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PBL SEM 3 > 9 - muscle and movement > Flashcards

9 - muscle and movement Flashcards

1
Q

location (typical), morphology, control, type of work, and activity (typical) of skeletal muscle

A
  • location = connected to bone
  • morphology = striated
  • control = voluntary
  • type of work = high power
  • activity (typical) = usually relaxed (however does have a basal muscle tone)
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2
Q

location (typical), morphology, control, type of work, and activity (typical) of cardiac muscle

A
  • location (typical) = heart
  • morphology = striated
  • control = involuntary
  • type of work = high power
  • activity (typical) = pump (cyclic)
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3
Q

location (typical), morphology, control, type of work, and activity (typical) of smooth muscle

A
  • location = hollow organs
  • morphology = smooth
  • control = involuntary
  • type of work = low power
  • activity = usually contracted (varies)
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4
Q

describe what happens in full at a neuromuscular junction

A
  1. AP arrives
  2. voltage-sensitive Ca++ channels open
  3. Ca++ enters the cell
  4. vesicle fusion - ACh exocytosis
  5. ACh diffusion in the synaptic cleft
  6. ACh-sensitive cation channels open
  7. Na+ in and K+ out
  8. end-plate membrane depolarises — End Plate Potential (EPP)
  9. AP forms = stimulus for muscle
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5
Q

thick vs thin filaments

A

thick - myosin
thin - actin

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6
Q

where does energy to shorten the muscle come from?

A

ATP hydrolysis

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7
Q

what shortens in a muscle contraction?

A

sarcomere

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8
Q

label this sarcomere

A
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9
Q

what makes up a muscle?

A

muscle cells or fibres = myofibrils = myosin + actin (myofilaments; thick and thin)

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10
Q

what are the myosin binding sites like at rest?

A

covered up by tropomyosin due to the absence of Ca++ — therefore actin and myosin can’t interact

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11
Q

what is the troponin complex and what does it do?

A
  • regulatory proteins — TnT, TnC and TnI
  • help moves tropomyosin out of binding sites in the presence of Ca++
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12
Q

what parts of the thin and thick filaments bind when they interact?

A

myosin head binds to actin filament at myosin binding site

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13
Q

describe the steps in a striated muscle contraction starting from the previous contraction

A
  1. ATP binds to myosin head, causing the dissociation of the actin-myosin complex
  2. ATP is hydrolysed, causing myosin heads to return to their resting conformation
  3. a cross-bridge froms and myosin head binds to a new position on actin
  4. P is released. myosin heads change conformation, resulting in the power stroke. the filaments slide past each other
  5. ADP is released
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14
Q

what triggers a muscle contraction?

A

increase in Ca++ —> exposes binding sites —> contraction

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15
Q

what forms the T-tubules?

A

invaginations of plasma membrane (sarcolemma)

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16
Q

what does the AP spread along in excitation-contraction coupling?

A

the sarcolemma

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17
Q

what stores the Ca++ at rest and then releases it when the T-tubule is depolarised?

A

sarcoplasmic reticulum

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18
Q

what pump is active at rest?

A

NaK pump

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19
Q

what is the Ca++ released through?

A

Ca++ release channels

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20
Q

increase in Ca++ = ?

A

stronger force of contraction

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21
Q

what are the 2 types of muscle contraction? how are they different?

A

isometric = muscle stays at constant length (but still generates force) (eg. lifting hand up against a table)

isotonic = muscle shortens (eg. weight lifting)

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22
Q

contraction is stronger and faster the…….?

A

closer the muscle initial length is to the optimum length

(too stretched/already contracted = worse contraction)

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23
Q

what is a muscle unit?

A

muscle fibres innervated by a single motor neuron

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24
Q

what is a motor unit?

A

muscle unit plus its motor neuron

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25
Q

what is a motor neuron pool?

A

collection of neurons innervating a single muscle

(UMN synapses on pool of LMNs - not 1 on 1)

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26
Q

fine vs coarse control

A

fine = few muscle fibres per motor unit

coarse = many muscle fibres per motor unit

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27
Q

typically a muscle is controlled by about ___ motor neurons — cell bodies in the spinal cord or brainstem

each motor neuron controls ___-___ muscle fibres scattered over the muscle

A
  • 100
  • 100-1000
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28
Q

type 1 muscle fibres:

myosin speed, Ca++ pump transport rate, diameter, oxidative capacity, glycolitic capacity, fatigue

A

myosin = slow
Ca++ pump transport rate = moderate
diameter = moderate
oxidative capacity = high
glycolytic capacity = moderate
fatigue = resistant

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29
Q

type 2B muscle fibres:

myosin speed, Ca++ pump transport rate, diameter, oxidative capacity, glycolitic capacity, fatigue

A

myosin = fastest
Ca++ pump transport rate = high
diameter = large
oxidative capacity = low
glycolytic capacity = high
fatigue = non resistant

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30
Q

type 2A muscle fibres:

myosin speed, Ca++ pump transport rate, diameter, oxidative capacity, glycolitic capacity, fatigue

A
  • myosin = fast
  • Ca++ pump transport rate = high
  • diameter = small
  • oxidative capacity = very high
  • glycolytic capacity = high
  • fatigue = resistant
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31
Q

what type of muscle fibres are resistant?

A

type 1 and 2A

32
Q

what muscle fibre type has the highest oxidative capacity?

A

type 2A

33
Q

what type of muscle fibre has the fastest myosin?

A

type 2B

34
Q

what muscle fibre type has the largest diameter?

A

type 2B

35
Q

what kind of respiration do type 1 muscle fibres use? use?

A

aerobic — long distance at low speed — fatigue resistant

36
Q

why do type 2B muscle fibres tire quickly?

A

rely on glycolysis

37
Q

how can you increase muscle force?

A
  1. increase recruitment of motor units
  2. increase firing rate of motor units
38
Q

what can you recruit?

A
  • fewer/more units
  • units of different sizes
39
Q

the CNS is lazy - you have to teach it to recruit more motor units. when is this evident?

A

1st few months of weight training == can lift more weight but dont see muscles getting bigger

40
Q

large vs small motor unit motor neuron

A

large = motor neuron is large, fast conduction, hard to excite

small = motor neuron is small, slow conduction, easy to excite

41
Q

large vs small other unit muscle fibres

A

large - many, type 2 (large, fast, glycolytic)

small - few, type 1 (small, slow, oxidative)

42
Q

large vs small motor unit recruitment/activity

A

large - recruited if a strong contraction is required, usually inactive

small - first to be recruited, frequently active

43
Q

describe the stretch reflex

A
  1. tendon tap
  2. stretch muscle
  3. stimulate muscle spindles
  4. excite motor neuron —> agonist muscle contraction
    excite inhibitory interneuron —> antagonist muscle relaxation
44
Q

what type of afferents in stretch reflex?

A

Ia, II

45
Q

what type of efferent in stretch reflex?

A

Aa efferent

46
Q

what type of motor neuron in stretch reflex?

A

a

47
Q

lower vs upper motor neuron lesion properties

muscle strength, paralysis, muscle tone, reflexes

A

> lower:
muscle strength = weakess
paralysis = flaccid
muscle tone = hypotonia
reflexes = hyporeflexia

> upper:
muscle strength = weakness
paralysis = spastic
muscle tone = hypertonia
reflexes = hyperreflexia

48
Q

why can you get twitching in a lower motor neuron lesion?

A

muscles respond to circulating ACh

49
Q

why do you get spastic paralysis and hypertonia in an upper motor neuron lesion?

A

sensitisation of LMN pools — respond in absence of innervation from motor cortex (still have wiring from spinal cord to muscle)

50
Q

why do you get hyperreflexia in an UMN lesion?

A

loss of a descending inhibitory pathway — get re-emergence of primitive reflexes

51
Q

what do the ventral and dorsal parts of the somite give rise to?

A

ventral — bone, cartilage, tendons

dorsal — skeletal muscle

52
Q

skeletal muscles from in _____?

A

subsequent waves

53
Q

what do invaginations of the cell membrane do?

A

increase SA = more receptor for ACh

54
Q

where are motor neurons found in spinal cord?

A

in anterior horn of spinal cord

55
Q

AP propagates along membrnae via _____ until it reaches ____

A

Na+ channels

T-tubule

56
Q

what is electrically coupled to T-Tubule?

A

sarcoplasmic reticulum

57
Q

what do type 1 muscle fibres contain to make them resistant to fatigue?

A

myoglobin — captures O2 and releases it when needed

58
Q

describe a muscle strain

A
  • commonly referred to as a “pulled” muscle
  • this injury can happen when the muscle is overstretched, overused, or used improperly
59
Q

describe a muscle tear

A
  • larger injury in which a muscle and the blood vessels that supply it are torn
  • typically takes a significant amount of force to cause this type of injury
60
Q

what is rhabdomyolysis?

A

a serious condition that occurs when muscle fibres die and their contents are released into the bloodstream

61
Q

what can rhabdomyolysis result in and why?

A

kidney failure — kidney responsible for filtering put the muscle byproducts

62
Q

symptoms of rhabdomyolysis

A

muscle pain, weakness, dark urine

63
Q

causes of rhabdomyolysis

A
  • crush injuries
  • car accidents
  • heatstroke
  • infections
  • intense exercise
  • seizures
  • use of cocaine or amphetamines
64
Q

what is muscle contusion?

A
  • also referred to as a muscle “bruise”
  • occurs when a blunt object strikes the body and crushes underlying muscle tissue, but does not break the skin
  • typically cause pain, swelling, and decreased range of motion
65
Q

muscle damage and regeneration

A
66
Q

what degrades and digests the debris of dead muscle?

A

neutrophil

67
Q

M1 macrophage classically divides into what? what do they promote?

A
  1. via IL-6 — satellite cell (like a stem cell) —> promotes regeneration
  2. M2 macrophage —> promotes inflammation
68
Q

what are chronic types of muscle damage?

A
69
Q

what is muscular dystrophy?

A

an X-linked recessive disease (more common in males) caused by mutation of dystrophin gene = the largest known gene coding for a cytoskeleton protein

70
Q

what is muscular dystrophy characterised by?

A

degeneration of skeletal muscle due to absence f dystrophin on muscle fibre membrane

71
Q

what happens to the calf in later stages of muscular dystrophy?

A

pseudohypertrophy of the calf — due to severe inflammation of gastrocnemius

72
Q

morphology of dystrophic muscle

A
73
Q

what is dystrophin?

A
  • coded for by the DMD gene
  • cytoplasmic protein
  • connects the sarcomeres to the membrane and other proteins to the basal lamina
  • protects from stress in contraction
74
Q

what happens in the absence of dystrophin?

A
  • increased probability that muscle membrane will be damaged
    —> Ca++ influx
    —> hypercontraction
    —> activation of Ca protease — destroys fibre
75
Q

what are the 2 forms of muscular dystrophy disease?

A
  1. mild form = Becker’s form — inframe mutation — amino and carboxyl left intact
  2. severe form = Duchenne’s form — frameshift mutation — protein not made
76
Q

what replaces fibres in muscular dystrophy?

A

fat infiltration and fibrosis

PBL SEM 3 (49 decks)

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