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KP322 > muscular system > Flashcards

muscular system Flashcards

1
Q

myofibrils

A

contain sarcomere for contraction, actin/myosin

actin = thick
myo = thin

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2
Q

satellite cells

A

undifferentiated cells, gives nuclei to muscle fibres

imp role in musc growth and repair…activated by training

initiates divide to inc nuclei…inc nuceli makes PROTEIn

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3
Q

motor unit

A

1 motor neuron and all assoc fibres it innervations

AP travels down t tubules into cell

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4
Q

NMJ

A

neuromuscular junction, where motor neuron and muscle cell meet

AP comes from nervous sys/somatic motor neuron

synaptic cleft separates neuron and cell
- AP stims NT release i.e. ACh in synaptic vessels
- travels across cleft to open Na channels
- generates end plate potential that continues AP
- AP travels along musc fibre membrane down t tubules, impacting all myofibrils

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5
Q

sliding filament theory

A

calcium released by of ATP, shortening of sarcomere

myosin binding site on actin opens for myosin head
- ca binds, shifting troponin-tropomyosin to allow myo head binding

2 ATP/crossbridge cycle…ATP needed to detach and reattach

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6
Q

excitation-contraction coupling

A

events causing depolarization of muscle that lead to muscle shortening

  1. AP from motor neuron releases ACh in NMJ
  2. ACh binds to receptors, causes end-plate potential
  3. depolarization of muscle leads to ca release from SR
  4. ca binds to troponin, which MOVES tropomyosin from myo binding site
  5. myosin head binds to actin = crossbridge
  6. power stroke, actin is PULLED and muscle shortens

when impulse ends, ca reputake into SR so muscle relaxes

ATPase breaks down ATP attached to crossbridge so myosin can bind to another actin

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7
Q

concentric contraction

A

musc length shortens, force > load

series elastic component

cross-bridge BRAKING EFFECT, process hindered if myosin-actin are bound too long

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8
Q

eccentric contraction

A

muscle elongates even tho trying to shorten

braking effect HELPS contraction, trying to resist lengthening

improves strength of contraction

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9
Q

what determines force of contraction

A
  1. type and number of MUs recruited
    - more MU and fast twitch = inc force
  2. initial muscle length: if optimal
  3. nature of neural stimulation of MUS: freq of stimulation
    - summation
    - tetanus
  4. contractile history: fatigued or primed
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10
Q

muscle twitch

A

one full contraction response

latent period, contraction, relaxation

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11
Q

orderly recruitment

A

small MUs have small threshold, are recruited first

large MUs are last to be recruited and first to be de-recruited

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12
Q

length-tension relationship

A

optimal length produces most force, falls off at greater length

optimal myosin-actin overlap to contract

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13
Q

tetanus vs summation

A

summation: fast firing so muscle doesn’t fully relax, force compounds

tetanus: maximum force production when optimal activation frequency

trained ppl recruit fewer MUs for easy motions

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14
Q

why don’t we recruit 100% muscle fibres

A

would tear muscle from tendon

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15
Q

post activation potentiation

A

when previous activity was non-fatiguing, will increase force production of contraction

because of more efficient cross bridges, ca sensitivity

not applicable to real life

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16
Q

force-velocity relationship

A

as velocity inc, force dec

17
Q

muscle fibre types

A

type 1/slow twich: slow oxidative
- red bcs low myosin ATPase
- activities less than 25% vo2max

type 2a: fast oxidative glycolytic

type 2x: fast glycolytic
- white bcs rich w myosin ATPase

18
Q

fibre type distribution

A

depends on muscle and needed function
- most ppl have 45-55% slow twitch

  1. genetics
  2. hormone concentrations
  3. exercise habits
19
Q

biochemical properties of musc fibres

A
  1. oxidative capacity: number of capillaries, myoglobin, mitochondria
  2. type of myosin ATPase isoform: speed of ATP degradation, fast twitch degrades fastest
  3. amount of contractile proteins in fibres: amount of act/myo determines number of crossbridges
20
Q

contractile properties of musc fibres

A
  1. max force production: force/unit of cross sectional area
    - large fibres = inc force
  2. speed of contraction: Vmax
    - myosin ATPase activity
    - rate of cb cycling
  3. max power output: power = force x velocity
  4. muscle fibre efficiency
21
Q

types of muscle biopsy

A

muscle biopsy: remove muscle piece, may NOT represent whole body

stain for ATPase isoform

  1. immunohistochemical staining: antibody binds to myosin protein, fibre determined by colour
  2. gel electrophoresis: ID myosin isofroms specific to fibre type
22
Q

why are muscle fibres different colours

A

myoglobin carries iron, which carries o2
- this is red in colours

oxidative fibres are red bcs are oxygenated, non-oxi are white

23
Q

fatigue

A

decline in muscle power output
- decrease in force generation and decrease in shortening velocity

in exercise:
- inability to maintain exercise intensity or power output
- sensations of tiredness and assoc w dec musc fatigue

reversible w recovery

24
Q

causes of fatigue in high intensity exercise vs long duration

A

high intensity: 60s
- accumulation of lactate, H, ADP, Pi, free radiacals
- diminishes cross bridges bound to actin

long duration exercise: 2-4hr
- musc factors i.e. accumulation free radicals, glyogen depletion, electrolyte imbalance

25
Q

system causes of muscular fatigue

A

CV system: delivery o2 blood, removal metabolites

energy supply system: inadequate ATP, issues w susbtrate depletion

neuromuscular system: dec neural drives, dec respond to MAPs

psychology: inc RPE

central governer model: must maintain homeostasis, prevent catastrophic failure
- body won’t let continue

thermoregulatory: critical core temp

26
Q

central vs peripheral fatigue

A

central fatigue: occurs w/in CNS…motor cortex –> SC
- pain, dec motivation
- reduced firing frequency of MUs

peripheral fatigue: w/in PNS…NMJ, sarcolemma, actin-myosin interaction
- impaired neuromuscular transmission leads to dec AP conductance to sarcolemma
- dec ca impairs cross-bridge cycling

27
Q

why is it hard to discover origin of fatigue

A

in muscle, compartmentalization w/in cell inc difficulty to determination

i.e. ATP may be depelted by myosin head, but is adequate in other cell areas

diffusion is often origin of fatigue
- i.e. dehydration, factors contrib to homeostasis distribution
- easier to ID correlations than causes of fatigue

28
Q

depletion hypothesis

A

peripheral fatigue

depletion of energy susbtrates i.e. ATP, PCr, glycogen
- must match restoration from other metabolic pathways or cause fatigue

initial rate of decline and extent of decline related to exercise intensity

glycogen: moderate intensity
- uniform depletion from fibre tupes
- carb loading can inc performance
- caffeine offsets fatigue

blood glucose:
- inc during short intense bursts
- falls w prologned exercise

TCA intermediates: decline causes dec capacity of krebs

29
Q

accumulation hypothesis

A

peripheral fatigue

buildup of lactate, pi, ca, ammonia

muscle acidosis: inhibits important processes
- ATP production releases H ions, cause pain

Po = max isometric force

ca accumulation is linked to mitochondrial coupling efficiency
- alteration in membrane potential
- can be caused by lactate

  1. dec ca leads to dec SR uptake…impaired EC coupling
  2. dec responsiveness to ca: H interference on troponin
  3. dec sensitivity to ca leads to dec force for given amount of ca -> musc can’t contract
30
Q

other metabolites involved in peripheral fatigue

A

potassium: released from contracting muscle
- dec cytosolic and inc plasma k content: release high enough to block nerve transmission in t tubules

sodium: increased na disrupts normal cell excitability

high na/k pump will inc performance

31
Q

oxygen and fatigue

A

o2 depletion in muscle can cause fatigue i.e. altitude, circulation issues

low o2 indicated by lactate accumulation and pcr depletion

can double oxidative capacity w training
- inc ffa use, spare glycogen

32
Q

neuromuscular fatigue

A

in CNS

exercise-induced decline in ability of musc to gen force/power that recovers w rest
- is MEASURABLE, not subjective like physical fatigue

33
Q

neuromuscular fatigue model

A

how interactions in brain impact muscle

fatigue can be bcs of nerve or muscle failure

34
Q

original vs new central fatigue hypotheses

A

origianl: to pass blood brain barrier and enter brain, transport protein binds to branched amino acid
- as prolong exercise, FFA primary source
- FFAs displace tryptophan from carriers and enter bloodstream
- compete w branched a.as to enter CNS
- in brain, tryptophan converted to serotonin
- serotonin causes lethargy

dopamine dec w activity = fatigue
- inc dopaminergic activity to prolong activity

35
Q

superimposed twitch technique

A

central fatigue

if superimposed twitch occurs, bcs CNS failed toa ctivate all MUs and is experiencing fatigue

apply shock when “contract as hard as you can”
- if 100% musc recruited, no twitch would occur

36
Q

supraspinal fatigue

A

produced by failure to generate output from motor cortex

brain or cortical fatigue

KP322 (7 decks)

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