P-ratio

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DwayneJohnson

New Member
So I'm very intrigued by this concept of partitioning ratio. I'm not the sharpest dude so I have to be honest I do tend to get lost in some of the scientific explanations from bryan or totentanz but I would love to get input on the following questions:

1) What sort of partitioning ratio does a genetically average male, age 30 and ~15% bodyfat have? In other words, suppose my maintenance calories (factoring in HST lifting) is 2200 calories and I add 500 calories to gain weight, so I eat 2700 calories per day. Over the course of 1 week, I will have overeaten by 500 x 7 days = 3,500 calories which is 1 lb of bodyweight. Of this 1 lb of bodyweight, how much can I hope to see go into muscle? and into fat? is is 70% muscle / 30% fat? better? worse?

2) I realize that factors affecting the p-ratio have been somewhat covered in the books but if you could just simplify things a bit for me and highlight the 3 or 5 most important things to do in order to maximize my p-ratio, what would you say they are?

Thanks again.
Dwayne
 
1: Tough to really say, as it is basically down to individual genetics. Also depends on training age and how close you are to your genetic limits. Obviously a newb will be able to gain more muscle compared to fat than a seasoned pro who is trying to eke out what little gains are left to him. 70:30 is probably a good ratio to plan on but again, it depends. At your size, you can probably make some pretty good muscle gains in comparison to fat still. A 1:1 ratio seems most common.

2:
1. Lifting weights improves partioning and is going to have the largest impact of anything you can do with regard to this.
2. Adequate protein consumption. Consuming more protein alone without even lifting already stimulates protein synthesis, though admittedly nowhere near the level of lifting.
3. Creatine can help a bit, it is a proven supplement. Just don't expect steroid like gains off of it, it is, however, something that will provide a consistent, small improvement in overall performance and growth.
4. Anabolic steroids improve p-ratio significantly, however depending on where you live, these can be highly illegal and so for the purposes of this discussion, not really relevant.
5. Some evidence indicates that bulking over 15% bodyfat may have a slightly negative impact on p-ratio.
 
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Apologies for bumping an old thread (thought it would be better than starting a new one)

In @Totentanz reply above he mentions that when bulking over 15% body fat there maybe a negative impact on a persons P-ratio, I assume that when dieting there will also be a threshold where if you fall below that body fat % there would also be a negative impact on P-ratio, just wondered where that is likely to happen.
 
It depends on the individual. If you were naturally lean before you started lifting, it might be as low as 8%. For many, it will probably be more like 10% or even 12.
 
Totentanz said:
It depends on the individual. If you were naturally lean before you started lifting, it might be as low as 8%. For many, it will probably be more like 10% or even 12.
Click to expand...

Thanks for that, I had assumed it was somewhere around 10-12% which is why now I will only bulk to say 15% and cut to no lower than 12% as this is probably low enough for someone nudging 50 - currently sitting at 14.4% according to a BodPod subject to the 'standard error of measurement'
 
I think you can safely bulk to 18-20% without worrying too much about it. But it doesn't really matter that much. The impact on p-ratio from getting too fat isn't terribly clear whereas the consequences of going too lean are well known.

It's important to keep in mind that p-ratio changes (for the worse) as you grow older and also as you become more advanced as a lifter.
 
Is there any way you can calculate, measure or determine your p-ratio. This would be really helpful when setting goals for a cycle in terms of muscle vs weight gain.
 
I would have thought the only true accurate method would be to have your body fat levels taken regularly by one of the following methods

Dexa scan

Hydrostatic Weighing

BodPod

Other than the above you could get a professional to use Harpenden calipers to ascertain body fat

Problem with all of this is the cost for regular testing.
 
Luke matthews said:
Is there any way you can calculate, measure or determine your p-ratio. This would be really helpful when setting goals for a cycle in terms of muscle vs weight gain.
Click to expand...

Here's the thing about the P-ratio. It constantly changes as the amount of muscle and fat (and activity level) you have on your body changes. Think of it this way, lets say you have a large sink with three drains. One drain goes to muscle, another drain goes to fat, and the last drain literally goes down the drain not to be seen again. Now, your P-ratio is the ratio of the size of the drains in your sink. People who carry a lot of fat have a large fat drain. When you dump a bucket of water in the sink, water goes down all drains, but more water goes down the fat drain by virtue of its size. The same is true for a person with a large muscle drain and small fat drain. Water goes down both drains but more goes to the muscle drain because its bigger.

As you can imagine, as a person who is fat begins to diet away the fat, their fat drain shrinks and can't drain as much water. Likewise their P-ratio will slowly shift. Same holds true for gaining weight. At first, a lot more water drains down the muscle drain "relative" to the fat drain. But the more you overeat, the larger the fat drain becomes so more water ends up diverting to the fat drain. Its not that the muscle drain gets smaller, its just that the fat drain gets bigger.

And like Totentanz said, genetics plays a role in how big each of your drains is to begin with. And as he also said, the most effective way to shift your p-ratio to favor muscle is to increase energy expenditure while weight training. This makes the fat drain shrink and enlarges the muscle and activity drains so you can eat more and gain less fat.
 
Awesome analogy, Bryan! I would point out, though - that when you are really lean - the body seems to be primed for fat gain moreso than muscle gain, but this is obviously a function of the varying degree of suppression of the HPTA and thyroid from extended dieting and single digit bf%

I also think, despite some of the current reductionistic belief, that nutrient timing becomes more important as you get leaner and more muscular - i.e. for the muscle sink to get preferential access to the bucket of water you should be placing a substantial amount of the daily food allotment in the 0-6hr period after a strenous workout.

I know you suggested in the past to have protein only post-workout, followed by carbs 30mins later to ensure a higher peripheral amino acid utilization - do you still think this is a viable idea?

There could potentially be benefits to a higher-than-optimal protein intake as well, if you want to limit fat gain in a surplus - Antonio et al. have suggested in various research the last couple of years that you can have a higher surplus with 3g/kg protein intakes - through TEF mostly. Thoughts about this?
 
Blade said:
Awesome analogy, Bryan! I would point out, though - that when you are really lean - the body seems to be primed for fat gain moreso than muscle gain, but this is obviously a function of the varying degree of suppression of the HPTA and thyroid from extended dieting and single digit bf%
Click to expand...

Excellent point, and absolutely true.

Blade said:
I also think, despite some of the current reductionist belief, that nutrient timing becomes more important as you get leaner and more muscular - i.e. for the muscle sink to get preferential access to the bucket of water you should be placing a substantial amount of the daily food allotment in the 0-6hr period after a strenuous workout.

I know you suggested in the past to have protein only post-workout, followed by carbs 30mins later to ensure a higher peripheral amino acid utilization - do you still think this is a viable idea?
Click to expand...

I have to admit, doing the review of literature for my dissertation gave me some new perspectives on nutrient timing. I think it is pretty clear that consuming whey (or EAAs+luecine) immediately after a workout does seem to maximize the rate of protein synthesis. For veteran lifters who have a relatively short-duration anabolic response to each training session I think this makes sense. I down 30-40 grams whey (+ creatine & HMB) immediately after my workouts. On days when I have to train late at night and only get one meal before bed, I'll leave a protein drink on my nightstand so when I get up to pee in the middle of the night, I can down another 20-30 grams of whey to try to take advantage of that window.

Back to how my views have changed... I used to feel that activating mTOR was the biggest priority of both training and eating. This meant prioritizing nutrient timing. Now however I'm thinking it might not matter as much as I thought. There is quite a bit of evidence that although timing protein intake around training maximizes protein synthetic rates, it doesn't seem to matter in the long term when looking at actual increases in muscle mass. Total daily protein intake is more important than when it is eaten. This makes sense from an evolutionary perspective in that the body could not depend on always having protein at specific times of the day. It would have to figure out a way to utilize the protein efficiently regardless of when it was eaten. This appears to be the case. That being said, I still feel it makes sense to push protein synthetic rates as high as you can get when the window is open following training.

Focusing only on mTOR for muscle growth is too narrow of a focus and ignores the other part of the equation namely, transcription and translation. A muscles ability or "capacity" to grow once protein synthesis is activated depends on the cell's transcriptional capacity and its translational capacity. Addition of new myonuclei by fusion of differentiated satellite cells determines the cell's transcriptional capacity. The number of ribosomes determines the cell's translational capacity. So the equation is training = transcription (myonuclei) > translation (ribosomes) > synthesis (mTOR).

The easiest part of the equation is activating mTOR. What appears to be the limiting factor for increases in actual muscle mass is mynuclei and ribosomes. I believe we have a good handle on how to increase satellite cell activity (proliferation > differentiation > fusion). What I'm currently investigating is how the variables of training effect robosomal biogenesis. I speculate that if we can maximize the stimulus for ribosomal biogenesis, it will have the greatest impact on actual accrual of muscle mass.

Blade said:
There could potentially be benefits to a higher-than-optimal protein intake as well, if you want to limit fat gain in a surplus - Antonio et al. have suggested in various research the last couple of years that you can have a higher surplus with 3g/kg protein intakes - through TEF mostly. Thoughts about this?
Click to expand...

When I up my protein during bulking phases my body temp hovers around 99-101 (Yes, it feels like having a fever too). So I have a strong TEF reaction to protein. My view is that it is definately helpful in the short term to boost protein intake as long as it is at least 50% greater than baseline intake. But this boost in protein deposition will slowly decline as the body adapts. In time, even 3g/kg/bw will not provide an advantage over 2g/kg/bw because of increased deamination and oxidation of the protein. How long does it work? It probably depends on both the individual (genetics) and environment (training and diet composition). It justifies cycling protein intake in my mind.
 
Blade said:
Awesome analogy, Bryan! I would point out, though - that when you are really lean - the body seems to be primed for fat gain moreso than muscle gain, but this is obviously a function of the varying degree of suppression of the HPTA and thyroid from extended dieting and single digit bf%
Click to expand...

Yes, and from what I've found, it's also highly related to adipose insulin sensitivity. The larger the size of a fat cell, the lower it's insulin sensitivity, so it's 'rejecting' more FFA per 'level of insulin' in the blood (this is why fatty acids end up in muscle , organs and visceral areas too). Smaller fat cells are more insulin sensitive so are pulling more FFA and glucose in.
 
Cool post Bryan!
Biogenesis, that seems to be a tricky factor in many functional areas (even for type 2 diabetes, who cannot properly accommodate for insulin resistance with beta cell neogenesis). For that, it seems to be a lot with genetics, but also related to intra-cellular lipids and their metabolites (such as ceramides), is there any links with those for muscle cells that you've seen?
 
NWlifter said:
Cool post Bryan!
Biogenesis, that seems to be a tricky factor in many functional areas (even for type 2 diabetes, who cannot properly accommodate for insulin resistance with beta cell neogenesis). For that, it seems to be a lot with genetics, but also related to intra-cellular lipids and their metabolites (such as ceramides), is there any links with those for muscle cells that you've seen?
Click to expand...
Here area few good links to ribosomal biogenesis in skeletal muscle:

https://www.ncbi.nlm.nih.gov/pubmed/24604615/

https://www.ncbi.nlm.nih.gov/pubmed/26507545/

https://www.ncbi.nlm.nih.gov/pubmed/26548696/
 
Thanks Bryan, interesting...
so 'exercise' is the biggest stimulation, leucine can increase the effect
They mention "even though it had no effect on the acute stimulation of protein synthesis." which confirms that post exercise PS increases are only significant, IF that level can be maintained, which makes sense. Increase it all you want, if you can't keep it later, it's not going to cause a long term accumulation of the tissue. I see mTOR and the Erk twins (lol) both as a path (tension and metaboic paths). They also mention myostatin.....
that is a varied and foggy path!
It does lead me to think though, that muscle cell insulin sensitivity is a big factor, that determines amino acid input during rest, and if leucine and other amino's not only provide substrates, but cause stimulation, then intracellular lipids and their metabolites could indeed hamper hypertrophy just as they hamper liver, pancreas and other cells from replication, neogenensis, sensitivity to nutrients, insulin, and all that....
 
Very interesting post, Bryan!

I also agree that there is definitely some missing pieces to understanding the whole puzzle, specifically as it pertains to mitochondrial and ribosomal biogenesis. We spent a lot of time looking into the importance of mitochondria for energy production (and the lack thereof) when I developed Energy Blueprint with Ari Whitten - and it ended up forming a cornerstone of the whole program.

I also tend to consider protein intake to cover the nightly fast to be important - perhaps even more important than post-WO supplementation (the only study strongly supporting this is Cribb et al.), as there are several studies to suggest:
https://www.ncbi.nlm.nih.gov/pubmed/28474785
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5188418/
https://www.ncbi.nlm.nih.gov/pubmed/19628107

Stokes et al. (2018) - Stu P managed to sneak in on this one, too - suggests that MPB is also an important part of the muscle remodeling process, so they kinda argue towards the opposite strategy - i.e. allowing periods of higher MPB to allow a higher muscle protein turnover and repair damage. They point out that it is just a theory, though - and I find no real support for it:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5852756/

Higher protein intake wrt TEF, do you think this will also diminish over time? I haven’t seen any long-term data on it, but I would think the deamination and oxidation process will keep TEF elevated.
 
Blade said:
Very interesting post, Bryan!

I also agree that there is definitely some missing pieces to understanding the whole puzzle, specifically as it pertains to mitochondrial and ribosomal biogenesis. We spent a lot of time looking into the importance of mitochondria for energy production (and the lack thereof) when I developed Energy Blueprint with Ari Whitten - and it ended up forming a cornerstone of the whole program.

I also tend to consider protein intake to cover the nightly fast to be important - perhaps even more important than post-WO supplementation (the only study strongly supporting this is Cribb et al.), as there are several studies to suggest:
https://www.ncbi.nlm.nih.gov/pubmed/28474785
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5188418/
https://www.ncbi.nlm.nih.gov/pubmed/19628107

Stokes et al. (2018) - Stu P managed to sneak in on this one, too - suggests that MPB is also an important part of the muscle remodeling process, so they kinda argue towards the opposite strategy - i.e. allowing periods of higher MPB to allow a higher muscle protein turnover and repair damage. They point out that it is just a theory, though - and I find no real support for it:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5852756/

Higher protein intake wrt TEF, do you think this will also diminish over time? I haven’t seen any long-term data on it, but I would think the deamination and oxidation process will keep TEF elevated.
Click to expand...

Interesting, it sounds similar to the old (and awkwardly termed) 'irrational hypertrophy' theory. Mel Siff spoke about it in Supertraining. Are you familiar with his idea Borge?
 
Yes, Siff proposed a lot of theories - some of them have later been proven, but I don’t think this is one of them. I think it was based on the notion of there being different types of muscle growth, e.g. sarcoplasmic vs. myofibrillar hypertrophy - and I don’t think we have solid evidence of this being a real variable in the process. Greg wrote a good piece on it here:
https://www.strongerbyscience.com/sarcoplasmic-vs-myofibrillar-hypertrophy/

...although I know e.g. Stu Phillips doesn’t think sarcoplasmic hypertrophy is even a thing:
https://twitpl.us/f8NN
 
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