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Sibiriak, recently I listened again to PEter Attia's interview on Steam talk, and it's confirmed his suggestion to take 5 grams of pure Leucine during workouts, in an attempt to keep the protein intake moderate.


As a matter of fact, that way he may make sure (probably) to trigger the cascade related to the Leucine + amminoacids signal via the RagGTPases.


In theory, we still need other amminoacids plus the necessary quantity of protein for new muscle tissue synthesis, the translational phase after the activation of mTOR.


Plus of course we need the mechanic signaling via mechanoreceptors→PI3K→PIP3→Akt, AND/Or the insulin/IGF-1 signal thru the same cascade  PI3K→PIP3→Akt and opther cascades, plus a favourable energetic environment trru the AMPK cascade.

Some other articles underline that the mechanoreceptors act thru LPD via phosphatidic acid, in a IGF-1 independent way.


That's why the bodybuilders like to overkill it, just to make sure not to forget about any of the numerous signals triggering MPS (muscle protein synthesis):


  • Pure BAAS intake (leucine signalling) while and before workout
  • Amminoacids (post workout meal)
  • Amminoacids (numerous proteic meals to make sure the translational process doesn't miss the raw material)
  • Insulin-IGF1 (simple sugar in the post workout meal together with amminos)
  • AMPK neutralization (simple sugar in the post workout meal together with amminos)
  • AMPK neutralization by Rest and recovery, avoiding excessive aerobic activitity
  • Proper training procedures to maximize the mechanoreceptors cascade

They also take numerous some targeted supplements like fosphatidic acid, insulin, various growth factors and hormones, androgens, sterodis. Not to speak about the diuretics needed to look extra shredded on contest days and who knows how many other chemical concoctions.


By applying all the above, they apply a faustian bargain as we know since most probably healthspan and longevity are compromised.

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In a CR framework, things are more complicated since we cannot overkill.


Keeping protein moderate may fail to provide the raw material needed for MPS. An extra amount from basic requirements is needed so we have here a double unknown, minimum requirement itself and MPS requirement.


In a CR or PR (protein restriction) framework, we automatically tend to inhibit the energy supply, so activating AMPk which inhibits mTOR amplification.


It still may be that skeletal muscle stimulation deroutes nutrients to muscle tissue, but it's all too evident that a systemic effect is almost unavoidable, since bodybuilders typically go thru periods of bulking (gaining muscle mass + fat mass in occasion of mTOR amplification) and pre-contest dieting, activating AMPK and loosing fat+some muscle mass in the process.


The only way we can try and boost mTOR activity in a CR context is by proper mechanical stress, which should also be optimized not to increase AMPK.


Maybe it's just impossible to grow muscle mass during CR.


Dr. Peter Attia is trying some CR mimetics, but he didn't provide detailed reports about such results as related to MPS. His energy ratio is still 20% protein, which is not little and his 20% carbs may be enough to provide sufficient IGF-1/insulin signaling, since he sure provides mechanical signaling.


My bottom line is that growing muscle by keeping systemic mTOR underamplified and local mTOR (muscles) overamplified may just be a chimaera.

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A very interesting review of the molecular issues of MPS is the following article, which sure deserves further discussion. Myostatin, SRF, other aspects are discussed which I didn't find in other articles. the article may also have been listed by Al Pater in his threads on CR literature.


Molecular Mechanisms Controlling Skeletal Muscle Mass
Kunihiro Sakuma1 and Akihiko Yamaguchi2

[1] Research Center for Physical Fitness, Sports and Health, Toyohashi University of Technology, 1-1 Hibarigaoka, Tenpaku-cho, Toyohashi, Japan

[2] Department of Physical Therapy, Health Sciences University of Hokkaido, Kanazawa, Ishikari-Tobetsu, Hokkaido, Japan

Abstract: The interplay between multiple signaling pathways regulates the maintenance of skeletal muscle. Under physiological conditions, a network of interconnected signals serves to coordinate hypertrophic and atrophic inputs, culminating in a delicate balance between muscle protein synthesis and proteolysis. Loss of skeletal muscle mass, termed “atrophy,” is a diagnostic feature of cachexia such as cancer, heart disease, and chronic obstructive pulmonary disease. Recent studies have further defined the pathways leading to gain and loss of skeletal muscle as well as the signaling events that induce post-injury regeneration. In this review, we summarize the relevant recent literature demonstrating these previously undiscovered mediators governing anabolism and catabolism of skeletal muscle.


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