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Does Exercise STOP the Effect of Fasting - Thomas DeLauer
mTOR
mTOR responds to signals from nutrients, growth factors, and cellular energy status and controls cell growth and proliferation based on this (by regulating protein synthesis)
In other words, whenever we have an increase in nutrition (mainly protein) and calories we essentially tell the body that plentiful times are here - our cells increase their working capacity and ATP production is increased
Cells increase division and we are then primed for growth and repair - mTOR is the protein that senses this
It’s important to realize that mTOR is neither good nor bad, but too much or too little can have negative consequences
You see, mTOR increases energy production, but also creates more junk products
Autophagy is the process that degrades these junk products, but it is only usually active when mTOR is decreased
The Good & Bad of mTOR Activation
The Good
mTOR activation allows us to put on more muscle (and fat) and we
increase various hormones such as IGF-1
mTOR increases ATP production and creates new mitochondria - it also increases mitochondrial metabolism (by activating PGC1a)
The Bad
Too much mTOR activation, however, contributes to a large number of human diseases, including cancer, obesity, type 2 diabetes, depression and neurodegeneration
Balance
A study published in the journal Cell Metabolism found that too little mTOR activation can be equally as bad as too much
The study found (in rats) that too little mTOR activity actually harms the liver - mice were fed an excess calorie diet, but given rapamycin to induce autophagy
Researchers found that persistent suppression of mTORC1 activity in the liver leads to low-level inflammation that is enhanced by feeding a HFD
Hepatocytes bearing deficient mTORC1 activity are less competent to cope with oxidative stress and other inflammation-related insults
Note: HCC is the fifth most common cancer subtype worldwide, with a median survival of 6–16 months after diagnosis
Persistent elevation of hepatic mTORC1 activity in the setting of overnutrition and obesity, or conversely, protracted suppression of mTORC1 activity induced by rapamycin and related drugs, sets in motion a spiraling sequence of pathologic events that promotes HCC.
Autophagy
The opposite side of the mTOR coin is the repair and recycling system - it’s activated with the mTOR switch is turned off
And, as we know, the main process that carries out repair and recycling in our cells is called autophagy
Autophagy is the mechanism our cells use to recycle damaged proteins and cell machinery (including mitochondria) and use their parts to make new machinery and new sources of energy - recycling old cellular machinery helps protect a cell from premature aging
Autophagy allows your cells to recycle used material for use as energy during stresses such as fasting, instead of breaking down valuable things such as muscle - preventing catabolism (breaking down) of muscle is always a good thing
Autophagy occurs at a low basal level in virtually all cells, being important in protein and organelle turnover - however, it may be up-regulated in times of need
When mTOR goes up, it shuts down autophagy - mTOR is sensitive to dietary amino acids (protein)
Fasting & Working Out
Journal - Autophagy
Fasting increase autophagy (as does caloric restriction and certain foods; EGCG, ginger, curcumin, etc.)
Explains that resistance training activates mTOR (as does protein, excess calories, IL-6, testosterone, etc.)
References
1) Jung CH , et al. (n.d.). mTOR regulation of autophagy. - PubMed - NCBI. Retrieved from
2) mTOR Pathways in Cancer and Autophagy. (n.d.). Retrieved from
3) Glick D , et al. (n.d.). Autophagy: cellular and molecular mechanisms. - PubMed - NCBI. Retrieved from
4) Autophagy fights disease through cellular self-digestion. (28, February). Retrieved from
5) Autophagy fights disease through cellular self-digestion. (28, February). Retrieved from
6) Resistance exercise initiates mechanistic target of rapamycin (mTOR) translocation and protein complex co-localisation in human skeletal muscle. (n.d.). Retrieved from
7) Short-term fasting induces profound neuronal autophagy. (16, August). Retrieved from
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