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Physiology > Muscle Part 1 > Flashcards

Muscle Part 1 Flashcards

1
Q

Compare the three types of muscles.

A
  1. Skeletal - striated: arranged in sarcomeres, (mostly) voluntary (somatic NS) (I.e., the diaphragm), attached to bone
  2. Cardiac - striated, involuntary (autonomic NS) - autorhythmicity (built-in rhythm), heart, intercalated discs
  3. Smooth - not striated, (mostly) involuntary, hollow organs
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2
Q

What are the 4 functions of muscles?

A
  1. Producing body movements - integrated functioning of skeletal muscles, bones, and joints; walking & running, localized movements (holding pencil)
  2. Stabilizing body positions - skeletal muscles stabilize joints & maintain body positions; postural muscles contract continuously when awake (I.e. Sustained contractions of neck muscles hold head upright)
  3. Storing and moving substances within the body - storage by sustained contractions of sphincters; prevents outflow hollow organs contents (food: stomach; urine: bladder); cardiac muscle contractions pump blood through blood vessels
  4. Generating heat - as muscle contracts it produces heat (thermogenesis), helps body temp regulation (shivering => involuntary)
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3
Q

What are the 4 properties of muscles?

A
  1. Electrical excitability - respond to certain stimuli by producing action potentials (chemical: NTs or hormones; autorhythmic electrical signals: pacemaker cells)
  2. Contractility - contract forcefully when adequately stimulated (Contraction => tension => if tension > resistance => movement)
  3. Extensibility - muscle stretches without being damaged (I.e. maintaining contractility)
  4. Elasticity - Return to its original length & shape after contraction or extension
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4
Q

What are the pathophysiological outcomes that can result from disruption of electrical excitability?

A
  1. Chemical
    - NTs => Dx: myasthenia gravis
    - Hormones => catecholamine storm (epi, norepi) => Dx: pheochromocytoma
  2. Autorhythmic electrical signals: pacemaker cells => Patho: cardiac pacemaker
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5
Q

What is a pathophysiological outcome to the contractility function of muscles?

A

Heart failure with reduced ejection fraction (HFrEF)
- inability of heart to contract & pump blood into vasculature

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6
Q

What is a pathophysiological outcome relating to the extensibility function of muscles?

A

muscle strain/tear

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7
Q

What is a pathophysiological outcome relating to the elasticity function of muscles?

A

Thoracic aortic aneurysm Marfan’s syndrome (connective tissue disorder)

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8
Q

Describe the embryonic development of skeletal muscle fiber:

A
  1. Embryonic development: myoblasts/satellite cells fuse with skeletal muscle fiber => immature skeletal muscle fiber
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9
Q

From largest to smallest, list the organization to a skeletal muscle fiber.

A

Skeletal muscle => fascicle => muscle fiber

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10
Q

Each fascicle is surrounded by ____ => continuous with _____

A

connective tissue; TENDON

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11
Q

Mature skeletal muscle fibers:

A
  1. Have multiple nuclei
  2. Contain satellite cells (myoblasts)
  3. Cannot undergo cell division
  4. Myofibrils: contractile elements
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12
Q

Describe the intracellular muscle structure of a skeletal muscle fiber.

A
  1. Sarcolemma - plasma membrane of muscle fiber
    - encloses sarcoplasm (cytoplasm), myofibrils, other organelles
    - Transverse (T) tubules - invaginate from sarcolemma
  2. Sarcoplasmic reticulum (SR) - fluid-filled system of membranous sacs encircling each myofibril (terminal cisternae on each end)
    - Triad = 1 T-tubule + 2 terminal cisternae of SR
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13
Q

Term for “muscle wasting”?

A

Muscular atrophy

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14
Q

Term for “muscle weakness”/”loss of flesh”

A

sarcopenia

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15
Q

In muscular atrophy, fibers decrease in size due to _______

A

progressive loss of myofibrils

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16
Q

What can cause muscular atrophy (2 possibilities)?

A
  1. Disuse: action potentials to inactive skeletal muscles greatly reduced => reversible (I.e. bedridden individuals, people with casts)
  2. Denervation: nerve supply to muscle disrupted/cut (6 mos-2yrs muscle shrinks ~1/4 original size; fibers irreversibly replaced by fibrous connective tissue)
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17
Q

Muscular hypertrophy - an increase in muscle fiber diameter due to ________

A

increased production of myofibrils, mitochondria, SR, and organelles

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18
Q

What causes muscular hypertrophy?

A

result of forceful, repetitive muscular activity (I.e. strength training)

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19
Q

The greater the number of myofibrils = ?

A

the greater the force of contractions

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20
Q

What is rhabdomyolysis?

A

striated + muscle + breakdown
Syndrome resulting from breakdown of skeletal muscle fibers with leakage of muscle contents (myoglobin = Mb) into circulation

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21
Q

What can cause myoglobin (Mb) circulation (MC)/rhabdomyolysis?

A

crush injury, overexertion, alcohol abuse, some medications

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22
Q

What are some signs/symptoms of Mb circulation from rhabdomyolysis?

A
  1. muscle pain
  2. tea-colored urine
  3. renal failure sx
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23
Q

What are the labs used for Mb circulation (MC)/rhabdomyolysis?

A
  1. urine myoglobin test (myoglobinuria)
  2. increase in creatine kinase
  3. increase in K+
  4. increase in creatine
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24
Q

What is the course of Mb once it gets into circulation due to rhabdomyolysis?

A

Mb in renal glomerular filtrate precipitates => renal tubular obstruction => renal damage

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25
Q

What are the repeating units of a myofibril?

A

sarcomeres

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26
Q

1 sarcomere unit = ____ to ____

A

Z-disc; Z-disc

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27
Q

holds thick filaments together at center of sarcomere

A

M-line

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28
Q

length of thick filaments of sarcomere; dark

A

A-band

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29
Q

thin filaments w/o thick filaments of sarcomere; light

A

I-band

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30
Q

Alternating A & I bands = ______

A

striations

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31
Q

What are the 3 types of muscle proteins?

A
  1. contractile proteins - generate force during contraction (myosin and actin)
  2. regulatory proteins - switch contractions on and off (tropomyosin and troponin)
  3. structural proteins - contribute to alignment, stability, extensibility, elasticity (titin/titan (towards end of z-disc) and dystrophin (stabilizing protein)
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32
Q

______ - group of inherited muscle-destroying diseases causing progressive degeneration of skeletal muscle fibers

A

muscular dystrophy

33
Q

Main component of thick filaments = ____

A

myosin (1 thick filament = ~300 myosin molecules)

34
Q

Myosin functions as ____ protein; how?

A

motor; chemical energy (ATP) => mechanical energy
- ATP-binding sites on myosin head bind ATP till time to contract

35
Q

main component of thin filaments =_____

A

actin

36
Q

individual actin molecules = ____

A

G-actin (globular) molecules

37
Q

linking of G-actin molecules to form ____

A

F-actin (fibrous) strands

38
Q

1 thin filament is composed of:

A
  • 2 F-actin strands (helix) + troponin (3 globular subunits) & tropomyosin (rod-shaped)
39
Q

rod-shaped regulatory muscle protein; in a relaxed muscle, blocks myosin from binding due to covering myosin binding sites on actin

A

tropomyosin

40
Q

regulatory muscle protein which holds tropomyosin in place

A

troponin

41
Q

What do the 3 globular subunits of troponin bind to?

A
  1. tropomyosin
  2. actin
  3. Ca2+
42
Q

When does the contraction cycle begin?

A

myosin binding sites exposed

43
Q

Explain sliding filament mechanism.

A

Muscle contraction: thin filaments move toward M-line of each sarcomere
I-band and H-zone narrow, eventually disappear when muscle maximally contracted
A-band (thick filaments) unchanged
Z-discs come together (sarcomeres shorten)
Sarcomere shortens => muscle fiber shortens => entire muscle shortens

44
Q

Outline the steps of the contraction cycle (4).

A

Ca2+ binds to troponin and causes conformation change => moves tropomyosin to expose myosin binding sites on F-actin
1. ATP hydrolysis - myosin head hydrolyzes ATP and becomes energized (“cocked”)
2. Attachment of myosin to actin - forms crossbridge
3. Power stroke - myosin crossbridge pivots (90-45 degree angle), pulling thin filament past thick filament and toward center of the sarcomere
4. Detachment of myosin from actin - after myosin head binds ATP

45
Q

How does rigor mortis effect the contraction cycle?

A
  • excess Ca2+, crossbridges form, but don’t have excess ATP to cause release of myosin head from actin
46
Q

What is the neuromuscular junction?

A

synapse between somatic motor neuron and skeletal muscle fiber

47
Q

somatic motor neuron action potential/action potential generated at muscle membrane = ____

A

end plate potential (EPP)

48
Q

How does end plate potential propagate through a muscle fiber?

A

in both directions away from NMJ along sarcolemma and T-tubules via continuous conduction

49
Q

1 AP in somatic motor neurons = _____ = ______

A

1 AP in skeletal muscle fiber; skeletal fiber contracts

50
Q

During a somatic motor neuron AP/end plate potential, acetylcholine is released, diffuses across synaptic cleft and binds to nicotine receptors on the ______

A

motor end plate = region of muscle fiber membrane opposite synaptic end bulbs

51
Q

When is an action potential generated in skeletal muscle fiber?

A

when region of sarcolemma adjacent to motor end plate depolarizes to threshold by an EPP

52
Q

What are the two phases of muscle action potential?

A
  1. Depolarization (Na+ open)
  2. Repolarization (Na+ closed, K+ open)
53
Q

low [Ca2+] in sarcoplasm and high [Ca2+] in sarcoplasmic reticulum (SR) is indicative of:

A

relaxed muscle

54
Q

What is excitation-contraction coupling?

A

sequence of events that links muscle action potential to muscle contraction

55
Q

Where does excitation-contraction coupling occur?

A

triads (1 T-tubule and 2 terminal cisternae)

56
Q

T-tubule and terminal cisternae are mechanically linked by what 2 groups of integral membrane proteins and what are their functions?

A
  1. Dihydropyridine (DHP) receptors - voltage sensors
  2. Ca2+ release channels - blocked by DHP receptors when T-tubule is at resting membrane potential
57
Q

What happens to DHP receptor and Ca2+ release channels when an action potential is generated?

A
  1. DHPR senses AP, undergoes conformational change (unstops Ca release channels)
  2. Ca2+ release channels open and Ca2+ released into sarcoplasm
  3. Ca2+ binds to troponin => conformational change => tropomyosin moves away from binding sites on actin => crossbridges form => contraction cycle
58
Q

lay term for tetanus

A

“lockjaw”

59
Q

What is the course of pathology of tetanus?

A

enters CNS => blocks release of inhibitory NTs from nerve terminals => unopposed muscle stimulation

60
Q

What are the 3 ways skeletal muscle fibers produce ATP?

A
  1. from creatine phosphate
  2. by anaerobic glycolysis
  3. by aerobic respiration
61
Q

What is the first source of ATP during muscle contraction?; Why is it the first source?

A

creatine phosphate; due to the very rapid formation of ATP from creatine phosphate (Creatine + ATP <=> Creatine phosphate + ADP_

62
Q

Which is the fastest method for skeletal muscle fibers to produce ATP?

A

creatine phosphate

63
Q

Stores of creatine phosphate and ATP provide enough energy for muscles to contract maximally for _____.

A

~15 seconds

64
Q

How do skeletal muscles produce ATP when muscle fiber’s creatine phosphate levels are depleted?

A

Anaerobic glycolysis = glucose is catabolized to generate ATP

65
Q

What are the steps to glycolysis under anaerobic conditions for skeletal muscle?

A

Glucose from blood or from breakdown of glycogen undergoes glycolysis: 1 glucose => 2 pyruvic acid molecules => 2 lactic acid molecules => 2 ATP
- most lactic acid diffuses out of skeletal muscle fiber into blood
- if produced rapidly, accumulates in muscle fibers & bloodstream (Sepsis)

66
Q

Compared to aerobic respiration, anaerobic glycolysis:

A
  • produces fewer ATPs
  • is faster
  • can occur when oxygen levels are low
67
Q

Anaerobic glycolysis provides enough energy for ______ of maximal muscle activity

A

2 minutes

68
Q

ATP production method that can only generate ATP when sufficient oxygen is available

A

aerobic respiration

69
Q

supplies enough ATP for muscles during periods of rest or light/moderate exercise

A

aerobic respiration

70
Q

Aerobic respiration provides enough energy that can last from ______ to _____

A

several minutes; an hour or more

71
Q

What are the 2 sources of oxygen for muscle tissue?

A
  1. O2 that diffuses into muscle fibers from blood
  2. O2 released by myoglobin within muscle fibers
72
Q

What are the steps to aerobic respiration of skeletal muscle fibers?

A

Pyruvic acid from glycolysis enters mitochondria => Krebs cycle => electron transport chain

73
Q

Compare to anaerobic glycolysis, aerobic respiration is:

A
  1. slower
  2. yields much more ATP (1 glucose = 30-32 ATP)
74
Q

What is muscle fatigue?

A

inability of muscle to maintain force of contraction after prolonged activity

75
Q

What are the reasons for muscle fatigue?

A
  1. Central fatigue - associated with the CNS; mechanism unclear (protective?)
  2. Muscle fatigue - energy availability (depletion of creatine phosphate); inadequate release of Ca2+ ions from SR; oxygen, glycogen, and ACh depletion; lactic acid buildup
76
Q

Oxygen consumption will _____ for a while after exercise; can recover in _____ to ____

A

increase; minutes to hours

77
Q

What are the muscles experiencing initially after exercise?

A

oxygen debt

78
Q

How does oxygen debt “pay back” metabolic conditions to resting levels?

A
  1. Converting lactic acid to glycogen stores in liver
  2. Resynthesizing creatine phosphate
  3. replacing O2 removed from myoglobin
79
Q

What is a better term for “oxygen debt”?

A

recovery oxygen intake

Physiology (8 decks)

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