Muscle Part 1 Flashcards
(79 cards)
1
Q
Compare the three types of muscles.
A
- Skeletal - striated: arranged in sarcomeres, (mostly) voluntary (somatic NS) (I.e., the diaphragm), attached to bone
- Cardiac - striated, involuntary (autonomic NS) - autorhythmicity (built-in rhythm), heart, intercalated discs
- Smooth - not striated, (mostly) involuntary, hollow organs
2
Q
What are the 4 functions of muscles?
A
- Producing body movements - integrated functioning of skeletal muscles, bones, and joints; walking & running, localized movements (holding pencil)
- 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)
- 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
- Generating heat - as muscle contracts it produces heat (thermogenesis), helps body temp regulation (shivering => involuntary)
3
Q
What are the 4 properties of muscles?
A
- Electrical excitability - respond to certain stimuli by producing action potentials (chemical: NTs or hormones; autorhythmic electrical signals: pacemaker cells)
- Contractility - contract forcefully when adequately stimulated (Contraction => tension => if tension > resistance => movement)
- Extensibility - muscle stretches without being damaged (I.e. maintaining contractility)
- Elasticity - Return to its original length & shape after contraction or extension
4
Q
What are the pathophysiological outcomes that can result from disruption of electrical excitability?
A
- Chemical
- NTs => Dx: myasthenia gravis
- Hormones => catecholamine storm (epi, norepi) => Dx: pheochromocytoma - Autorhythmic electrical signals: pacemaker cells => Patho: cardiac pacemaker
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
6
Q
What is a pathophysiological outcome relating to the extensibility function of muscles?
A
muscle strain/tear
7
Q
What is a pathophysiological outcome relating to the elasticity function of muscles?
A
Thoracic aortic aneurysm Marfan’s syndrome (connective tissue disorder)
8
Q
Describe the embryonic development of skeletal muscle fiber:
A
- Embryonic development: myoblasts/satellite cells fuse with skeletal muscle fiber => immature skeletal muscle fiber
9
Q
From largest to smallest, list the organization to a skeletal muscle fiber.
A
Skeletal muscle => fascicle => muscle fiber
10
Q
Each fascicle is surrounded by ____ => continuous with _____
A
connective tissue; TENDON
11
Q
Mature skeletal muscle fibers:
A
- Have multiple nuclei
- Contain satellite cells (myoblasts)
- Cannot undergo cell division
- Myofibrils: contractile elements
12
Q
Describe the intracellular muscle structure of a skeletal muscle fiber.
A
- Sarcolemma - plasma membrane of muscle fiber
- encloses sarcoplasm (cytoplasm), myofibrils, other organelles
- Transverse (T) tubules - invaginate from sarcolemma - 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
13
Q
Term for “muscle wasting”?
A
Muscular atrophy
14
Q
Term for “muscle weakness”/”loss of flesh”
A
sarcopenia
15
Q
In muscular atrophy, fibers decrease in size due to _______
A
progressive loss of myofibrils
16
Q
What can cause muscular atrophy (2 possibilities)?
A
- Disuse: action potentials to inactive skeletal muscles greatly reduced => reversible (I.e. bedridden individuals, people with casts)
- Denervation: nerve supply to muscle disrupted/cut (6 mos-2yrs muscle shrinks ~1/4 original size; fibers irreversibly replaced by fibrous connective tissue)
17
Q
Muscular hypertrophy - an increase in muscle fiber diameter due to ________
A
increased production of myofibrils, mitochondria, SR, and organelles
18
Q
What causes muscular hypertrophy?
A
result of forceful, repetitive muscular activity (I.e. strength training)
19
Q
The greater the number of myofibrils = ?
A
the greater the force of contractions
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
21
Q
What can cause myoglobin (Mb) circulation (MC)/rhabdomyolysis?
A
crush injury, overexertion, alcohol abuse, some medications
22
Q
What are some signs/symptoms of Mb circulation from rhabdomyolysis?
A
- muscle pain
- tea-colored urine
- renal failure sx
23
Q
What are the labs used for Mb circulation (MC)/rhabdomyolysis?
A
- urine myoglobin test (myoglobinuria)
- increase in creatine kinase
- increase in K+
- increase in creatine
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
25
What are the repeating units of a myofibril?
sarcomeres
26
1 sarcomere unit = ____ to ____
Z-disc; Z-disc
27
holds thick filaments together at center of sarcomere
M-line
28
length of thick filaments of sarcomere; dark
A-band
29
thin filaments w/o thick filaments of sarcomere; light
I-band
30
Alternating A & I bands = ______
striations
31
What are the 3 types of muscle proteins?
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)
32
______ - group of inherited muscle-destroying diseases causing progressive degeneration of skeletal muscle fibers
muscular dystrophy
33
Main component of thick filaments = ____
myosin (1 thick filament = ~300 myosin molecules)
34
Myosin functions as ____ protein; how?
motor; chemical energy (ATP) => mechanical energy
- ATP-binding sites on myosin head bind ATP till time to contract
35
main component of thin filaments =_____
actin
36
individual actin molecules = ____
G-actin (globular) molecules
37
linking of G-actin molecules to form ____
F-actin (fibrous) strands
38
1 thin filament is composed of:
- 2 F-actin strands (helix) + troponin (3 globular subunits) & tropomyosin (rod-shaped)
39
rod-shaped regulatory muscle protein; in a relaxed muscle, blocks myosin from binding due to covering myosin binding sites on actin
tropomyosin
40
regulatory muscle protein which holds tropomyosin in place
troponin
41
What do the 3 globular subunits of troponin bind to?
1. tropomyosin
2. actin
3. Ca2+
42
When does the contraction cycle begin?
myosin binding sites exposed
43
Explain sliding filament mechanism.
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
Outline the steps of the contraction cycle (4).
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
How does rigor mortis effect the contraction cycle?
- excess Ca2+, crossbridges form, but don't have excess ATP to cause release of myosin head from actin
46
What is the neuromuscular junction?
synapse between somatic motor neuron and skeletal muscle fiber
47
somatic motor neuron action potential/action potential generated at muscle membrane = ____
end plate potential (EPP)
48
How does end plate potential propagate through a muscle fiber?
in both directions away from NMJ along sarcolemma and T-tubules via continuous conduction
49
1 AP in somatic motor neurons = _____ = ______
1 AP in skeletal muscle fiber; skeletal fiber contracts
50
During a somatic motor neuron AP/end plate potential, acetylcholine is released, diffuses across synaptic cleft and binds to nicotine receptors on the ______
motor end plate = region of muscle fiber membrane opposite synaptic end bulbs
51
When is an action potential generated in skeletal muscle fiber?
when region of sarcolemma adjacent to motor end plate depolarizes to threshold by an EPP
52
What are the two phases of muscle action potential?
1. Depolarization (Na+ open)
2. Repolarization (Na+ closed, K+ open)
53
low [Ca2+] in sarcoplasm and high [Ca2+] in sarcoplasmic reticulum (SR) is indicative of:
relaxed muscle
54
What is excitation-contraction coupling?
sequence of events that links muscle action potential to muscle contraction
55
Where does excitation-contraction coupling occur?
triads (1 T-tubule and 2 terminal cisternae)
56
T-tubule and terminal cisternae are mechanically linked by what 2 groups of integral membrane proteins and what are their functions?
1. Dihydropyridine (DHP) receptors - voltage sensors
2. Ca2+ release channels - blocked by DHP receptors when T-tubule is at resting membrane potential
57
What happens to DHP receptor and Ca2+ release channels when an action potential is generated?
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
lay term for tetanus
"lockjaw"
59
What is the course of pathology of tetanus?
enters CNS => blocks release of inhibitory NTs from nerve terminals => unopposed muscle stimulation
60
What are the 3 ways skeletal muscle fibers produce ATP?
1. from creatine phosphate
2. by anaerobic glycolysis
3. by aerobic respiration
61
What is the first source of ATP during muscle contraction?; Why is it the first source?
creatine phosphate; due to the very rapid formation of ATP from creatine phosphate (Creatine + ATP <=> Creatine phosphate + ADP_
62
Which is the fastest method for skeletal muscle fibers to produce ATP?
creatine phosphate
63
Stores of creatine phosphate and ATP provide enough energy for muscles to contract maximally for _____.
~15 seconds
64
How do skeletal muscles produce ATP when muscle fiber's creatine phosphate levels are depleted?
Anaerobic glycolysis = glucose is catabolized to generate ATP
65
What are the steps to glycolysis under anaerobic conditions for skeletal muscle?
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
Compared to aerobic respiration, anaerobic glycolysis:
- produces fewer ATPs
- is faster
- can occur when oxygen levels are low
67
Anaerobic glycolysis provides enough energy for ______ of maximal muscle activity
2 minutes
68
ATP production method that can only generate ATP when sufficient oxygen is available
aerobic respiration
69
supplies enough ATP for muscles during periods of rest or light/moderate exercise
aerobic respiration
70
Aerobic respiration provides enough energy that can last from ______ to _____
several minutes; an hour or more
71
What are the 2 sources of oxygen for muscle tissue?
1. O2 that diffuses into muscle fibers from blood
2. O2 released by myoglobin within muscle fibers
72
What are the steps to aerobic respiration of skeletal muscle fibers?
Pyruvic acid from glycolysis enters mitochondria => Krebs cycle => electron transport chain
73
Compare to anaerobic glycolysis, aerobic respiration is:
1. slower
2. yields much more ATP (1 glucose = 30-32 ATP)
74
What is muscle fatigue?
inability of muscle to maintain force of contraction after prolonged activity
75
What are the reasons for muscle fatigue?
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
Oxygen consumption will _____ for a while after exercise; can recover in _____ to ____
increase; minutes to hours
77
What are the muscles experiencing initially after exercise?
oxygen debt
78
How does oxygen debt "pay back" metabolic conditions to resting levels?
1. Converting lactic acid to glycogen stores in liver
2. Resynthesizing creatine phosphate
3. replacing O2 removed from myoglobin
79
What is a better term for "oxygen debt"?
recovery oxygen intake
