Muscle adaptations to strength and endurance training Flashcards
what is the adaptation to endurance training
- increased oxidative enzyme activity
- increased mitochondrial content
= improved mitochondrial myogenesis
myogenesis
formation of new muscular tissue
what effect did one legged training show
- increased capillary density
- increased mitochondrial content
- increased peak oxygen uptake
master regulator of mitochondrial biogenesis
PGC-1
what doesPGC-1 do
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
what does PGC-1 bind to
NRF-1
what are NRF-1 and mtTFA
transcription factors that regulate mitochondrial genes in mitochndrial and nuclear DNA
what switch on PGC-1
- binding of AMP to AMPK
- camK from muscle contraction
- P38 from glycogen
angiogenesis
formation of new blood vessels
what processes increases capillary density
angiogenesis
- capillary per fibre and
- capillary per meter
what is the most beneficial increase in capillary growth
- more capillaries
- smaller muscle fibres
= faster diffusion
difference between capillary supply of muscles in endurance, sprinters and weightlifters
- 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
functional consequences of more capillaries
more capillaries = greater transit time = more chance for diffusion
effect of training on capillaries
increases capillary number
increases transit time
= more diffusion
what stimulates angiogenesis
exercise up regulates angiogenic growth factors such as VEGF
what is VEGF
vascular endothelial growth factor
master regulator of angiogenesis
what increases VEGF
- hypoxia
- mechanical signals, sheer stress
- increased energy stress AMPK
master regulator of angiogenesis
VEGF
glycogen of well trained athletes
well trained individuals have up to 2.5 times more intramuscular glycogen at rest
what causes difference in intramuscular glycogen in the well trained
increased sensitivity to insulin
- promotes glucose uptake to muscle
- GLUT4 25% higher in trained muscle
- increased activity of glycogen synthase
fat levels of well trained athletes
well trained individuals have higher intramuscular TAG around the mitochondria, at rest
why do well trained individuals have great intramuscular fat
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
when is intramuscular fat goof
- physiological
with exercise training.
lipid droplets accumulate around the mitochondria and give high influx through aerobic system for energy supply
when is intramuscular fat bad
- pathological
with inactivity and over feeding
lipid accumulates as FA by-products like ceramics which impair insulin signalling
what happens to intramuscular energy stores from endurance training
increased glycogen at rest
increased fat at rest
how does intramuscular fat lead to diabetes
FA intermediates block the pathway and so don’t get effective GLUT4 translocation, and glucose uptake into cell is limited
= hyperglycaemia
switching of fibre types
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
when does IIa -> IIx
with inactivity
when does IIx -> IIa
with activity
when does I-> IIa -> IIx
prolonged disuse such as spinal chord injury
when does IIa -> I
very difficult to achieve but shown possible with animal models using electrical stimulation
- calcium mediated calcineurin stimulation
what causes hypertrophy
mechanical overload
requirements of skeletal muscle in training
- explosive power comes from strength and speed
- power maintenance comes from fatigues resistance
when training, you will favour one over the other
what proves the need for exercises specificity
Dramatic increases in 1RM.
1RM can increase by 200% in 12 weeks, but that does not mean muscle has grown 200%
relationship between strength, isometric MVC and muscle mass
- 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
isometric MVC
maximal voluntary contraction
why is the increase in strength greater than increase in muscle size
- improved activation
- changes in muscle architecture
- selective hypertrophy of TII
how does improved activation increase strength
- 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
what changes in muscle architecture help strength
changes in pennation angle of fibres
how does selective hypertrophy of TII fibres improve strength
- 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
basic requirements for muscle growth
- net gain in protein
- provision of new nuclei
why are new nuclei needed in muscle growth
to maintain myonuclear domain
how is net gain in protein achieved for muscle growth
increased rate of synthesis and or decreased depreciation of protein
protein balance, normal conditions
protein synthesis = protein breakdown
muscle growth protein balance
net gain
MPS increased and/or
MPB decreased
anabolism
muscle atrophy, protein balance
net loss
MPS decreased and/or
MPB increased
catabolism
effect of strength training on MPS
Increases MPS for up to 72 hours because exercise simulates muscle proteins
effect of feeding AA on MPS
Increases MPS for 2-3 hours
- shows a dose-response
- saturation point when muscle becomes refractory (depolarised)
what is MPS regulated by
AKT
What is a negative regulator of MPS
myostatin; suppresses growth
nutritional stimulus of MPS
leucine; EAA
what can amplify MPS
nutrition and exercise and hence feeding time might be relevant, so two stimuli for leucine cascade
important regulator of MPS
P70s6K
what is activated by exercise to simulate MPS
IGF-1
Effect of exercise on MPS homeostasis
exercise has a synthetic response
this favours the left pathway = MPS
and inhibit the right pathway = MPB
What is the ceiling of a myonuclear domain
the max volume of cytoplasm that a nucleus can be responsible for
what part of muscle are essential for muscle replair
satellite cells - they are muscle stem cells
what are muscle stem cells called
satellite cells
process of hypertrophy in terms of muscle cells when MND initially small
- myonuclear domain initially small, well below ceiling
-hypertrophic stimuli makes muscle bigger - synthetic rate increase through nuclei transcription and translation
= hypertrophy occurs
process of hypertrophy in terms of muscle cells when MND initially large
- 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
when are satellite cells needed for hypertrophy
when MND are initially large they limit hypertrophy. Satellite cells are needed to produce more nuclei for hypertrophy to occur
when are satellite cells not needed for hypertrophy
when MND are initially small, hypertrophy can occur through transcription and translation
muscle memory
- neuromuscular memory e.g riding a bike
- cellular memory e.g satellite cells
summary of adaptations to endurance training
- 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
summary of adaptations to strength training that result in hypertropy
- 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
