2. nt/hormone receptor activity

25
Q

2 major mechanism for how skeletal muscle tension is graded/regulated

A
  1. frequency of AP
  2. # of motor units recruited

(doesn’t change length since its anchored)

26
Q

What is the basis of muscle fatigue (in skeletal muscles)?

A

Impairment at any of 4 points

  1. AP propagation potential into t-tubule
  2. Release of Ca2+ from SR
  3. Effect of Ca2+ on the myofilament interaction
  4. Force generation by the myofilaments
27
Q

How can impairment of AP cause muscle fatigue?

A

At high frequency stimulations, K+ builds up and Na+ is reduced in t-tubule network.

–> Reduction in AP amplitude or AP failure in inner part of t system

= outer part of fiber contracts, but not center

28
Q

Impairment of metabolic changes that cause muscle fatigue (steps 2-4)

A

Pi build up (from ATP hydrolysis)
Decrease in pH: (from H+ build up)

(2) Inhibits release of Ca2+ from SR
(3) Inhibits binding of Ca2+ to troponin
(4) Reduce contractile force of myosin-actin binding

29
Q

How does skeletal muscle use ATP during force generation?

A

It burns 2 ATPs to contract

  • It uses 1 ATP for each myosin-actin cycle
  • It uses 1 ATP for each Ca2+ ion pumped back into SR

(But ATP levels change very little bc of phosphocreatine)

30
Q

Length of sarcomere in:

  • resting muscle
  • contractile muscle
  • stretched muscle
A
  • resting muscle: 2.4 um
  • contractile muscle: 2.4 um
  • stretched muscle (to point of tearing): 3.6 um

more overlap with actin+myosin you have, the more tension you have for force generation.

31
Q

Describe the molecular basis of skeletal muscle diversity (fast and slow fibers)

A

Different skeletal muscle types have different mixes of oxidative and glycolytic energy-producing frameworks

(Fast twitch fibers, intermediate fibers, slow twich fibers)

32
Q

Fast twitch fibers

A

centered around glycolytic E production

quick burst, less sustainability

33
Q

Slow twitch fibers

A

Centered around oxidative phosphorylation to generate ATP
(postural or long distance)

-red in color bc of high myoglobin content

34
Q

Myostatin

A

Muscle growth regulator (inhibitor)

Controls the muscle mass you are genetically programmed to have

Normally more myoblasts are recruited to increase size and nuclei #.
Myostatin is made by muscles as a neg feedback mech.

35
Q

Structural/physiological differences between Cardiac muscle and skeletal muscle

A

Cardiac Skeletal
- Intercalated discs - none
- mononucleated - Multinucleated (periphery)
- cannot regenerate - Satellite Cells
damged tissue
- Gap junctions
(smooth muscle too)

36
Q

Why are smooth muscles just so damn smooth?

A
  1. No striations (sarcomeres aren’t lined up as nice)
  2. Extremely thin diameter
  3. Spindle-shaped cells
  4. Involuntary muscles (they just can help it)
37
Q

Explain contractions in smooth muscles (compared to skeletal/cardiac)

A
  1. instead of Ca2+ binding troponin as catalytic step for actin to bind to myosin, Ca2+ binds CALMODULIN
  2. Calmodulin binds CAMK
  3. CAMK phosphorylates myosin chains, allowing it to bind actin
  4. Contraction!
  5. Dephosphorylation of myosin = smooth muscle relaxes.

(slower than skeletal)

38
Q

What domains are found in Calmodulin (unit 1 refresher)

A

4 EF hands

-supplies electronegative environment for ion (Ca2+) coordination

39
Q

How does skeletal muscle develop?

A

Single cell –> multinucleate cells

  1. Satellite stem cells make new myoblast cells
  2. Myoblasts merge
  3. Get multinucleated cell
40
Q

Role of Satellite stem cells in skeletal muscle development/repair

A

They produce new skeletal muscle cells (muscle fiber)

New cells, instead of replacing the old muscle cells, they fuse with them –> bigger muscle fiber

41
Q

Physiological/structural response to exercise on skeletal muscle
(what happens when it gets damaged?)

A

Good thing our buddy satellite cells are there:
&raquo_space;Useful in exercise and repair of damaged muscle!

NOTE!
exercise does not add more muscle fibers, it increases the size of the muscle fibers you have (with fusion)

Atrophy is the opposite: reduces size of your muscle fibers

42
Q

Gap junction function in
Skeletal m:
Cardiac m:
Smooth m:

A

Skeletal m: nonexistent

Cardiac m: transmission of electrical current from one cell to the next (propagation of AP)
-Allows heart to contract synchronously!

Smooth m: synchronous contraction of gastroenteric smooth muscle (peristalsis)

43
Q

What does a “triad” in muscle consist of?

A

A t tubule sandwiched by 2 bulgy adjacent cisternae (end of SR.)

Parts of triad is linked VG sensitive Ca2+ channels
when AP reaches it, channel becomes activated.

M2M Unit 4 Vomit (9 decks)

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