12_Ctb 1.6 Skeletal Muscle

Front 1

What are the four basic tissues?

Back 1

Muscle, CT, Epithelium and Nerve

Front 2

Skeletal muscle is composed primarily of three types of cells, including:

Back 2

1. Skeletal Myocytes
2. Endothelial Cells (vascular)
3. CT

Front 3

What is the hierarchical order of skeletal muscle?

Back 3

1. Muscle
2. Fascicles
3. Skeletal Fibers (Myocytes)
4. Myfibrils
5. Myofilaments

Front 4

Is Sk m mono- or multi-nucleated?

Back 4

Multinucleated

Front 5

What is the name of the CT that surrounds gross muscles? What surrounds fascicles? What surrounds myofibers?

Back 5

1. Epimysium
2. Perimysium
3. Endomysium

Front 6

Myofibers (individual muscles cells) are wrapped in this CT. Since it is close to the cell, what is this CT tissue continuous with?

Back 6

1. Endomysium
2. Continuous with the basal lamina

Front 7

What demarcates the sarcomere? What protein does it contain?

Back 7

The Z-lines. Alpha actinin

Front 8

What is the plasma membrane of a sarcomere called?

Back 8

Sarcolemma

Front 9

Draw a sarcommere and include the A band, I Band, H band, M-line and the Z line.

Back 9

See p 55 of notes

Front 10

What enzyme is included in the M-line?

Back 10

MM-CK (MM-creatine kinase) for quick production of ATP

Front 11

What are the three major thin filament proteins?

Back 11

1. Actin
2. Troponin (3 isoforms, )
3. Tropomyosin

Front 12

In skeletal muscles, what allows depolarization waves to enter deep into the myofibers?

Back 12

Transverse tubules (T-tubules)

Front 13

In skeletal muscle, where is and what makes up a triad?

Back 13

At the A-I junction. Two SR membranes plus one T-tubule

Front 14

Striated muscles contract via a process called Excitation-Contraction coupling. Describe what happens in the Excitation phase.

Back 14

1. Acetylcholine binds to ACh receptors causing depolarization
2. Depolarization travels thru T-tubles and reaches SR via the Triad
3. SR releases Ca2+

Front 15

Describe what happens in the Contraction phase:

Back 15

1. Ca2++ binds troponin C --> tropomyosin moves, exposing active site
2. Cross-bridge (loaded with cleaved ADP and P) bind active site
3. Binding causes power stroke and contraction.

Front 16

What causes malignant hyperthermia?

Back 16

1. Autosomal dominant mutation of RYR (ryanodine receptor) in the SR membrane dysregulates Ca++ transport
2. This causes persistant muscle contraction and a life-threatening increase in body temp for pts under anesthesia.

Front 17

DONT FORGET: He put up new lecture notes on ANGEL

Back 17

DONT FORGET: He put up new lecture notes on ANGEL

Front 18

What causes Rigor Mortis?

Back 18

Adding ATP to a cross bridge is what causes it to release from actin. When a person dies, enough Ca enters cytoplasm of a sacromere bc the ATP driven Ca channel that keeps Ca in the SR is dysregulated. Ca is free to travel down its concentration gradient, causing muscle contraction. However, since there is no new generation of ATP, the muscle stays contracted until structural degradation occurs.

Front 19

If a pt was discovered to have the mutant ryanodine receptor mutation that causes malignant hyperthermia under anesthesia, how might they be treated?

Back 19

They could be treated with Dantrolene - a muscle relaxant that inhibits Ca release through the RYR channel.

Front 20

See p54 for lowdown on hierarchy. What surrounds a microfibril?

Back 20

Sarcoplasmic reticulum, 6 thin filaments, Triad

Front 21

What are the four energy sources used by skeletal m?

Back 21

1. Glycogen
2. ATP
3. Creatine phosphate
4. Fatty acid

Front 22

What is the difference between Type I and Type II muscle fibers?

Back 22

1. Type I: Red bc enriched in mitochondria and myoglobin for FA oxidation and oxidative metabolism to support continuous contraction AKA Slow Twitch fibers
2. Type II fibers: Fast twitch fibers with less myoglobin and modified for rapid, discontinuous contraction. They are primarily glycolytic or mixed oxidative/glycolytic.

Front 23

Sprinters typically have Type I or Type II muscle fibers? Marathon runners?

Back 23

Type II = sprinters; Type I = marathon runners

Front 24

Between what structures in skeletal muscle do stem cells reside? What is this area called?

Back 24

Between sarcolemma and basal lamina. The area is called the Cell Niche.

Front 25

1. Skeletal stem cells (aka satellite cells, skeletal myoblasts) rest in what phase of the cell cycle?
2. What triggers it to re-enter the cell cycle in G1?

Back 25

1. Resting in Go phase
2. Damage to the basal lamina releases Growth Factors that signals stem cells to re-enter cell cycle.

Front 26

Muscle stem cells are usually inhibited from growth by this GF:

Back 26

MyoSTATin (myoSTOPin)

Front 27

Describe how stem cells grow once they are stimulated to enter G1/cell cycle:

Back 27

1. They expand
2. The cells irreversibly withdraw from cell-cycle and fuse together
3. Form multinuclear muscle cells called "myotubes"
4. Myotubes undergo differentiation - capable of regenerating entire muscles.

Front 28

What is the underlying molecular cause of Duchenne Muscular Dystrophy?

Back 28

A mutated gene for dystrophin that stabilizes the myocyte cytoskeleton. Without it, the sarcolemma breaks down and dies.

Front 29

How long does it take to make new skeletal muscle cell after one is damaged?

Back 29

21 days

Front 30

Prednisone and Gentamicin are current best treatments for DMD. How do they work?

Back 30

DMD mutations are typically premature stop codons. Prednsone and Gentamicin enable translational read-through of the stop codons.

Front 31

What does Dystrophin doe in the cell?

Back 31

It serves as a structural anchor for many proteins.

Front 32

Why is dystrophin so commonly mutated?

Back 32

Bc it's HUGE 2.6 million bp (ave is 12,000 bp).