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Exercise & Environment > Muscle adaptations to strength and endurance training > Flashcards

Muscle adaptations to strength and endurance training Flashcards

1
Q

what is the adaptation to endurance training

A
  • increased oxidative enzyme activity
  • increased mitochondrial content
    = improved mitochondrial myogenesis
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2
Q

myogenesis

A

formation of new muscular tissue

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3
Q

what effect did one legged training show

A
  • increased capillary density
  • increased mitochondrial content
  • increased peak oxygen uptake
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4
Q

master regulator of mitochondrial biogenesis

A

PGC-1

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5
Q

what doesPGC-1 do

A

master regulator of mitochondrial biogenesis

  • increased PGC-1 causes increased expression of transcription factors
  • e.g NRF-1 and mtTFA
  • these regulate mitochondrial genes encoded in nuclear and mitochondrial DNA
  • PGC1 also binds to NRF-1
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6
Q

what does PGC-1 bind to

A

NRF-1

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7
Q

what are NRF-1 and mtTFA

A

transcription factors that regulate mitochondrial genes in mitochndrial and nuclear DNA

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8
Q

what switch on PGC-1

A
  • binding of AMP to AMPK
  • camK from muscle contraction
  • P38 from glycogen
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9
Q

angiogenesis

A

formation of new blood vessels

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10
Q

what processes increases capillary density

A

angiogenesis

  • capillary per fibre and
  • capillary per meter
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11
Q

what is the most beneficial increase in capillary growth

A
  • more capillaries
  • smaller muscle fibres
    = faster diffusion
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12
Q

difference between capillary supply of muscles in endurance, sprinters and weightlifters

A
  • endurance athletes will have more capillaries per fibre to increase oxygen supply
  • weightlifters will muscle growth to a greater extent than their increase of capillaries; this means they are less well perfused than endurance atheletes when looking at capillaries/mm muscle
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13
Q

functional consequences of more capillaries

A

more capillaries = greater transit time = more chance for diffusion

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14
Q

effect of training on capillaries

A

increases capillary number
increases transit time
= more diffusion

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15
Q

what stimulates angiogenesis

A

exercise up regulates angiogenic growth factors such as VEGF

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16
Q

what is VEGF

A

vascular endothelial growth factor

master regulator of angiogenesis

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17
Q

what increases VEGF

A
  • hypoxia
  • mechanical signals, sheer stress
  • increased energy stress AMPK
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18
Q

master regulator of angiogenesis

A

VEGF

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19
Q

glycogen of well trained athletes

A

well trained individuals have up to 2.5 times more intramuscular glycogen at rest

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20
Q

what causes difference in intramuscular glycogen in the well trained

A

increased sensitivity to insulin

  • promotes glucose uptake to muscle
  • GLUT4 25% higher in trained muscle
  • increased activity of glycogen synthase
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21
Q

fat levels of well trained athletes

A

well trained individuals have higher intramuscular TAG around the mitochondria, at rest

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22
Q

why do well trained individuals have great intramuscular fat

A

favourable adaptation to metabolise fat and reserve glucose for the brain.

they will expend the same amount of energy during a given exercise, but will metabolise more fat and less CHO than untrained

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23
Q

when is intramuscular fat goof

A
  • physiological
    with exercise training.
    lipid droplets accumulate around the mitochondria and give high influx through aerobic system for energy supply
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24
Q

when is intramuscular fat bad

A
  • pathological
    with inactivity and over feeding
    lipid accumulates as FA by-products like ceramics which impair insulin signalling
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25
Q

what happens to intramuscular energy stores from endurance training

A

increased glycogen at rest

increased fat at rest

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26
Q

how does intramuscular fat lead to diabetes

A

FA intermediates block the pathway and so don’t get effective GLUT4 translocation, and glucose uptake into cell is limited
= hyperglycaemia

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27
Q

switching of fibre types

A

depends on definition of muscle fibre type

  • defined biochemically; can adapt from glycolytic to oxidative
  • based one their MHC, very difficult to achieve but shown possible in animal studies
28
Q

when does IIa -> IIx

A

with inactivity

29
Q

when does IIx -> IIa

A

with activity

30
Q

when does I-> IIa -> IIx

A

prolonged disuse such as spinal chord injury

31
Q

when does IIa -> I

A

very difficult to achieve but shown possible with animal models using electrical stimulation
- calcium mediated calcineurin stimulation

32
Q

what causes hypertrophy

A

mechanical overload

33
Q

requirements of skeletal muscle in training

A
  • explosive power comes from strength and speed
  • power maintenance comes from fatigues resistance

when training, you will favour one over the other

34
Q

what proves the need for exercises specificity

A

Dramatic increases in 1RM.

1RM can increase by 200% in 12 weeks, but that does not mean muscle has grown 200%

35
Q

relationship between strength, isometric MVC and muscle mass

A
  • small increase in CSA can result in big increase in isometric force
  • big increase in strength can occur with only a small increase in isometric MVC
36
Q

isometric MVC

A

maximal voluntary contraction

37
Q

why is the increase in strength greater than increase in muscle size

A
  • improved activation
  • changes in muscle architecture
  • selective hypertrophy of TII
38
Q

how does improved activation increase strength

A
  • increased drive to agonists=
    increased AP firing rate or synchronised for efficiency which improves activation
  • decreased drive to antagonists =
    protective co-contraction is switched off
39
Q

what changes in muscle architecture help strength

A

changes in pennation angle of fibres

40
Q

how does selective hypertrophy of TII fibres improve strength

A
  • higher force per unit area potential
  • more sensitive to exercise overload than TI
    OR, TII fibres are now being switched on when they previously weren’t because of selection order
41
Q

basic requirements for muscle growth

A
  • net gain in protein

- provision of new nuclei

42
Q

why are new nuclei needed in muscle growth

A

to maintain myonuclear domain

43
Q

how is net gain in protein achieved for muscle growth

A

increased rate of synthesis and or decreased depreciation of protein

44
Q

protein balance, normal conditions

A

protein synthesis = protein breakdown

45
Q

muscle growth protein balance

A

net gain
MPS increased and/or
MPB decreased
anabolism

46
Q

muscle atrophy, protein balance

A

net loss
MPS decreased and/or
MPB increased
catabolism

47
Q

effect of strength training on MPS

A

Increases MPS for up to 72 hours because exercise simulates muscle proteins

48
Q

effect of feeding AA on MPS

A

Increases MPS for 2-3 hours

  • shows a dose-response
  • saturation point when muscle becomes refractory (depolarised)
49
Q

what is MPS regulated by

A

AKT

50
Q

What is a negative regulator of MPS

A

myostatin; suppresses growth

51
Q

nutritional stimulus of MPS

A

leucine; EAA

52
Q

what can amplify MPS

A

nutrition and exercise and hence feeding time might be relevant, so two stimuli for leucine cascade

53
Q

important regulator of MPS

A

P70s6K

54
Q

what is activated by exercise to simulate MPS

A

IGF-1

55
Q

Effect of exercise on MPS homeostasis

A

exercise has a synthetic response
this favours the left pathway = MPS
and inhibit the right pathway = MPB

56
Q

What is the ceiling of a myonuclear domain

A

the max volume of cytoplasm that a nucleus can be responsible for

57
Q

what part of muscle are essential for muscle replair

A

satellite cells - they are muscle stem cells

58
Q

what are muscle stem cells called

A

satellite cells

59
Q

process of hypertrophy in terms of muscle cells when MND initially small

A
  • myonuclear domain initially small, well below ceiling
    -hypertrophic stimuli makes muscle bigger
  • synthetic rate increase through nuclei transcription and translation
    = hypertrophy occurs
60
Q

process of hypertrophy in terms of muscle cells when MND initially large

A
  • MND close to ceiling
  • same size muscle, but 2 myonuclei instead of 4 little ones
  • will impair muscle’s drive to hypertrophy
  • new nuclei are added from satellite cells
    = hypertrophy
61
Q

when are satellite cells needed for hypertrophy

A

when MND are initially large they limit hypertrophy. Satellite cells are needed to produce more nuclei for hypertrophy to occur

62
Q

when are satellite cells not needed for hypertrophy

A

when MND are initially small, hypertrophy can occur through transcription and translation

63
Q

muscle memory

A
  • neuromuscular memory e.g riding a bike

- cellular memory e.g satellite cells

64
Q

summary of adaptations to endurance training

A
  • increased size and number of mitochondria for oxygen utilisation
  • increased capillary density for increased transit time for oxygen delivery
  • increased storage of fat and glycogen in muscles
  • short towards fat metabolism in sub maximal exercise
  • fibre type conversion; IIx -> IIa is possible, II->I is difficult and unlikely
65
Q

summary of adaptations to strength training that result in hypertropy

A
  • increased strength and power involves both neural and muscular adaptations
  • muscular hypertrophy requires net gain in protein
    muscular hypertrophy usually requires increase in myonuclei by satellite cells
  • resistance will initially causes MPB but eventually MPS, via the AKT/mTOR signalling pathway
  • feeding of EAA stimulates MPS but saturates

Exercise & Environment (14 decks)

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