It's been established that the rate of synthesis is higher when Cho consumed immediately post exercise but the more applicable questions are whether or not this results in different absolute storage over a more relevant time frame and whether or not the increased rate of resynthesis leads to improvements in performance during secondary bouts of glycogen depletion exercise, ie multiple, hour long sporting events sequentially

E: what I'm suggesting is that in the scope of our exercise on this forum (weightlifting) where we only exercise for an hour bout each day, absolute glycogen synthesis may not really be different after a 24 hour period whether or not you consume Cho immediately post or not

This post was edited by cloudkicker on May 10 2014 10:56am

So basically you temporarily have more glycogen?

Does the depletion and regeneration of glycogen do anything other than refuel you?

This post was edited by tommyd323 on May 10 2014 11:16am

Just some proof high reps > low reps for hypertrophy http://www.ncbi.nlm.nih.gov/m/pubmed/20711498/

Instead of seeing a steadily increasing, plateauing, and then decreasing synthesis rate you see an anormally high synthesis rate that tapers off over time. So greater synthesis rates at the onset of recovery that approach normal rates over time.

If i had to speculate I would say greatly increased g6p concentrations in the myocyte stimulate massive glycogen synthesis because you have combined uptake effects of insulin from the meal consumption and also calcium mediated translocation of glut4 transporters to the cell membrane as a result of exercise. Both of these serve to increase glucose uptake by the myocyte and a massive flux through glycogenesis is the result.

"Evidence-based recommendations for natural bodybuilding contest preparation: nutrition and supplementation"

http://www.jissn.com/content/pdf/1550-2783-11-20.pdf

Alan Aragon is also a part of this

Already read it, way ahead of u haha, too many things they advise just to be on the safe side in my opinion, when they even say there's no evidence for the advantage of it.

hey

I'm looking for articles about anxiety, depression, medication, how the brain works under stress etc

thanks

its all bullshit

"Irisin stimulates muscle growth-related genes and regulates
adipocyte differentiation and metabolism in humans"

http://libgen.org/scimag/index.php?s=10.1038%2Fijo.2014.42

Eh.. what are you interested in specifically? How the brain works under stress is probably much different than depression, and generally, meds for anxiety vs depression will be different, and the disorders themselves are generally different (ie amygdala vs hippocampus or other regions). Narrow your selection or just ask a question and I may be able to answer.



As for this;

- Irisin/FNDC5 (irisin precursor) is upregulated during muscle differentiation
- Irisin increased IGF-1 levels and decreased myostatin levels, in a dose-response relationship
- Irisin increased PGC1-alpha 4 isoform, which is known to boost IGF-1 and decrease myostatin.. so it seems unclear whether or not Irisin itself can induce the changes in IGF/myo, or whether it simply activates the Isoform of PGC-1 alpha, which subsequently causes the changes. It doesn't seem to work through the PI3k - Akt - mTOR pathway, but an ERK one.
- Exogenous use of Irisin eventually downregulates/attenuates PGC 1 alpha and FNDC5 levels, suggesting a feedback loop, much like injecting test or thyroid hormones
- Inhibits adipogenesis --> inhibits lipid accumulation, PPAR-gamma, Fatty acid synthase, and adipocyte protein 2
- Inhibits adiponectin expression from adipocytes, which I find odd.
- Induces genes for mitochondrial biogenesis and "browning" of WAT through increasing fat energy expenditure PGC, UCP1, etc). Also upregulates genes for lipid and glucose metabolism (GLUT4, HSL, PPAR-alpha, etc)
- Despite all this, Irisin ostensibly decreases lipolysis. May be through an overall smaller amount of fat to be liberated from the irisin treatment though (increases HSL and ATGL, whilst decreasing FAS)
- Irisin probably exerts its effects via autocrine/paracrine means, like other myokines
- In vitro - needs more studies, but may be promising



Be careful at looking at only the acute protein synthesis rates and measures of anabolism immediate PWO.
I posted a study or two that found no correlation between acute measures of protein synthesis, and longer term hypertrophy