Too Much Protein?

[Braaq]

I wont, for reasons I posted in the big drama topic.

But I'll give you a link on this matter (note: this is a one time thing, just so people can see that everytime I have been saying somehing my information was correct and subsequently that of Tim was wrong)

Why do you feel the need to "prove Tim wrong" all the time? And why is this just a one time thing? Post supporting articles for your arguements more often, it will only help you when proving a point. Not only would you not be in a "I'm right, you're wrong" tiff but you will also be helping members by teaching them on the subject. You clearly have a lot of knowledge on the subject (although sometimes I think you think you say you know more than you do but that is far from being just you, there are many on here) so share it with us constructively.

 

[BigBen]

I wont, for reasons I posted in the big drama topic.

But I'll give you a link on this matter (note: this is a one time thing, just so people can see that everytime I have been saying somehing my information was correct and subsequently that of Tim was wrong)

Also the not so geeky guys might like this. It is easy readable and written by Layne Norton:

http://agro-food-industry.teknoscienze.com/pdf/norton_AF2_09.PDF

Have they done any subsequent studies on their conclusions and amounts of lean muscle mass gained in comparison to other methods of diet? Ie the most common splitting yr meals up. What would be considered a large protein meal in relation to the athletes bodyweight? I have been for larger meals with more time in between feeding but my reasoning is related to hormone release and food timing.

 

[jornT]

Have they done any subsequent studies on their conclusions and amounts of lean muscle mass gained in comparison to other methods of diet?

I'm not sure who you mean with they? The idea of a protein synthesis refractionary period dates from 2001. There is a 24h study in humans but there have been no chronic studies on LBM and it would not supprise me if those will not happen anytime soon, because the diet protocol would be a MAJOR bitch and adherence would be likely very low and impossible to track.

Ie the most common splitting yr meals up. What would be considered a large protein meal in relation to the athletes bodyweight?

0,05g of leucine/kg bodyweight.

It is funny that you posted that study b/c i have been for larger meals with more time in between feeding for a while but my reasoning is related to hormone release and food timing.

Plz eleborate.

 

[BigBen]

I'm not sure who you mean with they? The idea of a protein synthesis refractionary period dates from 2001. There is a 24h study in humans but there have been no chronic studies on LBM and it would not supprise me if those will not happen anytime soon, because the diet protocol would be a MAJOR bitch and adherence would be likely very low and impossible to track.

Just scientists in general on this topic.

Plz eleborate.

Well for example when you eat a large meal the body releases a large amount of insulin (Responsible for allowing amino acids and glucose to enter cells). When you fast for a period of time the body releases a spike of growth hormone(responsible for increasing protein synthesis, lipolysis, increases levels of fatty acids in the blood and increases growth of cells not just the hypertrophy of them. With the types of fats/foods i have them eating and the structure of the diet i can make an athlete leaner bigger and stronger with less food as a result of the effects of food on their hormone production and the type of training i have the athlete use.

 

[jornT]

Acute hormone fluctuations are largely irrelevant in the bigger picture in my opinion. It takes chronic superphysiological doses in order to have significant effects.

Well for example when you eat a large meal the body releases a large amount of insulin (Responsible for allowing amino acids and glucose to enter cells).

Carbohydrate induced insulin release has no effect on skeletal muscle protein synthesis, however it does have influence on skeletal muscle degradation (Borsheim et al., 2004), with maximal inhibition at a plasma level of 15 µU/ml (Rennie et al., 2006) which can easily be archieved by protein only meals (Koopman et al., 2007a). Additional insulin has no benefits on skeletal muscle protein synthesis.

When you fast for a period of time the body releases a spike of growth hormone(responsible for increasing protein synthesis, lipolysis, increases levels of fatty acids in the blood and increases growth of cells not just the hypertrophy of them.

I'm not sure what you mean with growth of cells but not just hypertrophy? Do you mean hyperplasia?

Although GH increases protein synthesis, it is not in skeletal muscle (Yarasheski et all, 1992). GH has some influence on lipolysis, but this effect is very small and only occurs when insulin is low, therefore you would lose the benefical effect of insulin on protein degradation. Furthermore, fasting results in increased AMPK and decreased mTOR, inhibiting protein synthesis.

 

[BigBen]

Acute hormone fluctuations are largely irrelevant in the bigger picture in my opinion. It takes chronic superphysiological doses in order to have significant effects.

They are a part of the big picture.[COLOR]

Carbohydrate induced insulin release has no effect on skeletal muscle protein synthesis, however it does have influence on skeletal muscle degradation (Borsheim et al., 2004), with maximal inhibition at a plasma level of 15 µU/ml (Rennie et al., 2006) which can easily be archieved by protein only meals (Koopman et al., 2007a). Additional insulin has no benefits on skeletal muscle protein synthesis.

I am not concerned about the insulins effect on protein synthesis their are much stronger variables than insulins effecting that. I am concerned with the insulins effect on allowing glucose and amino acids to pass into muscle cells. Muscle cels whose sensitivity to glucose is determined by training,dietary carbohydrates and glycogen super compensation. their are other factors in place like training and growth hormone and testosterone production that effect muscle protein synthesis that are more relevant.

I'm not sure what you mean with growth of cells but not just hypertrophy? Do you mean hyperplasia?

Yes, in anatomy and physiology discussions that is how cell growth is defined, the division of cells.

Although GH increases protein synthesis, it is not in skeletal muscle (Yarasheski et all, 1992). GH has some influence on lipolysis, but this effect is very small and only occurs when insulin is low, therefore you would lose the benefical effect of insulin on protein degradation. Furthermore, fasting results in increased AMPK and decreased mTOR, inhibiting protein synthesis.

I cannot agree that growth hormone does not have an effect on muscle protein synthesis b/c growth hormone acts on every cell that has receptors for it. IGF-1 increases as GH increases as well. Growth hormone does have an effect on lipolysis directly or indirectly. I agree insulin does have to be low for levels of GH to to be raised as found in the body naturally(without drug supplementation)

 

[jornT]

I am not concerned about the insulins effect on protein synthesis their are much stronger variables than insulins effecting that. I am concerned with the insulins effect on allowing glucose and amino acids to pass into muscle cells. Muscle cels whose sensitivity to glucose is determined by training,dietary carbohydrates and glycogen super compensation. their are other factors in place like training and growth hormone and testosterone production that effect muscle protein synthesis that are more relevant.

All myofibril hypertrophy has to occur through protein synthesis. If something has no effect of protein synthesis, it does not contribute to actual growth of contractible fibers. If you think that insulin increases sarcoplastic hypertrophy, I would like to see something to back that up.

Yes, in anatomy and physiology discussions that is how cell growth is defined, the division of cells.

Skeletal muscle is stuck in G0 and does no enter cell division.

I cannot agree that growth hormone does not have an effect on muscle protein synthesis b/c growth hormone acts on every cell that has receptors for it. IGF-1 increases as GH increases as well. Growth hormone does have an effect on lipolysis directly or indirectly. I agree insulin does have to be low for levels of GH to to be raised as found in the body naturally(without drug supplementation)

Muscles might have receptors, but that does not say anything about it the effect of ligand/receptor binding. For example, GH has an anabolic effect on non skeletal muscle proteins, but a catabolic effect on adipose tissue. And in another type of tissue, skeletal muscle tissue, it has been found to have no effect on synthesis (see the paper, it is not a speculation)

I agree with you that GH has influence on lipolysis, but if you try to stimulate GH by fasting, you lose the bigger picture: fasting has a negative influence on protein synthesis for example.

 

[Braaq]

Muscles might have receptors, but that does not say anything about it the effect of ligand/receptor binding. For example, GH has an anabolic effect on non skeletal muscle proteins, but a catabolic effect on adipose tissue. And in another type of tissue, skeletal muscle tissue, it has been found to have no effect on synthesis (see the paper, it is not a speculation)

Yup, pretty much:

Skeletal muscle is the major constituent of lean body mass and a major determinant of energy expenditure both at rest and during physical activity. Growth hormone, in turn, influences muscle mass as well as energy expenditure. Growth hormone substitution in adults increases muscle mass by 5-10%, but part of the effect is attributed to rehydration rather than protein accretion. In addition, GH regulates substrate metabolism in muscle and in particular antagonizes insulin-stimulated glucose disposal. This effect is linked to increased free fatty acid (FFA) flux but the molecular mechanisms remain unclear. During fasting, GH-induced insulin resistance may be favorable by reducing the demand of gluconeogenesis from protein. But in the postprandial phase, GH exposure may compromise glucose tolerance via the same mechanisms. Understanding the mechanisms whereby GH antagonizes insulin-stimulated glucose disposal in muscle is an important future research field with implications for a variety of clinical conditions ranging from malnutrition to obesity and type 2 diabetes.

Effects of GH in human muscle and fat.
Jorgensen JO, Rubeck KZ, Nielsen TS, Clasen BF, Vendelboe M, Hafstrom TK, Madsen M, Lund S
Pediatr Nephrol. 2009 Nov 10;

I agree with you that GH has influence on lipolysis, but if you try to stimulate GH by fasting, you lose the bigger picture: fasting has a negative influence on protein synthesis for example.

Just to back this up:

CONTEXT: Whether GH promotes IGF-I production or lipolysis depends on nutritional status, but the underlying mechanisms remain unknown. OBJECTIVE: To investigate the impact of fasting on GH-mediated changes in substrate metabolism, insulin sensitivity, and signaling pathways. DESIGN: We conducted a randomized crossover study. SUBJECTS: Ten healthy men (age 24.3 +/- 0.6 yr, body mass index 23.1 +/- 0.4 kg/m(2)) participated. INTERVENTION: A GH bolus administered 1) postabsorptively and 2) in the fasting state (37.5 h). Skeletal muscle and adipose tissue biopsies were taken, and a hyperinsulinemic-euglycemic clamp was performed on both occasions. MAIN OUTCOME MEASURES: Metabolic clearance rate (MCR) of GH, substrate metabolism, and insulin sensitivity were measured. Biopsies were subjected to Western blotting for expression of signaling proteins and to RT-PCR for expression of suppressor of cytokine signaling protein 3 and IGF-I mRNA. RESULTS: Fasting was associated with reduced MCR of GH (P < 0.01), enhanced lipolytic responsiveness to GH, decreased insulin sensitivity (P < 0.01), and reduced IGF-I bioactivity (P = 0.04). After the GH bolus, phosphorylation of signal transducers and activators of transcription protein 5b (pSTAT5b) were observed in both conditions; however, the phospho-STAT5b/STAT5b ratio was significantly decreased in the fasting state (muscle P = 0.02 and fat P = 0.02). CONCLUSION: The combination of fasting and GH exposure translates into enhanced lipolysis, reduced IGF-I activity and insulin sensitivity, and blunted activation of the Janus kinase (JAK)/STAT pathway. Whether this change in signaling activity is related to the change in MCR of GH and/or the concomitant shift in the metabolic effects of GH merits future attention.

Impact of fasting on growth hormone signaling and action in muscle and fat.
Moller L, Dalman L, Norrelund H, Billestrup N, Frystyk J, Moller N, Jorgensen JO
J Clin Endocrinol Metab. 2009 Mar ; 94(3): 965-72

 

[Ironslave]

GH isn't a very potent enhancer of skeletal muscle protein synthesis, though it is pretty potent in fat metabolism. GH's effects are exerted mainly through IGF-1 as alluded to, but there are both hepatic and local IGF-1. The latter accounts for only 25% of total IGF-1 but is responsible for the skeletal growth, while the former being involved in fat/cho metabolism.

One thing GH does in acute action is increase sensitivity to catecholamines, even in absence of any direct lipolytic action. Further, I don't agree that GH is really lipolytic only in the absence of insulin. Cortisol has been shown to attenuate lipolysis and stimulate LPL in the presence of insulin, while GH inhibits it. (Ottosson et al 2000). Endogenous GH release during exercise is also in fact an independent predictor of fat oxidation while epinephrine was not (Gibney, 2007.... this is an excellent paper).

Still a little ways to go Jorn :gaysign:




1. Effects of Cortisol and Growth Hormone on Lipolysis in Human Adipose Tissue. The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 2 799-803

2. The Growth Hormone/Insulin-Like Growth Factor-I Axis in Exercise and Sport. Endocrine Reviews 28 (6): 603-624

 

[dilatedmuscle]

my brain exploded...

 

[El Freako]

My digestive functions just reversed themselves and I just shat in my mouth.

 

[dilatedmuscle]

My digestive functions just reversed themselves and I just shat in my mouth.

....

 

[jornT]

1. Effects of Cortisol and Growth Hormone on Lipolysis in Human Adipose Tissue. The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 2 799-803

That study is in vitro. High plasma levels of both insulin and growth hormone are unlikely, as rises in glucose after oral or intravenous administration to normal individuals will inhibit GH release and the GH response to GHRH (Davies et al. 1984; Sharp et al. 1984; Garrel et al. 1989).

However GH may be more more potent than I thought on fat metabolism based on a quick peak at your other reference. I will look into that, but I can already add that GH release is one of the MANY responses to fasting and you have to take them all into account. Again, look at the bigger picture.

 

[Ironslave]

That study is in vitro. High plasma levels of both insulin and growth hormone are unlikely, as rises in glucose after oral or intravenous administration to normal individuals will inhibit GH release and the GH response to GHRH (Davies et al. 1984; Sharp et al. 1984; Garrel et al. 1989).

However GH may be more more potent than I thought on fat metabolism based on a quick peak at your other reference. I will look into that, but I can already add that GH release is one of the MANY responses to fasting and you have to take them all into account. Again, look at the bigger picture.

Yes, but it's still with human cells which is a plus. And of course you're right it's one of the many responses to fasting... want to know what the biggest contributing to fasting on lipolysis is? Not eating!

 

[jornT]

Yes, but it's still with human cells which is a plus. And of course you're right it's one of the many responses to fasting... want to know what the biggest contributing to fasting on lipolysis is? Not eating!

I do not care much about the origin of a cell line when it tests a mechanism that is unlikely to occur in vivo in the first place.

Also lipolysis =/= fatloss.

 

[BigBen]

All myofibril hypertrophy has to occur through protein synthesis. If something has no effect of protein synthesis, it does not contribute to actual growth of contractible fibers. If you think that insulin increases sarcoplastic hypertrophy, I would like to see something to back that up.

You are looking to directly. Insulin does play a role in muscle growth. Translation occurs in Rough ER. How do amino acids enter the cells sarcoplasm? Insulin.


Skeletal muscle is stuck in G0 and does no enter cell division.

Muscle cells do divide in the presence of Growth hormone. If they did not what is responsible for muscle growth(the division of cells) during puberty?

Muscles might have receptors, but that does not say anything about it the effect of ligand/receptor binding. For example, GH has an anabolic effect on non skeletal muscle proteins, but a catabolic effect on adipose tissue. And in another type of tissue, skeletal muscle tissue, it has been found to have no effect on synthesis (see the paper, it is not a speculation)

[COLOR"Orange"]http://diabetes.diabetesjournals.org/content/41/4/424.abstract


[/COLOR]

I agree with you that GH has influence on lipolysis, but if you try to stimulate GH by fasting, you lose the bigger picture: fasting has a negative influence on protein synthesis for example.

If you have athletes eat round the clock every 4 hours(thats is on average how long it takes the stomach to empty after a solid food meal) then what is the harm? whats the purpose of force feeding someone every two hours when their stomach has not fully emptied yet and causing digestion issues when you can wait and then have the person eat a larger meal every 3-4 hours. How much could really have been lost in a 3-4 hour period of not eating? The over all food intake is more relevant to bodyweight than what a 3-4 hour period between meals does to the body concerning the metabolism. Thats why i say take the break, let the stomach empty, and benefit from the hormones.

 

[jornT]

You are looking to directly. Insulin does play a role in muscle growth. Translation occurs in Rough ER. How do amino acids enter the cells sarcoplasm? Insulin.

This is not how science works. In science you measure things, and after it you try to understand the working mechanism and then test again if it actually works like that.

What you do is use a theoretical concept to try to predict an outcome.

So again, please show actual data that insulin increases protein synthesis or LBM. I already showed you that it does not.

Muscle cells do divide in the presence of Growth hormone. If they did not what is responsible for muscle growth(the division of cells) during puberty?

Burden of proof is all yours. What you are now doing is making a statement that is correct untill some else proves it wrong. Plz present any data about hyperplasia during puberty.

[COLOR"Orange"]http://diabetes.diabetesjournals.org/content/41/4/424.abstract

Ben, could you eleborate more in your posts, because I'm find myself guessing what you mean.



Diabetes. 1992 Apr;41(4):424-9.

Growth hormone stimulates skeletal muscle protein synthesis and antagonizes insulin's antiproteolytic action in humans.
Fryburg DA, Louard RJ, Gerow KE, Gelfand RA, Barrett EJ.

Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut.

We examined the effects of a combined, local intra-arterial infusion of growth hormone (GH) and insulin on forearm glucose and protein metabolism in seven normal adults. GH was infused into the brachial artery for 6 h with a dose that, in a previous study, stimulated muscle protein synthesis (phenylalanine Rd) without affecting systemic GH, insulin, or insulinlike growth factor I concentrations. For the last 3 h of the GH infusion, insulin was coinfused with a dose that, in the absence of infused GH, suppressed forearm muscle proteolysis by 30-40% without affecting systemic insulin levels. Measurements of forearm glucose, amino acid balance, and [3H]phenylalanine and [14C]leucine kinetics were made at 3 and 6 h of the infusion. Glucose uptake by forearm tissues in response to GH and insulin did not change significantly between 3 and 6 h. By 6 h, the combined infusion of GH and insulin promoted a significantly more positive net balance of phenylalanine, leucine, isoleucine, and valine (all P less than 0.05). The change in net phenylalanine balance was due to a significant increase in phenylalanine Rd (51%, P less than 0.05) with no observable change in phenylalanine Ra. For leucine, a stimulation of leucine Rd (50%, P less than 0.05) also accounted for the change in leucine net balance, with no suppression of leucine Ra. The stimulation of Rd, in the absence of an observed effect on Ra, suggests that GH blunts the action of insulin to suppress proteolysis in addition to blunting insulin's action on Rd.

PMID: 1607069 [PubMed - indexed for MEDLINE]




I'm not fully sure why you posted this study, as all this says that in a previous! study GH has been found to have an effect on skeletal muscle protein synthesis. If you want to present your case, track that study down, but note it is an infusion study so I'm afraid that it will be a superphysiological dose.

If you have athletes eat round the clock every 4 hours(thats is on average how long it takes the stomach to empty after a solid food meal) then what is the harm? whats the purpose of force feeding someone every two hours when their stomach has not fully emptied yet and causing digestion issues when you can wait and then have the person eat a larger meal every 3-4 hours. How much could really have been lost in a 3-4 hour period of not eating? The over all food intake is more relevant to bodyweight than what a 3-4 hour period between meals does to the body concerning the metabolism. Thats why i say take the break, let the stomach empty, and benefit from the hormones.

You now talk about eating every 3-4h, that is something diffrent than fasting.

Also, you ask how much could really be lost in that time. Let's reverse that, what is a little (if any?) physiological GH pulse going to archieve in a even shorter time frame.

 

[BigBen]

This is not how science works. In science you measure things, and after it you try to understand the working mechanism and then test again if it actually works like that.
What you do is use a theoretical concept to try to predict an outcome.

So basically you just accept and reject science as it fits your argument then? I wasn't aware that the action of insulin was a theory. So don't have your athletes eat any carbohydrates then if i am wrong. Reject my theory with full belief in what your saying.



So again, please show actual data that insulin increases protein synthesis or LBM. I already showed you that it does not.
I did not say insulin increases protein synthesis. Insulin is a factor in muscle cell hypertrophy. If it is not then again train your athletes and provide them with diets that give them constantly low levels of insulin.



Burden of proof is all yours. What you are now doing is making a statement that is correct untill some else proves it wrong. Plz present any data about hyperplasia during puberty.


I didnt know that basic anatomy and physiology needed an explination. This is first year learning in under graduate when you learn the function of hormones.

Ben, could you eleborate more in your posts, because I'm find myself guessing what you mean.



Diabetes. 1992 Apr;41(4):424-9.

Growth hormone stimulates skeletal muscle protein synthesis and antagonizes insulin's antiproteolytic action in humans.
Fryburg DA, Louard RJ, Gerow KE, Gelfand RA, Barrett EJ.

Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut.

We examined the effects of a combined, local intra-arterial infusion of growth hormone (GH) and insulin on forearm glucose and protein metabolism in seven normal adults. GH was infused into the brachial artery for 6 h with a dose that, in a previous study, stimulated muscle protein synthesis (phenylalanine Rd) without affecting systemic GH, insulin, or insulinlike growth factor I concentrations. For the last 3 h of the GH infusion, insulin was coinfused with a dose that, in the absence of infused GH, suppressed forearm muscle proteolysis by 30-40% without affecting systemic insulin levels. Measurements of forearm glucose, amino acid balance, and [3H]phenylalanine and [14C]leucine kinetics were made at 3 and 6 h of the infusion. Glucose uptake by forearm tissues in response to GH and insulin did not change significantly between 3 and 6 h. By 6 h, the combined infusion of GH and insulin promoted a significantly more positive net balance of phenylalanine, leucine, isoleucine, and valine (all P less than 0.05). The change in net phenylalanine balance was due to a significant increase in phenylalanine Rd (51%, P less than 0.05) with no observable change in phenylalanine Ra. For leucine, a stimulation of leucine Rd (50%, P less than 0.05) also accounted for the change in leucine net balance, with no suppression of leucine Ra. The stimulation of Rd, in the absence of an observed effect on Ra, suggests that GH blunts the action of insulin to suppress proteolysis in addition to blunting insulin's action on Rd.

PMID: 1607069 [PubMed - indexed for MEDLINE]




I'm not fully sure why you posted this study, as all this says that in a previous! study GH has been found to have an effect on skeletal muscle protein synthesis. If you want to present your case, track that study down, but note it is an infusion study so I'm afraid that it will be a superphysiological dose.

That is all it needs to say. That is the point i was making, GH increases skeletal muscle protein synthesis.

You now talk about eating every 3-4h, that is something diffrent than fasting.

I guess i gshould have better defined fast then. 3-4 hours is what i had always ment.

Also, you ask how much could really be lost in that time. Let's reverse that, what is a little (if any?) physiological GH pulse going to archieve in a even shorter time frame.

GH peaks 3-4 hours after a meal. What good does it do? Well if you only look at 1 meal, not much but if you look at total GH production, it is higher. That was in a book entirely about GH i read almost 2 years ago jorn you will have to excuse me for not remembering the title. And i will understand if that is not good enough reason for you bc it wouldnt be for me if someone presented the argument to me like that either. But i read all the information and studies that went along with the theory of meal timing GH release and their regards to performance and body composition.

 

[Justwonderin]

the other day for my post work out meal i ate a llama. you can never have enough protein

 

[jornT]

I actually believe you are not being antagonistic on purpuse. I think that this is going on:

Inertia is the idea that individuals prefer not to change their attitudes, behaviors, and beliefs rather than to change them, all things being equal (Knowles & Linn, 2004).

If freedom to engage or not engage in a behavior is threatened or denied, motivational arousal is prompted to restore lost freedom
(Brehm & Brehm, 1981)

Ofcourse, you could argue that it is the other way around. However, that is unlikely the case, since your argurments are very weak from a scientific point of view.

Let's take a look at what we discussed so far. Your theory:

Well for example when you eat a large meal the body releases a large amount of insulin (Responsible for allowing amino acids and glucose to enter cells). When you fast for a period of time the body releases a spike of growth hormone(responsible for increasing protein synthesis, lipolysis, increases levels of fatty acids in the blood and increases growth of cells not just the hypertrophy of them. With the types of fats/foods i have them eating and the structure of the diet i can make an athlete leaner bigger and stronger with less food as a result of the effects of food on their hormone production and the type of training i have the athlete use.

I asked you if you ment hyperplasia with the growth of cells and you said that was the case. I explained you that muscle cells do not enter cell division and your responeded:

Muscle cells do divide in the presence of Growth hormone. If they did not what is responsible for muscle growth(the division of cells) during puberty?

Now this concerns me for several reasons:

a) This is extremly basic knowledge. Now this does not have to be a big problem, as it could have been just a slip of a solid knowledge base.
b) after I explained you that muscle cells do not enter cell division, you continued to defence your argument. This is highly indicative of inertia and reactance, since you could have checked my information in a minute, but apparently did not.
c) You tried to back your argument with a logical fallacy: shifting the burden of proof. You try to make it sound that your statement is true unless someone can prove it wrong, which is not how if works.
d) besides that your logic was flawed, you should provide data, and not logic to your arguments. That is how science works.

I mentioned the burden of proof before, and this is how you responded:

I didnt know that basic anatomy and physiology needed an explination. This is first year learning in under graduate when you learn the function of hormones.

This looks to me like it's written in a condescending way, but I'm willing to give you the benefit of the doubt and ignore it. However, this is no way an argument. In the Netherlands we learn the basic functions of insulin in high school (as well as the diffrence in stabile, labile and permant cells). That the functions of hormones can be summerized in a few major effects does not mean that the hormones are not extremly complex. Whole books can be written about insulin and its effects, with half or more of the concepts unfamiliar to you.

As mentioned, my bachelor thesis was about the effects of protein on exercise induced skeletal muscle protein synthesis and hypertrophy. In alot of studies there is carbohydrate co-ingestion so I had to study the effects of insulin on muscle in-dept. Do you think I didn't learn anything from that, because I already was taught the effects of insulin in high school? Should I also have told my thesis supervisor, that he should have stopped doing his research on insulin as everthing is know about it already?

I already showed you that insulin has no effects in muscle protein synthesis while the burden of proof was all yours. You have a theory, plz present data to back it up or admit that it is just a guess. Show us that insulin increases hypertrophy (either sarcoplastic or myofibrillar I don't care). And don't come with arguments as I didn't know that the function of insulin was theory. If that was the case, it would be really easy for you to dig up the data. Furtermore, once you found data that insulin increases sarcoplastic hypertrophy, present data that infrequent peaks with the same AUC are more effective compared to more regular intervals.


We also talked about growth hormone. The last part of the discussion:

I'm not fully sure why you posted this study, as all this says that in a previous! study GH has been found to have an effect on skeletal muscle protein synthesis. If you want to present your case, track that study down, but note it is an infusion study so I'm afraid that it will be a superphysiological dose.

That is all it needs to say. That is the point i was making, GH increases skeletal muscle protein synthesis.

Note how I posted this BEFORE you posted your abstract:

It takes chronic superphysiological doses in order to have significant effects.

Some time after that you posted your abstract to which I responded with with one of the qoutes above. Note how you do not say anything about my remark of a supraphysiological dose. That tells me, you did not actually read the study (or actually, the other study that it mentions) and checked wheter a supraphysiological dose was used. Which in turn tells me, that you simply started searching for a study that was supportive of your argument, rather than taking my remarks into account and actually trying to figure out the truth (again, indicating inertia and reactance).

So I pointed out again that we're talking about physiological doses in the above quote and you respond to it with 'that is all it needs to say'. Is that how you do you research Ben? If I can find an abstract that says that spice X induced tumor cell apoptosis in n in vitro study, do I have a cure for cancer? You know that you have to take data into context (I hope)(as we're still talking about hormone manipulation with your eating plan) and you still don't do it after I pointed it out several times (again, intertia and reactance)

GH peaks 3-4 hours after a meal. What good does it do? Well if you only look at 1 meal, not much but if you look at total GH production, it is higher. That was in a book entirely about GH i read almost 2 years ago jorn you will have to excuse me for not remembering the title. And i will understand if that is not good enough reason for you bc it wouldnt be for me if someone presented the argument to me like that either. But i read all the information and studies that went along with the theory of meal timing GH release and their regards to performance and body composition.

Ben, you already showed us that you misinterpreted data. How can I be sure that the autor and/or you made the correct conclusions when you don't even know what you read?

As of yet, you have failed to back any of your arguments, while several have been shown to be wrong.

So if you want to continue this debate in an evidence based manner (if you don't want to it in an evidence based manner I am done with it) take the following into account:
a) do not use logic but data
b) be able to present references. If you can't find data, how can you be sure it's out there, you remember it correctly and interperted it correct?
c) interpretend data correctly (not sure if you did it wrong on purpose or not)

Taken the above factors into account, I recommend you to do a extensive literature study and post the results here once your done.