The BBM general model

[quark]

No, the goal of a strength training program is to generate increases in force production.

Based on our understanding of the physiology of force production, we know that the fundamental factors include:

1) Genetic/Epigenetic predisposition (not modifiable with training) [see comments on epigenetics, resulting in removal of the word]
2) Anthropometry, muscle origins/insertions (not modifiable with training)
3) Neuromuscular adaptation, including skill + recruitment (modifiable with training)
4) Muscular hypertrophy (modifiable with training)
5) Psychological factors (modifiable with training & education)

Given that 1 & 2 aren't modifiable, we'll exclude them from discussion for now.

#3 Requires regular practice and exposure to heavy loads.

#4 Requires sufficient training volumes, the specific dose of which depends on the individual's baseline training status and anabolic sensitivity. The only way to sustainably train at higher volumes of work is for them to be delivered at an appropriate intensity that both allows for sufficient motor unit recruitment, but is also recoverable (both within and between workouts). This latter factor requires sufficient work capacity / recovery capacity, which is trainable by training more.

#5 Requires education and practice, as well as "immunization" against nocebo.

Well, I suppose I just laid out our general model, and perhaps an outline for a few book chapters ...

https://forum.barbellmedicine.com/forum ... #post10065

[Stenson]

Sounds reasonable.


They're doing good work over there. I think the split from SS is the best thing that coulda happened for them.

[AaronM]

Fahve points for his general model? Pharaoh would be proud

[chrisd]

Surely epigenetic factors are modifiable, that's what training achieves. Demethylation of muscle protein synthesis genes is an epigenetic modification that comes about through appropriate exercise.

Doctors!

[Austin]

Fahve points for his general model? Pharaoh would be proud

Lol, god damn it...

Surely epigenetic factors are modifiable, that's what training achieves. Demethylation of muscle protein synthesis genes is an epigenetic modification that comes about through appropriate exercise.

Doctors!

Whoops! Of course, you are correct. I frequently lump those together in my mind and mistyped while rapid-fire answering all the forum questions this morning Will fix.

[BigDave]

Surely epigenetic factors are modifiable, that's what training achieves. Demethylation of muscle protein synthesis genes is an epigenetic modification that comes about through appropriate exercise.

Doctors!

Yes! Although I see Austin has already responded.

Of additional interest, some of these changes seem to be heritable. We know that major stresses (famine, for example) affect the offspring through epigenetics, but animal data suggests that less extreme scenarios do too. For example, obese mice methylate the shit out of PGC1a (big player in making mitochondria) and pass that on to their offspring, but exercise prevents that. There is not great data in humans, for obvious reasons, but it seems likely that very trained and healthy people are passing on a better epigenetic "starting point" for their kiddos.

[PatrickDB]

There is not great data in humans, for obvious reasons, but it seems likely that very trained and healthy people are passing on a better epigenetic "starting point" for their kiddos.

I would guess the effect here probably pales in comparison to the fact that trained and healthy people are passing on much better genetic starting points to their kiddos (given the genetic selection bias for "trained and healthy").

[stevan]

Good job Baraki!

[chrisd]

Surely epigenetic factors are modifiable, that's what training achieves. Demethylation of muscle protein synthesis genes is an epigenetic modification that comes about through appropriate exercise.

Doctors!

Yes! Although I see Austin has already responded.

Of additional interest, some of these changes seem to be heritable. We know that major stresses (famine, for example) affect the offspring through epigenetics, but animal data suggests that less extreme scenarios do too. For example, obese mice methylate the shit out of PGC1a (big player in making mitochondria) and pass that on to their offspring, but exercise prevents that. There is not great data in humans, for obvious reasons, but it seems likely that very trained and healthy people are passing on a better epigenetic "starting point" for their kiddos.

To be fair to Austin. Some epigenetic factors are not modifiable, but their influence can be moderated. It's a pretty mind boggling branch of genetics if you did your first genetics course in the early eighties when the genetic code was seen as a blueprint.

Ideas like 'genetically predetermined limits ' may not fit.

[PatrickDB]

Ideas like 'genetically predetermined limits ' may not fit.

Pump the brakes, bro. I don't think epigenetic influences are nearly this important.

[platypus]

Surely epigenetic factors are modifiable, that's what training achieves. Demethylation of muscle protein synthesis genes is an epigenetic modification that comes about through appropriate exercise.

Doctors!

Yes! Although I see Austin has already responded.

Of additional interest, some of these changes seem to be heritable. We know that major stresses (famine, for example) affect the offspring through epigenetics, but animal data suggests that less extreme scenarios do too. For example, obese mice methylate the shit out of PGC1a (big player in making mitochondria) and pass that on to their offspring, but exercise prevents that. There is not great data in humans, for obvious reasons, but it seems likely that very trained and healthy people are passing on a better epigenetic "starting point" for their kiddos.

I can't tell if you guys are making this stuff up or if those are actual words.

[chrisd]

Surely epigenetic factors are modifiable, that's what training achieves. Demethylation of muscle protein synthesis genes is an epigenetic modification that comes about through appropriate exercise.

Doctors!

Yes! Although I see Austin has already responded.

Of additional interest, some of these changes seem to be heritable. We know that major stresses (famine, for example) affect the offspring through epigenetics, but animal data suggests that less extreme scenarios do too. For example, obese mice methylate the shit out of PGC1a (big player in making mitochondria) and pass that on to their offspring, but exercise prevents that. There is not great data in humans, for obvious reasons, but it seems likely that very trained and healthy people are passing on a better epigenetic "starting point" for their kiddos.

I can't tell if you guys are making this stuff up or if those are actual words.

It's an actual thing.

You can (or could, maybe still can) do a Coursera course entitled "The Epigenetic Control of Gene Expresssion".

In a way it's kind of obvious. Genes are expressed, the way in which they are expressed is influenced by the environment. Sit in sunshine, the genes for melanin secretion get expressed. Genes can be 'switched off' by methylation of the start sequence. This can happen because of environmental factors. Stop exerting yourself, less need for muscle protein synthesis, methylate the genes, sarcopaenia.

The freaky bit comes when you look at inheritance. Ova are present in the embryo, they are formed during gestation. Genes in these ova can be methylated or demethylated in response to the mother's environment. This will affect the grandchildren.

The crack about 'genetically predetermined limits' refers tot he fact that genes determine how an organism will respond to an environment. there may be tendencies towards certain phenotypical limits, but these are tendencies, not some blueprint. If you had taken some of the manlets who overcompensate by lifting heavy barbells and given them decent doses of growth hormones during childhood, they would have grown to the proper height for an adult male, i.e six foot.

[MattNeilsen]

You can (or could, maybe still can) do a Coursera course entitled "The Epigenetic Control of Gene Expresssion".

Thanks for the recommendation - I was just about to ask for one. I’ll look up the course. Epigenetics has interested me for a while but I haven’t spent the time studying it.

[anelson]

If you had taken some of the manlets who overcompensate by lifting heavy barbells and given them decent doses of growth hormones during childhood, they would have grown to the proper height for an adult male, i.e six foot.

Come on, man, no need to talk about Skillin that way...

[chrisd]

Anyway, it's a decent enough five point model. So well done BBM.

[KyleSchuant]

Genes are expressed, the way in which they are expressed is influenced by the environment.[...]

The freaky bit comes when you look at inheritance. Ova are present in the embryo, they are formed during gestation. Genes in these ova can be methylated or demethylated in response to the mother's environment. This will affect the grandchildren.

[Stenson]

Posted in BBM facebook group by Austin:



OK folks, brace yourselves: in an attempt to hammer this home I’m going to lay this argument out as clearly as I can:

1) The evidence shows that strongest predictor of force production capacity is the amount of muscle mass someone carries -- and this becomes even more true once basic neurological adaptations (e.g., skill and neuromuscular recruitment) have taken place. In other words, in post-novice trainees, the amount of muscle you have seems to make the biggest difference in how strong you are.

2) The neurological adaptations necessary to lift relatively heavy weights are best developed by handling relatively heavy weights (in other words, you MUST handle heavy weights to improve and demonstrate top-end force production using the muscle mass you already have). No one is arguing that at all, and the evidence is clear here.

3) Increases in muscle mass result from the process of muscular hypertrophy. The evidence unequivocally demonstrates the role of training volume as the primary driver of muscular hypertrophy, with data showing an incremental benefit to each additional set performed per week. Additionally (and very interestingly), there is also evidence showing that anabolic signaling progressively increases as you increase intensity from 20% 1RM to around 60%-70% … but above that, you don’t seem to get any higher anabolic signaling by using heavier weights. This helps to explain why you can get the SAME hypertrophic outcomes using weights ranging from 30% 1RM to 90% 1RM. (And has all been measured *myofibrillar* hypertrophy. The idea that using different intensities give you different proportions of sarcoplasmic vs. myofibrillar hypertrophy is bullshit.)

4) So, once we have someone who has developed the basic skills to perform the lifts, and has developed some of the necessary neurological adaptations in terms of neuromuscular recruitment (for our purposes, say, once they’ve finished the novice program), we need to get them MORE JACKED. This means that training volume per unit time MUST increase, *for everyone* (… which, of course, requires a reduction in average intensity). Note that doing the opposite — reducing training volume, increasing training intensity, and eating more — is an *incredibly* stupid way to train for gaining muscle mass (unless you’re artificially sensitized to training by being on tons of drugs, in which case you can do anything, like one heavy set per week, and make progress).

5) We have evidence showing that older trainees generate a lower anabolic response to training compared to younger trainees at low training volumes. However, we also have data showing that increasing this training volume for older trainees increases (and nearly normalizes) their anabolic response. This is the exact same phenomenon we see with protein intake. Similarly, there is evidence that anabolic signaling decreases the more “trained” you become (you effectively become desensitized to anabolic stimuli, i.e. more training resistant), and therefore need MORE TRAINING the more advanced you get. Duh.

6) It is true that an untrained older person is more likely to have a poorer recovery capacity than a younger person … though untrained people in general have poor recovery capacities. Fortunately, training with more volume and more frequency 1) improves your recovery capacity (evidenced by, among *many* other things, the rate of MPS after training), and 2) stimulates the Repeated Bout Effect, which protects you from the effects of muscle damage and DOMS … meaning you don’t get as sore — unless, of course, you’ve been told that as soon as you turn 35 years old you become crippled, unable to recover from anything because your testosterone is in the low-normal range. (In fact, we have evidence that fear-avoidance and catastrophizing behavior worsen the perceived severity of DOMS after training … and I’ll be talking more about this soon).

7) SO, the bottom line: Waiting as long as humanly possible before increasing someone’s training volume and frequency (or, *decreasing* it) means you are also 1) Waiting as long as humanly possible to develop the necessary work capacity to 2) TOLERATE the amount of training necessary, in order to 3) Stimulate enough anabolism and therefore gain enough muscle, in order to 4) Keep increasing long-term strength potential. On top of this, constantly TELLING people they can’t recover from doing an extra set and REMINDING them of how sore and achy they’ll get, further compromises this entire process from a psychological standpoint.

If you aren’t already familiar with this stuff, with physiology in general, and with the current literature, there is a WHOLE LOT to digest here. But that’s the argument we’ve been laying out in these podcasts.
"""

[quark]

@Austin just posted some supporting papers:

This is just a quick set of papers I was able to pull together in 20 min (numbered to reflect the above post). There are numerous additional sources available on this stuff.

1) LOADS of evidence cited here:
https://www.strongerbyscience.com/size-vs-strength/
https://journals.lww.com/nsca-jscr/Abst ... 95442.aspx

2) https://www.ncbi.nlm.nih.gov/pubmed/28834797 showing that training at > 60% 1RM gets you stronger than training at < 60% 1RM. But if you take the sets far enough, you can get equivalent hypertrophy all the way down to ~30% 1RM.

3) https://www.ncbi.nlm.nih.gov/pubmed/27433992 showing higher weekly training volumes produce more hypertrophy in a dose-response fashion. (And as an aside, effect of weekly set volume on strength: https://rd.springer.com/article/10.1007 ... 018-0872-x )

Apparent plateau of anabolic signaling in young vs old: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2670034/

4) This is a logical conclusion from #1-3 above

5) Young vs. old response to training volume https://academic.oup.com/biomedgerontol ... 170/604729

Young vs. old anabolic signaling response to protein (one of numerous sources)
https://www.ncbi.nlm.nih.gov/pubmed/15596483/

Attentuation of anabolic signaling / desensitization in trained individuals:
https://www.ncbi.nlm.nih.gov/pubmed/16267123
https://www.ncbi.nlm.nih.gov/pubmed/18032468
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4387748/

6) Search literally any paper related to the Repeated Bout Effect

Fear and DOMS:
https://www.ncbi.nlm.nih.gov/pubmed/17277648
https://www.ncbi.nlm.nih.gov/pubmed/21419575

We are happy to refine our thinking and change our minds if presented with compelling evidence (in fact … this is exactly what we did when initially presented with this stuff, since at one point we both used to train and program in “SS fashion”). We will not accept an argument where all this evidence is rejected in favor of “that has not been my experience” for the same reason we do not cite our own experience as evidence here – we are all victims to confirmation bias, whether we like it or not.

Finally, I fully anticipate responses like “that’s not what WE do”, and rejecting studies using a leg extension, for example … without realizing why something like a single-joint training study helps to eliminate numerous confounders (skill/technique/experience, coaching, fear, etc.) and illustrate the underlying physiology (after all, it’s still muscle contraction, which is the whole point here). This is to say that picking out a flaw like that in one of the above studies is not going to make this model topple like a house of cards.

In order to reject our hypothesis, any single one of the following will need to be convincingly shown:

1) Evidence that within-individual changes in muscle size do not significantly result in increased strength performance.

2) Evidence that training volume is NOT the driving factor in hypertrophy (in other words … evidence showing a higher intensity, lower volume program produces more hypertrophy than a lower intensity, higher volume program).

3) Evidence that older adults demonstrate an equivalent (or greater) training response to younger individuals at low training volumes and/or dietary protein intakes.

4) Evidence that recovery rate does NOT improve with training.

[mgil]

Lookit losers, Rip said that SS is the only folks doing the science in regards to getting stronger. That’s why you’ve seen such drastic changes to the Rx over the past decade!

LOL

[slowmotion]

Great stuff, thanks!