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CR / IF + BCAAs (leucine) ?


sirtuin

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I'm curious what the group's opinion is on using supplemental branched chain amino acids (leucine in particular) to limit the catabolic effects that calorie restriction and fasting have on muscle tissue.

 

With intermittent fasting / calorie restriction I believe growth hormone is elevated, which is itself implicated in certain cancers.  I believe that the drop in mtor / igf-1 might provide some protection against this in the context of calorie / protein restriction.  However, I'm not sure what the effect is when supplementing branched chain amino acids / leucine, which strongly activate mtor/igf-1, over the rise in growth hormone produced with CR / IF.

 

Is supplementing BCAAs / Leucine a smart hack around the catabolic effect of CR / IF on muscle tissue, or does this negate the anti-aging benefits and introduce new risks?

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Since Leucine increases IGF-1 (at least in skeletal muscles [1]), and the IGF-1 pathway is pretty strongly implicated in the beneficial effects of CR, I'd be reluctant to supplement with leucine or other branched chain amino acids for fear of negating the beneficial effects of CR.

 

--Dean

 

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[1] The FASEB Journal vol. 29 no. 1 Supplement 819.2, April 2015

 

L-Leucine Increases Skeletal Muscle IGF-1 Peptide But Has No Effect on Akt/mTOR Signaling in Response to Resistance Exercise in Trained Men

 

David Church1, Neil Schwarz3, Mike Spillane3, Sarah McKinley2, Tom Andre2, Jeffery Stout1, Jay Hoffman1 and Darryn Willoughby2
 

http://www.fasebj.org/content/29/1_Supplement/819.2.short?related-urls=yes&legid=fasebj;29/1_Supplement/819.2

 

Abstract
 
Background: Leucine ingestion following resistance exercise (RE) increases muscle protein synthesis via mammalian target of rapamycin complex 1 (mTORC1) at a dose of 3g. It has also been shown that skeletal muscle (SM) IGF-1 activates mTORC1. It is plausible that leucine can increase SM IGF1, elucidating another mechanism in which mTORC1 activity might be up-regulated.
 
 Purpose: The effect of a single threshold dose of L-leucine given immediately after RE on serum leucine and IGF1, and SM IGF1, IGF1 receptor (IGF1R), Akt, mTOR, and p70S6K.
 
 Methods: 9 resistance-trained men performed two separate testing sessions of 4 sets of 8-10 reps at 75-80% 1-RM on the angled leg press and knee extension exercises. Immediately after, 3g of L-leucine (LEU) or placebo in the form of gelatin capsules was ingested. Venous blood was obtained before, 0.5-, 2-, and 6-hr post-exercise, and a muscle biopsy obtained before, 2- and 6-hr post-exercise. A repeated measures ANOVA (treatment x time) for each criterion variable was performed.
 
 Results: Increases were noted in serum [leucine] in LEU group (p=0.04), muscle IGF1 at 2-hr (p=0.03) and 6-hr (p=0.04), with no changes observed in serum IGF-1 (p=0.99), IGF-1R (p=0.84), Akt (p=0.55), mTOR (p=0.09), and P70S6K (p=0.98).Conclusion: 3 g of L-leucine following a RE session does not appear to influence serum [iGF1] or mTORC1 signaling, but did preferentially increase IGF1 peptide content in SM.
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