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PHSI 208 > Skeletal muscles > Flashcards

Skeletal muscles Flashcards

1
Q

Sk muscles are primarily innervated by the somatic NS

A

ya

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2
Q

where is the origin of a sk muscle?

A

closest to the trunk (centre of the body) or the more stationary bone

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3
Q

where is the insertion of a sk muscle?

A

more distal or more mobile attachment

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4
Q

what is the purpose of a flexor?

A

brings bones together

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5
Q

what is the purpose of an extensor?

A

moves bones away from each other

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6
Q

what are antagonistic muscle groups?

A

flexor/extensor pairs

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7
Q

what is the epimysium?

A

connective tissue that wraps around the muscles

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8
Q

what is the perimysium?

A

wraps around the muscle fascicles & individual muscle fibres

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9
Q

go over sarcomere

A

ya

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10
Q

what are the brain regions involved in voluntary muscle movement?

A
  • premotor cortex (motor associa2on) -basal ganglia
  • thalamus
  • midbrain
  • cerebellum
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11
Q

what is a motor unit?

A

A single motor neuron and all the muscle fibres it innervates

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12
Q

The area where the motor neuron makes synap2c contact with the muscle fibre is known as the neuromuscular junc2on

A

ya

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13
Q

what innervates muscle fibres, and give general info

A

alpha motor neuron; Large, myelinated axon; 15-120 m/sec

• Each axon branches and innervates several muscle fibers (cells); causes muscle fibres to respond simultaneously

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14
Q

Number muscle fibers / motor unit varies
– <10 for delicate precise work
– >100 for powerful, less precise contrac2ons

A

ya

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15
Q

briefly describe ALS

A

Neurodegenera2ve motor neuron disease

Upper and/or lower motor neurons degenerate leading to muscle atrophy and weakness from disuse

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16
Q

10% of ALS cases are genetically inherited as dominant traits
25% of these are due to a muta2on in gene(s) producing superoxide dismutase
- enzymes that catalyze the dismuta2on of superoxide (O2−) into oxygen and hydrogen peroxide
- Important an2oxidant defense

A

ya

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17
Q

what causes the death of ALS patients?

A

eventually resp failure

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18
Q

what are the components of a NMJ?

A
  1. Presynaptic motor neuron filled with synaptic vesicles
  2. The synaptic cleft
  3. The postsynaptic membrane of the skeletal muscle fibre
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19
Q

what is the motor end plate?

A

Region of sarcolemma at the neuromuscular junction

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20
Q

what is the purpose of junction folds in the motor end plate?

A

increases surface area, increases amount of receptors on the muscle—can respond to more neurotransmitter

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21
Q

what do motor neuron vesicles contain?a

A

Ach

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22
Q

what receptors are present on the postsyn memrbane (sarcolemma of the muscle fibre)?

A

nicotinic ACh receptors

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23
Q

nACh receptor general info

A

Member of cys-loop receptor family of ligand gated ion channels; classified as a monovalent ca2on channel (permeable for Na+ and K+.); requires two ACh molecules to bind to allow a net influx of Na to depol the muscle fibre (K effluxes as well)

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24
Q

Na+ entry through nACh generates an excitatory end-plate poten2al (EPP) that spreads to adjacent voltage gated Na+ channels on the sarcolemma and ini2ates an ac2on poten2al

A

ya

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25
Q

how is ACh recycle?

A

Acetylcholine in the synap2c cle^ can diffuse away or is broken down to acetate and choline by the enzyme acetylcholinesterase.
Choline is transported back into the motor neuron and combined with Acetyl CoA produced from mitochondria by the enzyme choline acetyltransferase to make acetylcholine.

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26
Q

how is ACh put into syn vesicles?

A

ACh-H exchanger moves ACh into the synap2c vesicle and H+ out; A vesicular, ATP fueled, proton pump creates a proton electrochemical gradient (posi2ve voltage and low pH) that drive this process to keep the H conc high in the syn ves

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27
Q

what is myasthenia gravis?

A

means severe weakness of muscle (especially facial muscles); Disorder of neuromuscular transmission
• Can be restricted to extraocular muscles or generalized; an autoimmune disorder–body produces an2bodies that bind to ACh receptors; Impedes ac2va2on of AChR and eventually decreases number.
• Degenera2on of postjunc2onal folds

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28
Q

how is MG treated?

A

Acetylcholinesterase
Inhibitors or immunosuppressant–> allows ACh to sit in syn. cleft for a long time—>can create a larger EPP using the nACh receptors still present

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29
Q

T tubs wrap around each muscle fibre

A

ya

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30
Q

Specialized Ca2+ storage organelles known as sarcoplasmic re2culum are strategically organized with the T-tublules

A

ya

31
Q

what is EC coupling?

A

The process by which electrical excita2on of the surface membrane triggers an increase of [Ca2+]i

32
Q

where do the t tubs connect with the sarcomere?

A

A and I band

33
Q

describe the initiation of a muscle AP

A

ACh from somatic motor neuron axon terminal binds to nACh receptors in the junctional folds; this causes the cell to depol (Na influx); the AP flows through the T tub where it reaches an L-type Ca channel (DHP) which is mechanically linked to a RyR; the conf change in the DHP channel causes RyR to open, allowing an increasing in cytosolic Ca–>bind to troponin complex, exposing myosin binding sites on actin->contraction
–RyR can also be opened by CICR–NOT vital in sk muscle

34
Q

where does Ca bind on the TNC?

A

to low affinity sites

35
Q

where is most Ca stored in SR?

A

in terminal cisternae

36
Q

what is the purpose of DHP channel in sk muscles?

A

voltage gated calcium channel—L-type;—job is NOT to cause an influx of Ca, but to sense the voltage change—still allows an influx of Ca

37
Q

what shortens during sarcomere contraction?

A

H zone and I band

38
Q

why is uptake into the SR the major mechanism to decrease Cai?

A

if the Na-Ca pump of ATP-dependent Ca pump were major, this would eventually deplete the cell (and therefore, the SR) of Ca

39
Q

how is Ca reuptaken into the SR?

A

through the SERCA pump (sarcoplasmic and endoplasmic re3culum Ca2+-ATPase)–high Ca conc in SR inhibits SERCA pump

40
Q

how is inhibited of the SERCA pump delayed in the SR?

A

Ca binding proteins exist; such as calsequestrin–localized to the triad region
-forms a complex with the Ca2+ release channels (RyR), not only buffers Ca2+ but also unloads Ca2+ near RyR facilita3ng EC coupling.

41
Q

where does anaerobic metabolism taking place?

A

in the sarcoplasm (cytoplasm)

42
Q

what is muscle fatigue?

A

a decrease in muscle tension as a result of previous contrac6le ac6vity

43
Q

what is central fatigue?

A

feeling of 6redness and a desire to cease ac6vity.

*Precedes physiological fa6gue–protective mechanism prevent cell damage

44
Q

why may we feel fatigue?

A

Low pH from acid produc6on during ATP hydrolysis may influence the sensa6on of fa6gue perceived by the brain.
-likely only the case in cases of maximal exertion–maintain pH pretty tightly

45
Q

what is peripheral fatigue?

A

problems with excitation-contraction coupling:
–At the T tub: With repeated AP firing, K+ builds up in the T-tubules and extracellular space changing the threshold for AP’s in the muscle fibre.
–Within the muscle fibre
-Build up of inorganic phosphate, ADP, H+ and reduc6on of ATP
-substances can act directly or indirectly to cause fa6gue; Sarcoplasmic re*culum
-reduced Ca2+ reuptake (SERCA inhibited) -reduced Ca2+ release (RyR inhibited); Pi can inhibit the SERCA pump
when there is a lot of Pi around, it binds to Ca—>can’t be taken up by SERCA pump; Troponin C
-decreased Ca2+ sensi6vity leading to decreased cross- bridge cycling;
myosin head: -release of Pi and ADP during cross bridge cycle slowed by sarcoplasmic accumula6on

46
Q

peripheral fatigue in short

A

Failed excita6on-contrac6on coupling at the t-tubule
• Decrease in the rate of Ca2+ release, reuptake, and storage by the sarcoplasmic re6culum
• Decreased ac6va6on of thin filament proteins by Ca2+
• Direct inhibi6on of the binding and power- stroke mo6on of the myosin cross-bridges

47
Q

what is the difference between slow and fast fibres?

A

-Slow fibres contain myosin with slower ATPase ac6vity (TYPE I) -Fast fibres contain myosin with more rapid ATPase ac6vity (TYPE II)–therefore rates of CBC differ

48
Q

Fibres containing a large amount of mitochondria have a high capacity for oxida6ve phosphoryla6on and are classified as oxidave fibres
-surrounded by blood vessels and contain a large amount of myglobin
to aid in oxygen delivery
-Fibres containing few mitochondria but an abundance of glycoly6c enzymes and a large store of glycogen are classified as glycolyc fibres

A

ya

49
Q

study slide 11 of muscles 4

A

ya

50
Q

what determines force/tension development of a sk muscle?

A

• Force/muscle cell – Fibre diameter
– Fa0gability
– Ini0al resting length
– Frequency of activation (# of APs–summation)
• Number of muscle cells ac0vated – Number of muscle cells/ motor unit – Number of motor units ac0vated

51
Q

why does muscle length affect tension generated?

A

sarcomeres too short–too much overlap–can’t shorten as effectively; sarcomeres too stretched–not enough overlap for CBC

52
Q

how is summation possible in sk muscles?

A

not all Ca leaves the SR from one AP, and not all myosin-binding sites have been exposed; Ca conc remains elevated for a longer period of time–>more CBC–> higher tension

53
Q

what is tetanus and the types?

A

a maintained contraction to repeated stimuli; unfused and fused

54
Q

what is unfused tetanus?

A

reaches steady state of contracton but stimuli are far enough apart that the muscle fibre slightly relaxes between stimuli

55
Q

what is fused tetanus?

A

the stimulation rate is fast enough that the fibre does not relax, instead it reaches maximum tension and remains there

56
Q

what is a motor unit?

A

a single alpha motor neuron and all the muscle fibres it innervates
–one mn innervates one fibre type

57
Q

what is a motor neuron pool?

A

the group of all motor neurons innervation a single muscle

58
Q

what is the size principle?

A

as the stimulus increases, larger and stronger neurons on the motor neuron pool are recruited

59
Q

what is asynchronous recruitment

A

during submaximal contraction, CNS modulates firing rates of motor neurons to allow different motor units to undergo contraction–> attempt to prevent fatigue

60
Q

what is isometric contraction?

A

creating a force (tension) without moving a load; muscle remains at constant length; tension increases?

61
Q

what is isotonic contraction?

A

a constant load is moved and muscle length shortens

62
Q

what is the difference between concentric and eccentric contraction?

A

muscle shorts while generating a force; muscle lengthens while generating a force

63
Q

isometric conctrations–sarcomeres change length (shorten) but muscle does not change length–elastic elements lengthen which allows for sarcos to shorten

A

ya

64
Q

what is muscle adaptation?

A

changes in the muscle capacity/ability upon usage/lack of usage

65
Q

how can a muscle adapt to demands?

A
  1. ATP-synth capacity; 2. muscle cross-section; 3. muscle fibre type (myosin) transition; 4. increased strength without hypertrophy
66
Q

what ways can ATP-synth capacity be increased?

A

increase in mito; increase capillary density; increase in glycolytic enzymes

67
Q

what is hypertrophy and atrophy?

A

hypertrophy: increase in area; atrophy: decrease in area

68
Q

how is strength increased without hypertrophy?

A

mods of neural pathways–

  • -increased synchronization of recruitment of motor units
  • -enhanced ability to recruit fast-glycolytic motor neurons
  • -reduc6on in inhibitory afferent inputs from tendon sensory receptors
69
Q

what is motor learning?

A

a change in the capability of responding resulting from practice or novel experience

70
Q

muscle mass can increase via hypertrophy or hyperplasia

A

ya

71
Q

what is hyperplasia

A

generation of new muscle fibres–not shown in adult humans; thought either if a muscle fibre becomes too large it’ll split or myosatellite cells involved in muscle repair may form new muscle fibres (occurs in development)

72
Q

what is hyperplasia

A

generation of new muscle fibres–not shown in adult humans; thought either if a muscle fibre becomes too large it’ll split or myosatellite cells involved in muscle repair may form new muscle fibres (occurs in development)

73
Q

what is cachexia?

A

weakness/wasting due to chronic disease

PHSI 208 (32 decks)

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