Another write-up from Brad.. I enjoy that his interest is purely in terms of hypertrophy, good to see someone avidly exploring the topic and doing actual studies

"How long should you rest between sets for hypertrophy?"

His write-up on his site:

http://www.lookgreatnaked.com/blog/how-long-should-you-rest-between-sets-for-hypertrophy/

The actual literature review:

http://www.ncbi.nlm.nih.gov/pubmed/25047853

His conclusion: "In conclusion, the literature does not support the hypothesis that training for muscle hypertrophy requires shorter rest intervals than training for strength development or that predetermined rest intervals are preferable to auto-regulated rest periods in this regard."

One interesting study he cites is here: http://www.ncbi.nlm.nih.gov/pubmed/16095405

- It notes no difference in muscle CSA in groups resting either 2 vs 5 minutes, over a span of 6 months.

Irrespective of these, Brad also notes: "That said, the paucity of controlled studies on the topic make it difficult to draw concrete conclusions. Certainly we know that shortening the duration of rest between sets increases metabolic stress, which is known to stimulate muscle remodeling. We also know that well-trained individuals such as bodybuilders are able to sustain a high percentage of their repetition maximum with rest periods as short as a minute. Could the combination of these factors may provide an additional hypertrophic stimulus — albeit a small effect — over time in well-trained subjects? Could other factors such as increased hypoxia and cell swelling also contribute to such a response?"

And again, as I said what's exciting, he's trying to elucidate on these things.

Irrespective of the conclusion, I sincerely doubt for PURE mass, a group resting 4-5 mins vs a group resting 60-90 secs would have the same results, for the exact reasons he outlined - more robust metabolic stress looking from a mechanistic perspective

Hmmmm

http://www.sciencedaily.com/releases/2014/07/140711153329.htm

Apparently a meta analysis of some 343 studies shows that, indeed, organic foods are nutritionally superior.

Of course, through all that processing or gmo etc., the foods going to lose some nutrients and be inferior. However usually the food gets fortified with extra nutrients.

At least this is what I thought.

i remember hearing a looong time ago on TV that frozen vegetables were better than fresh, nutritionally..have no clue if that true or not though.

"Hypercaloric diets with increased meal frequency, but not meal size, increase intrahepatic triglycerides: A randomized controlled trial"

http://onlinelibrary.wiley.com/doi/10.1002/hep.27149/full

Study notes that through increasing meal frequency, there's an augmented propensity to store more highly deleterious liver (hepatic) fat.
This is something I talked about in the article on fasting - the ramifications of chronic mTOR stimulation, even in the "healthy" lifestyle groups, and how it's certainly not nearly as healthy as other interventions. Well, here's at least some preliminary proof.
For health, fasting >>
and until a study can actually note a difference in hypertrophic outcomes between a 16hr (or so, just arbitrary) fast group and a typical "bro" meal freq (aka 6-8), there's no reaso to think there should be.

Doesn't that kind of support lean bulking with IF?

Also it's kinda hard to eat so much in a small time frame IMO.

hepatic TG storage is more of a general health problem than a body composition problem. a fatty liver becomes vulnerable to inflammation and scarring damage

Ahh okay so it's on your insides (liver) compared to under your skin.

yeah

"Beta-2 Adrenergic Agonists Enhance Intracellular Calcium Signaling in Pancreatic Beta Cells"

http://professional.diabetes.org/Abstracts_Display.aspx?CID=55209

Maybe I was being naive before, but I was denoting the catecholamines, period, to inhibit insulin secretion, yet cause glucagon secretion. Apparently the beta 2 adrenergic receptors cause both?

It's also interesting that the beta 2 adrenergic receptors causes increase in cytosolic Ca2+.. the canonical b2 signaling pathway is the alpha subunit dissociation --> adenylyl cyclase --> cAMP --> PKA & Epac proteins --> CREB and other effectors

However, I know the beta-gamma subunits dissociate and activate other pathways like PLC-beta, and different channels such as Ca2+ specific ones, even some tyrosine kinase signaling. Tbh I guess this secondary signaling explains the increase in cytosolic Ca2+.. it's just that the beta-gamma subunits are usually so rarely talked about in signaling I didn't think they contributed enough to matter, or under a specific condition (such as this?). Interesting. I need to revisit my lit review on Norepi signaling and modulation of T cells then.. this would explain certain MAPK signals.
I guess this means the alpha-1 adrenergic receptor also stimulates insulin secretion then, as it's Gq coupled and thus activates PLC --> PIP2 --> IP3 & DAG --> Ca2+ , CaMK , PKC, calcineurin.

These are just random thoughts, I was just surprised because I always think: sympathetic nervous system signaling = insulin secretion inhibited.
However, it may still require a strong impetus from glucose or other incretins to ACTUALLY release the insulin, and this will just potentiate it, perhaps.