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Physiology and Pharmacology > Lecture 17 > Flashcards

Lecture 17 Flashcards

1
Q

What are functions of skeletal muscles?

A

Produce movement of body parts: simple motion or coordinated movement
Support soft tissues: support the weight and shield visceral organs
Maintain posture and body positions: allows standing position
Communication: speech, expression, and writing
Control of openings and passageways: voluntary control of movements of digestive and urinary tracts
Maintain body temperature: heat released through muscle contraction participants in control of body temperature

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2
Q

What are universal characteristics of muscles?

A

Responsiveness (excitability)
- capable of response to chemical signals, stretch or other signals and responding with electrical charges across the plasma membrane
Conductivity
- local electrical charge triggers a wave of excitation that travels along the muscle fiber
Contractility
- shortens when stimulated
Extensibility
- capable of being stretched
Elasticity
- returns to its original resting length after being stretched

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3
Q

How are the myofibril structure surrounded by connective tissues?

A

Also present in bundles of cells and surrounding muscle fibers

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4
Q

What is epimysium and perimysium?

A

Blood vessels and nerves bring nutrients and electrical activity needed for contraction
Some muscles have cells 50-60cm but some are about 5cm

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5
Q

How do myoblasts fuse to form skeletal muscle fibers?

A 
Plasma membrane (sarcolemma) from invaginations contribute to propagation of nerve signal to cell contractile units
Sarcolemma is rich in glycogen and packed with bundles of proteins that organize into myofibrils
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6
Q

What do myofibrils contain repeated units of?

A

Sarcomeres (functional unit)

  • Many composed of thick and thin filaments
  • Thick filaments lie in center while thin overlap between two sarcomeres
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7
Q

What is the Dark band?

A

Situated in center

Mainly composed of thick filament

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8
Q

What is Light band?

A

Mainly composed of thin filament

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9
Q

What are Z-lines?

A

Show one sarcomere

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10
Q

What is contraction?

A

Sliding of thick and thin filaments

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11
Q

How many myosin heads do thick filaments contain?

A

300

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12
Q

How often does each head cycle?

A

5 times/s

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13
Q

What is the thick filament mainly made of?

A

Myosin

- one domain is a myosin head (globular) and the myosin chain (rod)

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14
Q

How are thick and thin filaments organized?

A

In opposite directions

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15
Q

Where do proteins anchor onto?

A

Filaments and Z-line:

made of 15 000 amino acids

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16
Q

What do the spring-like structures?

A

Allows whole filament to stretch and recoil

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17
Q

What is protein essential for?

A

Extensibility and elasticity

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18
Q

What is thin filament mainly made of?

A

Actin

Very stable in length and state

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19
Q

Why is the Z-disc anchored to CapZ and tropomodulin?

A

Maintains uniformity across sarcomere, the length of filament

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20
Q

What does nebulin act as?

A

molecular ruler (repeat units contain binding sites for the actin): set actual length of actin

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21
Q

What is actin partly associated with?

A

troponin and tropomyosin

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22
Q

Why do myosin heads can bind to filaments of actin?

A

Operating movement that pulls filament of actin towards them in opposite directions - contraction

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23
Q

What are the steps of myosin heads binding to filaments of actin?

A
  1. Myosin rod and head attached to specific binding site on actin filament
  2. Myosin head needs to detach from binding site (ATP onto myosin head)
  3. ATP - ADP + Pi: ADP remains bound to hinge region
  4. Myosin head comes back to resting protein
  5. Myosin head moves to another binding site
  6. Pi released changes conformation at level of hinge, allowing thin filament to slide past thick filament. 300 heads simultaneously carrying out sliding at fast speed
    - very powerful and rapid contraction
24
Q

How is contraction initiated?

A
  1. Electrical signal from motoneuron to skeletal muscle
  2. At the neuromuscular junction, depolarization of membrane is triggered, activating voltage-gated Ca channels. This increases intracellular Ca then initiates release of neurotransmitter
  3. ACh will bind to receptors at postsynaptic membrane which triggers entry of Na then causes depolarization of sarcolemma. This initiates voltage-gated Ca channels so Ca is released at sarcoplasmic reticulum
  4. Ca finds its way to troponin
  5. TroponinC is capable of binding to Ca which triggers a change of conformation between complex of troponin and tropomyosin
    - masking of myosin head binding site
  6. Troponin and tropomyosin prevent myosin head from binding
    - electrical signal
    - binds
    - initiates contraction (need to have mechanism to end)
25
Q

What is the function of AChE in contraction?

A

AChE will degrade ACh causing repolarization of membrane, no longer released from sarcoplasmic reticulum

26
Q

What is critical in muscle contraction?

A

neuromuscular junction

27
Q

What is a toxin that affects Na channels?

A

Tetrodotoxin

28
Q

What is a toxin that affects Ca channels?

A

w-conotoxin

29
Q

What is a toxin that affects K channels?

A

Dendrotoxin (from Mamba snake)

30
Q

What are toxins that affects ACh release?

A 
Tetanus toxin (tetanus; lockjaw)
Botulinum toxin (botulism)
31
Q

What is a toxin that affects AChR channel?

A

d-tubucurarine (curare)

32
Q

What is the most common cause of food poisoning?

A

Botulinum toxin (botulism)

33
Q

What bacteria does the botulinum toxin originate from?

A

Clostridium botulinum (botulus: sausage)

34
Q

What symptoms do Botulinum toxin cause?

A

Muscle weakness; paralysis leading to death

35
Q

How does the botulinum toxin act on ACh release?

A

Endoproteinase that cleave proteins required for exocytosis of ACh in autonomic nervous system

36
Q

What are the symptoms at different stages?

A

1st: dry mouth, double vision
2nd: gastrointestinal (diarrhea, vomiting)
3rd: Paralysis of limbs, respiratory muscles
- strives and preserves and salamis
- released pores which are highly resistant to high temperatures and low oxygen conditions, each bacteria strain releases different toxin types

37
Q

What is essential for exocytosis?

A

synaptogamine

38
Q

What are the clinical uses of botulinum toxins?

A

Treatment of strabismus (cross-eyedness) by injection into peri-ocular muscles
Blepharospasm (uncontrolled eyelid movements)
Cosmetic treatments (Botox: ToxinA)
- removes wrinkles by causing slight paralysis in muscles in skin

39
Q

Are all muscles equivalent in their energy consumption?

A

Slow fibers: metabolically economical

Fast fibers: metabolically expensive

40
Q

How do the different muscle fibers act against fatigue?

A

Slow oxidative: resistant
Fast oxidative: resistant
Fast glycolytic: fatiguable

41
Q

What are the colors in the different muscle fibers?

A

Slow oxidative: red
Fast oxidative: red
Fast glycolytic: white

42
Q

What are the different metabolisms for different muscle fibers?

A

Slow oxidative: oxidative
Fast oxidative: oxidative
Fast glycolytic: glycolytic

43
Q

What are the different glycogen contents of different muscle fibers?

A

Slow oxidative: low
Fast oxidative: abundant
Fast glycolytic: high

44
Q

What are the differences in ATP synthesis in different muscle fibers?

A

Slow oxidative: aerobic
Fast oxidative: aerobic
Fast glycolytic: anaerobic

45
Q

What are the different levels of mitochondria in different muscle fibers?

A

Slow oxidative: high
Fast oxidative: higher
Fast glycolytic: fewer

46
Q

Where are the different muscle fibers located?

A

Slow oxidative: soleus
Fast oxidative: gastrocnemius
Fast glycolytic: biceps, brachii

47
Q

What are the differences between slow and fast fibers_

A

Slow fibers are half the diameter of fast fibers take longer to contract after nerve stimulation
Fast fibers take 10 msec or less to contract

48
Q

What are the aerobic conditions of muscle metabolism?

A 
Cells generate ATP through aerobic metabolism in mitochondria or through glycolysis (anaerobic) in the cytoplasm
Aerobic metabolism (moderate activity, slow fibers)
49
Q

What is aerobic exercise?

A

Typically is a sustained, low level exercise (jogging, distance swimming)
Stimulation of slow fibers
Converstion from fast glycolytic to fast oxidative
Increased fatigue resistance, blood capillaries (no change in muscle strength)

50
Q

What are the anaerobic conditions of muscle metabolism?

A

Glycolytic metabolism (peak activity, fast fibers)

  • advantage: produces ATP in absence of oxygen
  • disadvantage: ATP yield is low and toxic products are generated
  • can have lactic acid reabsorbed into the bloodstream, converted back into oxygen
51
Q

How is creatine transported into the muscles?

A

Creatine is ingested from the diet and transported to muscles via bloodstream

52
Q

What is creatine present is muscles are?

A

95% of creatine is present as:
P-creatine (60%)
Creatine (40%)

53
Q

What is the enzyme that catalyses the synthesis and degradation of P-creatine?

A

creatine kinase

- has cytoplasmic and mitochondrial isoforms

54
Q

What does creatine provide?

A

readily source of energy in the first minutes of intense exercise

55
Q

How is creatine recycled?

A

Recycled into P-creatine into mitochondria at rest

56
Q

What does creatine do?

A

Stores energy within muscles
Allows rapid release of ATP in first few minutes of stimulation of fast fibers
Activate creatine kinase
Anaerobic exercise produces boost of energy which is why fast fibers have rapid response
Mitochondria rebind ATP which is transported back to sarcoplasm
No change in muscle fiber type but can cause hypertrophy (enlargement of muscle fibers)

57
Q

How does fatigue occur?

A

Muscle fatigue is the progressive weakness of muscle contraction until no response. It takes place when:

  • ATP synthesis decreases due to shortage of glycogen (aerobic conditions)
  • Lactic acid levels rise and lower the pH of sarcoplasm, which prevents normal functioning of muscles (anaerobic conditions)
  • failure from motorneurons (production of ATP due to reduced availability of Ca)

Physiology and Pharmacology (27 decks)

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