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Nutrition Leucine

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Or isn’t this the other way - genetics for your habbits in early childhood already.

Based on my understanding on the studies on the matter, no.

Without a doubt there is some kind of genetic predisposition towards athleticism. I'm sure that will encourage a child to partake in sports etc.

However, the nervous system etc of a child develop at an age where they do not, for example, actively compare themselves with others, and the development happens in part based on the behaviour of the children. They play, and they should play hours upon hours every single day. Encouraging this play and providing various opportunities for it develops athletes. I stress that a lot of this development happens quite early.

A child can grow in the country, play outside for hours a day, climb trees, jump on rocks, swim, run, tumble, wrestle, etc. As a negative example take a child with overprotective parents, no chance for outside play, no chance for inside play, just staring at screens for all day. Comparing these two extreme examples, I don't think genetics get to say a lot between these two.
 
Is there a huge difference in effect between taking bcaa vs whey? Say take some bcaa at noon, whey at 4pm, eat at 8pm. Or whey at noon, bcaa at 4pm, eat at 8pm. Or straight up bcaa at noon and 4pm and have a meal and whey at 8pm.
 
Any guesses? Insulin.

@Snowman great post. I made Kenny the below question before, maybe you have an idea how insulin and mtor (or muscle growth) are related?

I have a question maybe you can help me with. Do you know if total calories and insulin response play a part in mtor? In other words: is it the same to eat 3 grams of leucine in a 1000 calorie meal, including a bunch of carbs that trigger insulin, compared to a 3 gram dose of leucine in BCAA format?

I have this doubt because I ate very little protein for a few years, and muscle mass was not all that different from when I do eat protein. I eat mostly fruit and veggies then. So maybe the insulin response makes muscles grow to some degree?
 
@Oscar.....taken from the leucine research paper quoted originally:

"We were surprised that the standardized breakfast (6 g protein, 60 g carbohydrate, and 11 g fat) resulted in a significant FSR increase. We can only speculate about the reason for this, taking into account that the FSR increase is a result of increased incorporation in muscle proteins of available AAs from the precursor pool. In our study, the protein-bound enrichment in muscle noticeably increased in both groups, but reached higher levels in the test group. An increase in protein-bound enrichment was observed in other studies after a bolus of protein (33, 44), but to a lower extent also after carbohydrates with fat (i.e., no protein, with an insulin peak of 51 mU/L) (33). This suggests that insulin and AAs are both contributing factors. In our study, the plasma precursor pool may have been slightly influenced by the larger protein amount in the test product. From these analyses, we can speculate that the muscle protein synthetic response in the control group was a result of a combination of the insulin response—related to the provision of carbohydrate—and the small amount of AAs from the breakfast. Because our subjects were not sarcopenic and insulin resistant, it is possible that the sensitivity of muscle protein synthesis to even a low amount of protein, such as in the breakfast in combination with a high insulin response, was able to increase muscle protein synthesis."
 
@Oscar.....taken from the leucine research paper quoted originally:

"We were surprised that the standardized breakfast (6 g protein, 60 g carbohydrate, and 11 g fat) resulted in a significant FSR increase. We can only speculate about the reason for this, taking into account that the FSR increase is a result of increased incorporation in muscle proteins of available AAs from the precursor pool. In our study, the protein-bound enrichment in muscle noticeably increased in both groups, but reached higher levels in the test group. An increase in protein-bound enrichment was observed in other studies after a bolus of protein (33, 44), but to a lower extent also after carbohydrates with fat (i.e., no protein, with an insulin peak of 51 mU/L) (33). This suggests that insulin and AAs are both contributing factors. In our study, the plasma precursor pool may have been slightly influenced by the larger protein amount in the test product. From these analyses, we can speculate that the muscle protein synthetic response in the control group was a result of a combination of the insulin response—related to the provision of carbohydrate—and the small amount of AAs from the breakfast. Because our subjects were not sarcopenic and insulin resistant, it is possible that the sensitivity of muscle protein synthesis to even a low amount of protein, such as in the breakfast in combination with a high insulin response, was able to increase muscle protein synthesis."
Thanks Ali. Right under my nose. I'll read that paper in detail.
 
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how insulin and mtor (or muscle growth) are related?
@ali to the rescue (which is good, his answer is more specific than mine). I just know that mTor is activated by both insulin and protein. In someone who is eating discreet meals and either A) is insulin sensitive or B) eating low enough carbs that they can mimic insulin sensitivity, then mTor is turned on and then off again throughout the day. For someone with hyperinsulinemia (they have high insulin levels all the time) then their mTor pathway is going to look like the sad little cancer mice. But they'll still probably die of something else (i.e. heart disease) before the cancer gets them.
It's worth pointing out that all mTor activation is not equal; we have to look at the context in which it happens. Both the protein and insulin are activating a variety of other pathways beside just mTor. So mTor activation in the context of just protein vs. just insulin vs protein+insulin are all going to look a little different. An issue we see with this sort of science is that we often place a lot of importance on the thing that we kind of understand. We assume that, because we're familiar with it, it must be super important. There are a variety of pathways besides mTor that are doing lots of things, and while we can use our understanding of the mTor pathway to improve our understanding of the system, we can't place it on a pedestal. I digress...

To answer your question, @Oscar, I think studies like this as well as the experience of many athletes and coaches (including yourself) tell us that you can maintain muscle mass reasonably well on a lower protein diet, but it can be difficult to build muscle. We see this on low protein/high fat diets (like classic keto) as well as low protein/high carb diets. It seems reasonable to me to say that part of the reason why you can maintain mass on a high carb diet is due to mTor activation via insulin. I'm less sure what the mechanism might be with something like keto, but it may still have to do with insulin, in that a high degree of insulin sensitivity might allow mTor to be activated by the small amount of insulin that is released in response to protein. I'm not sure if better tissue insulin sensitivity actually translates to better mTor activation, so that's just me thinking out loud. Again, I think we have to recognize that there are going to be a multitude of other pathways being activated as well.

It's worth recognizing, in light of the various dietary practices followed by everyone here, that at least a moderate levels of carbohydrate and high levels protein are needed for someone looking to maximize muscle growth. There are a variety of other contexts in which we can increase muscle mass, but the process is going to be slower if you're restricting one of those macronutrients. As tends to be the case with most basic science discoveries, our understanding of mTor supports this idea that we have long known based on accumulated experience.
 
Not to resurrect a sleeping thread, but a couple of more variable that I would consider in this conversation.

Dr. McGill coined, at least for me, a wonderful expression, "self-selecting." It's in one of his book with pictures of Tour de France riders, and the explanation - I'll paraphrase - that just because that group of 150 people can have healthy spines after pedaling with flexed lumbar spines for 7 hours a day doesn't mean it's a healthy activity, it just means you're looking at the people for didn't get injured, the survivors and thrivers. I think it's an important thing to keep in mind when looking at any profession- or sport-specific group of people.

The other things is that, for the survivors and thrivers, we know that volume is a key factor in muscle hypertrophy. If you do something that takes enough muscle to do, and you do it enough, and you survive/thrive, your muscle will likely grow to meet the demands you've placed upon them. But this is a formula - enough of the right kind of physical tasks, plus the right genetics, plus sufficient nutrition, plus sufficient rest.

Just my very amateur opinion as a mid-60's aged 150 pounder. I can tell you that, when I do the Rite of Passage, my arms and shoulders get bigger.

-S-
 
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