what does phosphorylated Akt target
mTOR
what are the 2 effects that progestin can have
- anti-androgenic
- androgenic
what are 5 changes that happen when someone takes OC
- decreased estrogen
- decresed progesterone
- decreased free testosterone
- decreased IGF-1
- increased cortisol
what are 2 key regulators in the muscle hypertrophy using the mTOR pathway
- IGF-1
- mTOR
what is the difference between anti-androgenic and androgenic
anti-androgenic block androgen recptors while androgenic minic the effects of androgens
was there explanations for excluding women in research studies
some research papers have justificaiton but most of them did not
what does enhanced translational capacity do
this increases ribosomal translational capacity
what does IGF-1 do to the cell
it binds to the cell surface and cause Akt to be recruited from cytosol
what does increaesd human growth hormone do
this increases circulating IGF-1
what does mTOR do
it targets S6K1 and 4E-BP1, this enhances translational capacity
what are the effects of reduced estrogen and progesterone and what does this do
they can lower bone mineral density and cause injury
what are 2 mechanisms that contribute to muscle hypertrophy
- increased translation capacity through mTOR signalling
- increased translation capacity through addition of myonuceali
what is the basics for muscle hypertrophy to occur
protein synthesis needs to be higher than protein breakdown
what does mTOR inhibition show
it reduces hypertrophy and shows the impact that it has on hypertrophy and muscle recovery
what are the most common OCs comprised of
ethinyestradiol and progestin
what happens when Akt is recruited
it goes to the cell membrane where it is phosphorylated and activated
what do OC do
they surpress endogenous estradial and progesterone, which surpress ovulation/thicken cervial mucus
do older adults have the same mTOR and AKT protein content after having similar stimulation of a muscle compared to a younger adult
no, older adults mTOR and AKT protein content is less
What are the 5 steps that cause increased protein synthesis
- IGF-1
- AKT
- mTOR
- S6K1/ 4E-BP1
- Ribsome biogensis 5’-TOP translation/ Cap-depedent translation
what happens to S6K1 and 4E-BP1 portein content after resitance training in young adults
it is increased
what are 4 ways we can increase protein syntehsis in the myofibre
- increasing protein intake
- increasing stimulus of muscle associated with exercise
- adding nuclei via satellite cells (has code for protein)
- increasing ribsomes so that we allow for increased protein synthesis
knowing what we know about the mTOR and satellite cells, what are some possible conculsions that we can come to
because muscles initially seem to hypertrophy even without the addition of satellite cells this could imply that mTOR pathway has a significant role to play in intially muscle hypertrophy, the addition of satellite cells has an effect on long term muscle hypertrophy. This indicates that the mTOR pathways might also have a threshold
what happens to Akt when muscle is hypertrophyed
it causes increase Akt and phosphorylated Akt increase
what is local IGF-1 called
mechano-growth factor
