I changed my mind on this lol.
After trying to put it together, I couldn't find enough true aspects of it.. ESPECIALLY in regards to resistance training. Quite abstruse
It boils down to;

Sympathetic overtraining - occurs first.. leads to sympathetic nervous predominance. You have an increase in circulating epi/norepi, but a decrease in beta receptors, thus decreased catecholamine sensitivity. You then have subsequently decreased performance

Parasympathetic overtraining - occurs last.. it's PSNS predominance. You have decreased CNS drive, decreased hypothalamic-pituitary action/drive, both decreased epi/norepi and beta receptors, and lower overall energy availability.

It seems before true manifestation, there's a change in acute hormonal responses, before the resting levels begin to shift.
There's overall HPA axis alterations and thus decreased ACTH, GH, LH, and FSH.

There also seems to be differences in neurotransmitters.. this is one of the abstruse aspects I talked of.. it's more well known in endurance OT than resistance. In resistance however, it seems that hippocampal serotonin is inhibited/not sensitized to release from the chronic stress.. this also downregulates the HPA axis.
Further, this next bit is a bit of an extrapolation on my part but meh.. in the mesencephalon (midbrain), is the raphe nucleus, which is the major region of serotonergic neurons, which innervates the hippocampus. The raphe nuclei also heavily innervate the locus coeruleus, which is the main site of norepinephrine secreting neurons. So, if the hippocampal serotonin is decreased, it stands to reason that a lot of the decrease in sympathetic drive stems from the raphe nucleus.. and thus serotonin may play a large role in overtraining.

second link doesn't work...

"Are you synched with your CHRONO? Chrono, the last piece of the circadian clock puzzle?
All organisms, from mammals to fungi, have daily cycles controlled by a tightly regulated internal clock, called the circadian clock. The whole-body circadian clock, influenced by the exposure to light, dictates the wake-sleep cycle. At the cellular level, the clock is controlled by a complex network of genes and proteins that switch each other on and off based on cues from their environment.
Most genes involved in the regulation of the circadian clock have been characterized, but Akihiro Goriki, Toru Takumi and their colleagues from RIKEN and Hiroshima University in Japan and University of Michigan in the United States knew that a key component was missing and sough to uncover it in mammals.
In the study, the team performed a genome-wide chromatin immunoprecipitation analysis for genes that were the target of BMAL1, a core clock component that binds to many other clock genes, regulating their transcription.
The authors characterize a new circadian gene that they name Chrono. They show that CHRONO functions as a transcriptional repressor of the negative feedback loop in the mammalian clock: the protein CHRONO binds to the regulatory region of clock genes, with its repressor function oscillating in a circadian manner. The expression of core clock genes is altered in mice lacking the Chrono gene, and the mice have longer circadian cycles.
"These results suggest that Chrono functions as a core clock repressor," conclude the authors.
In addition, they demonstrate that the repression mechanism of Chrono is under epigenetic control and links, via a glucocorticoid receptor, to metabolic pathways triggered by behavioral stress.
These findings are confirmed by another study by the University of Pennsylvania, also published in PLOS Biology today. In the study, John Hogenesch and his team prove the existence of Chrono using a computer-based analaysis."

Very nice. More advancement/understanding.

http://www.bodyrecomposition.com/fat-loss/another-look-at-metabolic-damage.html

Lyle McDonald on "metabolic damage"

http://www.alanaragon.com/an-objective-look-at-intermittent-fasting.html

Alan Aragon on IF

"Differential Muscle Hypertrophy Is Associated with Satellite Cell Numbers and Akt Pathway Activation Following Activin Type IIB Receptor Inhibition in Mtm1 p.R69C Mice"

http://www.sciencedirect.com/science/article/pii/S0002944014001849

JUst in case you didn't realize, the Activin Type 2 receptors are what myostatin binds to.
The differential effects and corresponding to satellite cell number is pretty cool though



http://www.ncbi.nlm.nih.gov/pubmed/17627483

This is insane lol..
" low concentrations of 2,4-dinitrophenol (DNP) upregulate neuronal cAMP and tau levels, promote neurite outgrowth and neuronal differentiation and block the oligomerization and neurotoxicity of Abeta."

brb DNP (low dose) is good for your brain
Had to briefly look into that tbh. It signals through ERK and controls transcription of a few hundred genes. Unexpected to say the least

This post was edited by Balla on Apr 19 2014 02:16pm

http://www.bodyrecomposition.com/muscle-gain/reps-per-set-for-optimal-growth.html

i tot dis was interderasting

cliffs: 5-8 reps

This is great



Disagree on a few points, but Alan is of course only looking at studies that may have examined the issue
The major benefit of IF for me, is appetite control, for instance.
I also profoundly disagree with the notion put forth about breakfast.. especially the cognitive function. For me personally, breakfast makes me much sloppier/lazier in general and slows down my cerebration/cognitive function, without a doubt.
I think there's a lot of variables with the breakfast issue though.. such as they'd typically look at epidemiology and find correlations between populations. That can sometimes be fallacious, as is seen with the evidence for eating more frequently vs fewer meals, and the higher frequency eating tends to be leaner/healthier.. clearly asinine physiologically, but that's the "trend".
I also think not enough "health" benefit was touched on from chronic IF. He did talk about blood lipids, neuroprotection (of which is also largely mediated by GDNF, not ONLY BDNF), and insulin sensitivity, however there's probably more. Fasting will obviously lower insulin secretion and increase glucagon secretion.. one, lower insulin pathways/fasting will induce FOXO pathways (from Akt not being activated), which binds to IREs and upregulates PGC1alpha as well as upregulating transcription of several antioxidant genes. The glucagon response augments (through CREs) the PGC1alpha expression and these lead to increased mitochondrial efficacy/function and greater antioxidant capacity. You also have an increased AMPK response from short term fasting. Unfortunately, I didn't even realize the time and I have to go.. later tonight or tomorrow now I want to go into more detail into AMPK and Sirtuin expression and benefits of (and how it applies to short term fasting).

Eh, lyle keeps trying to push the explosive strength as the biggest contributor to hypertrophy for a very long time. Still, the evidence is stacked against him.

So you believe around 12-15 is best for hypertrophy right? Like sarcoplasmic hypertrophy? But isn't there way less sarcomeres than myofibrils in the muscle or am I confused? I just want your reasoning.