Too Much Protein?

[MrChewiebitums]

and here i was wondering whether i should put that extra tablespoon of whey

 

[BigBen]

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.

You can not seriously think that i would fall victim to such a simple theory on behavior. All behavior theories by the way have one flaw and that is that none of them are verifiable.

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



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:



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.

I did check your information. I looked driectly into a 2009 anatomy and physiology that states that GH is responsible for muscle cell hyperplasia during puberty. Now if the text is incorrect I need to see, not one, but a series of studies saying so.[COLOR]
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.

Actually the more basic the statement and more common the knowledge the less evidence is necessary proving the statement is true bc the statement is more universally accepted. I would say that insulin not being a factor in muscle growth is more outside of the realm of common knowledge and more against the grain of what is accepted. Meaning that more than one study is required to prove a point as everything i have ever read disagrees with the statement "insulin plays no role in muscle growth." Your statement requires more evidence backing it b/c your statement was more specialized than the statement I made. Your statement is less common knowledge and therefore requires more evidence backing the claim.
d) besides that your logic was flawed, you should provide data, and not logic to your arguments. That is how science works.

No my logic is not flawed. My presentation was not as strong as it could have been and that is what bugs you. I made the mistake of assuming we know the same information as we are both graduates of 4 year nutrition programs and constantly read material on the matter.

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



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.

Absolutely, I do not know every function of insulin or every possible reaction that it is responsible for in the body, but neither do 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?

You should have learned a lot, and that is great. But you are kind of making an over extension of the point i was making about insulin by inferring if you know a few functions of insulin that you should stop learning about it all together and of course you should not. And that is not what I was saying either.

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.

Jorn, if insulin has no effects on muscle cell hypertrophy i challenge you to train your athletes and maintain a low insulin level to show true belief in your theory. The idea that insulin plays no role in muscle cell hypertrophy, even if it is a secondary role, is ridiculous. If insulin plays no role in muscle cell hypertrophy then i need answers from you with your knowledge to the following questions:
1.why do bbers who supplement it gain 10-20lbs of lean muscle?
2. How does glucose enter into the cell for cellular respiration?
3. What is more efficiently used than glucose to make ATP? ATP is for some of the steps in protein synthesis. This last question comes from the fact that glucose passes into the cell from the action of insulin.


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





Note how I posted this BEFORE you posted your abstract:



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.

I did respond actually. I said that I disagreed with you that hormones are a factor even if they are not of supraphysiological dosages.

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).

You are mistaken. And this is a serious slipper slope argument.

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)

I posted the study b/c you made the comment that growth hormone does not have any effect on skeletal muscle protein synthesis, and I said that it does. I am well aware of the context the study was done in and i was pointing out that your statement is not true in all cases. And again you are looking to directly at what i am saying. When GH levels raise so do IGF-1 levels. I mentioned this before. IGF-1 does many beneficial things for an athlete one of them being muscle cell hyperplasia.





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?

This was funny. No you already showed that when i make a statement you can take that statement and try to make it appear as if I have misinterpret the data by incorrectly stating the reason I posted the study. That to is a fallacy.

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

HGH, Insulin, IGF-1 and the importance of muscle cell energy (ATP) in the role of protein synthesis. The roles of HGH insulin, and IGF-1 are relevant.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2439518/?tool=pmcentrez







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.

 

[tim290280]

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.

 

[jornT]

Yes annoyed, will not take the time for proper lay out, and will not try to keep it nice as other don't do so either. Furtermore you continue your argument in a non evidence based manner, good job!

I thought you wouldn't reply to my posts anymore?

I also thought it was childish that I laughed at your posts? But when you do it, it is ok right? Ofcourse, there is the diffrence that when I did it was actually for a good reason.


You can not seriously think that i would fall victim to such a simple theory on behavior. All behavior theories by the way have one flaw and that is that none of them are verifiable.

Fall victim to a simply theory? Do you think this is only is something that applies to low IQ people or something (which would make it all the more relevant)

Also, I wouldn't call it a flaw, you could argue that is a weakness, but let's not get into semantics. It is not verifiable to see if they apply to you in this discussion (although I build a very strong case and anyone with some sort of sociological background is likely to confirm it) but the theories an sich are verifiable is that is what you ment. But I expect you to understand sociology about as good as you do physiology, so what would you know?

I did check your information. I looked driectly into a 2009 anatomy and physiology that states that GH is responsible for muscle cell hyperplasia during puberty. Now if the text is incorrect I need to see, not one, but a series of studies saying so.[COLOR]

What part of POST REFERENCES!!!! did you not get?

Actually the more basic the statement and more common the knowledge the less evidence is necessary proving the statement is true bc the statement is more universally accepted. I would say that insulin not being a factor in muscle growth is more outside of the realm of common knowledge and more against the grain of what is accepted. Meaning that more than one study is required to prove a point as everything i have ever read disagrees with the statement "insulin plays no role in muscle growth." Your statement requires more evidence backing it b/c your statement was more specialized than the statement I made. Your statement is less common knowledge and therefore requires more evidence backing the claim.

LULZ. Epic strawman again. When did I say that insulin did not play a role in muscle growth? I questioned your theory that eating with less regular intervals would increase hypertrophy and then you tried to use some random logic to explain it. Big diffrence. Just because insulin plays 'a role' (note that I explained exactly under which circumstances in previous posts) is something totally diffrent from the claims you originally made.

No my logic is not flawed. My presentation was not as strong as it could have been and that is what bugs you. I made the mistake of assuming we know the same information as we are both graduates of 4 year nutrition programs and constantly read material on the matter.

Who cares about how long someone studied? That doesn't prove anything about your knowledge or who is right. Also, don't you do some study to become a dietician? That is much lower level bro, sorry.

Absolutely, I do not know every function of insulin or every possible reaction that it is responsible for in the body, but neither do you.

Never claimed I did. You on the other hand where the one who said you didn't need to back on your claims because insulin was explained in the first year (or high school) and that is why I said you don't half of what insulin does and how. And I do know alot more about it than you do, especially with relation to muscle growth.


Jorn, if insulin has no effects on muscle cell hypertrophy i challenge you to train your athletes and maintain a low insulin level to show true belief in your theory. The idea that insulin plays no role in muscle cell hypertrophy, even if it is a secondary role, is ridiculous. If insulin plays no role in muscle cell hypertrophy then i need answers from you with your knowledge to the following questions:
1.why do bbers who supplement it gain 10-20lbs of lean muscle?
2. How does glucose enter into the cell for cellular respiration?
3. What is more efficiently used than glucose to make ATP? ATP is for some of the steps in protein synthesis. This last question comes from the fact that glucose passes into the cell from the action of insulin.

Again, straw man, see above.
I also would like to respond to AGAIN you use (flawed) logic instead of data and that you start the very first question talking about SUPRAPHYSIOLOGICAL doses which I said about 10 times that is not relevant to your theory. I will not bother to answer your questions if you do not adress the points I asked you to do first, namely, argue in a evidence based manner.

I posted the study b/c you made the comment that growth hormone does not have any effect on skeletal muscle protein synthesis, and I said that it does. I am well aware of the context the study was done in and i was pointing out that your statement is not true in all cases. And again you are looking to directly at what i am saying. When GH levels raise so do IGF-1 levels. I mentioned this before. IGF-1 does many beneficial things for an athlete one of them being muscle cell hyperplasia.


Data, it is where?

Strawman, supraphysiological doses blablabla repeat x10

This was funny. No you already showed that when i make a statement you can take that statement and try to make it appear as if I have misinterpret the data by incorrectly stating the reason I posted the study. That to is a fallacy.

Huh, I posted before that study that we were talking about physiological doses and you started to strawman and try to turn it into 'a role' in hypertrophy.

HGH, Insulin, IGF-1 and the importance of muscle cell energy (ATP) in the role of protein synthesis. The roles of HGH insulin, and IGF-1 are relevant.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2439518/?tool=pmcentrez

OK? I also asked you before to be more specific in what you say. Could you plz tell me what part of the above study proves what, and why that is relevant to our argument? Notice how when I reference something, it is a specific line, not a whole paper which leaves the other guessing what it means? That is how you reference, you learn it in your first year.


Now if you could argue in an evidence based manner, I have no problem to continue this discussion in a decent manner.

 

[BigBen]

Yes annoyed, will not take the time for proper lay out, and will not try to keep it nice as other don't do so either. Furtermore you continue your argument in a non evidence based manner, good job!

Thats the pot calling the kettle black isn't it? Wasn't your initial post in this thread one word? Very scientific Jorn.

I thought you wouldn't reply to my posts anymore?

I also thought it was childish that I laughed at your posts? But when you do it, it is ok right? Ofcourse, there is the diffrence that when I did it was actually for a good reason.




Fall victim to a simply theory? Do you think this is only is something that applies to low IQ people or something (which would make it all the more relevant)

No, I do not think that behavior theories apply only to lower level IQ's. Inertia would apply to any person who attaches their emotions to their beliefs. I have taught my self to not attach my emotions to any of my beliefs for that exact reason. So when my beliefs are challenged the only preference I have in the discussion is for the truth.

Also, I wouldn't call it a flaw, you could argue that is a weakness, but let's not get into semantics. It is not verifiable to see if they apply to you in this discussion (although I build a very strong case and anyone with some sort of sociological background is likely to confirm it) but the theories an sich are verifiable is that is what you ment. But I expect you to understand sociology about as good as you do physiology, so what would you know?

For someone so deeply rooted in scientific method you do an awful lot of guess work and assuming when making judgments on me. Inertia is a behavioral response to the stimulus of a challenged belief.

And for the record sociology is the science or study of the origin, development, organization, and functioning of human society.

Psychology, which inertia wold fall under, is the science of the mind or of mental states and processes, the science of human and animal behavior, the sum or characteristics of the mental states and processes of a person or class of persons, or of the mental states and processes involved in a field of activity, mental ploys or strategy.



What part of POST REFERENCES!!!! did you not get?

The part where you got emotionally attached to your scientific beliefs and are becoming very defensive when they are questioned.

GH has direct effects on most tissues, including skeletal muscle (d'Ercole et al., 1984; Gostelli-Peter et al., 1994; Jorgensen et al., 2006).

GH stimulates the synthesis of IGF-I in most tissues (Figure 1Figure 1; d'Ercole et al., 1984; Gostelli-Peter et al., 1994).

There are two main mechanisms by which muscle mass may be increased: hypertrophy or an increase in myofibre size and hyperplasia or an increase in myofibre number.

GH regulates postnatal body growth.(Savage et al., 1993; Zhou et al., 1997; Efstratiadis, 1998)



LULZ. Epic strawman again. When did I say that insulin did not play a role in muscle growth? I questioned your theory that eating with less regular intervals would increase hypertrophy and then you tried to use some random logic to explain it. Big diffrence. Just because insulin plays 'a role' (note that I explained exactly under which circumstances in previous posts) is something totally diffrent from the claims you originally made.

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.

Insulin rapidly activates protein synthesis by activating components of the translational machinery including eIFs (eukaryotic initiation factors) and eEFs (eukaryotic elongation factors). In the long term, insulin also increases the cellular content of ribosomes to augment the capacity for protein synthesis.Department of Biochemistry and Molecular Biology, University of British Columbia, 2350 Health Sciences Mall, Vancouver, Canada V6T 1Z3. cgpr@interchange.ubc.ca PMID: 16545079 [PubMed - indexed for MEDLINE



Protein synthesis also depends on the energy status in the muscle as it is an ATP-dependent process(Bolster et al., 2002)

ATP is most efficiently created out of glucose and oxygen. ATP is synthesized in the mitochondria. Mitochondria is located on the INSIDE of cells. Glucose must be transported to the inside of cells to be utilized by the mitchondria for ATP synthesis.

Glucose is transported by GLUT4 (a glucose transporter protein) to the plasma membrane of a muscle cell. The hormone insulin, on the outside of the cell binds, to a receptor on the plasma membrane. That binding then sends a signal to increase the amount of GLUT4 on the surface of the cell. This increases the amount of glucose taken from the outside of the cell to the inside.
Source(s):
The World of the Cell by Becker et. al





Who cares about how long someone studied? In light of the following statement you made.That doesn't prove anything about your knowledge or who is right. This seems quite contradictory doesn't it? Also, don't you do some study to become a dietician? That is much lower level bro, sorry.Who cares if i studied dietetics. That does not mean i do not know anything beyond dietetics.




Data, it is where?

Strawman, supraphysiological doses blablabla repeat x10

Huh, I posted before that study that we were talking about physiological doses and you started to strawman and try to turn it into 'a role' in hypertrophy.

So as originally stated.

when you eat a large meal the body releases a large amount of insulin.

http://jcem.endojournals.org/cgi/content/full/88/6/2706
This investigation revealed that significantly enhanced incretin responses occurred in types 1 and 2 diabetic patients and in lean and obese healthy subjects during a large meal test vs. a small meal test.

Second, we found that the ß-cell sensitivity to glucose tended to increase in both type 2 diabetic patients (29%) and obese healthy subjects (22%) during the large meal, compared with the small meal. The change in ß-cell sensitivity was seen in spite of only a minor insignificant increase in plasma glucose. The increased insulin response during the large meal could, therefore, reflect an increased secretion of incretin hormones. I put the above information in my post b/c i did not want to take the bolded red text out of context. But you can see that as meal size increases so does the insulin response.

I made it clear how insulin was relevant to protein synthesis by this:
Protein synthesis also depends on the energy status in the muscle as it is an ATP-dependent process(Bolster et al., 2002)

ATP is most efficiently created out of glucose and oxygen. ATP is synthesized in the mitochondria. Mitochondria is located on the INSIDE of cells. Glucose must be transported to the inside of cells to be utilized by the mitchondria for ATP synthesis.

Glucose is transported by GLUT4 (a glucose transporter protein) to the plasma membrane of a muscle cell. The hormone insulin, on the outside of the cell binds, to a receptor on the plasma membrane. That binding then sends a signal to increase the amount of GLUT4 on the surface of the cell. This increases the amount of glucose taken from the outside of the cell to the inside.
Source(s):
The World of the Cell by Becker et. al



What was originally said of growth hormone:

When you fast for a period of time the body releases a spike of growth hormone.

Now I will say I should have more clearly defined fast. I mean a period of 3-4 hours between meals. That was a my mistake. Now what I did not include in my initial post intentionally was what i have the athletes do in between meals regarding supplementation of amino acids. I left that out on purpose b/c you did not share all of the information on a the topic that i wanted to know, so i did not share all of my information I had that you were interested in hearing.

http://74.125.95.132/search?q=cache...wth+hormone+secretes&cd=6&hl=en&ct=clnk&gl=us

A study was carried out in 15 male volunteers to evaluate qualitatively the secretion of growth factors following stimulation by oral amino acids. the results showed that oral administration of a combination of two amino acids (1200 mg l-lysine plus 1200 mg l-Arginine Pyroglutamate) provoked a release of pituitary somatotrophin and insulin. This phenomenon was reproducible and the growth hormone secreted in response to this stimulation had biological activity (as demonstrated by radiorecepter assay and somatomedin induction).

We could demonstrate that the association of the two amino acids does result in the release of biological-active hormone able to affect peripheral cellar receptors and thus growth in general.

Insulin is, of course, an equally important factor in cell growth. Even if there are some uncertainties regarding the bioactivity of the substance assayed, there is no doubt the amino acids stimulated insulin as well as HGH: hence, both of the physiologically important growth factors are affected. It should also be noted that the hypoglycemia which follows the insulin peak is a further stimulus to HGH secretion.

Probably the most significant aspect of our findings is that these HGH responses have demonstrated following oral administration of the amino acid complex.

References

Cited References used in the above study can be obtained from Bio Corp., 204 East 2nd Avenue, Suite 408, San Mateo, California 94401, 1-800-246-9004
The above study clearly demonstrates the effectiveness of blending specific amino acids to achieve increased levels of growth hormone production.

So with that understood. We can look at growth hormones relationship with IGF-1.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2439518/?tool=pmcentrez


GH has direct effects on most tissues, including skeletal muscle (d'Ercole et al., 1984; Gostelli-Peter et al., 1994; Jorgensen et al., 2006).

GH stimulates the synthesis of IGF-I in most tissues (Figure 1Figure 1; d'Ercole et al., 1984; Gostelli-Peter et al., 1994).

In summary, normal GH/IGF-I function does have a role in the development and maintenance of muscle mass, as gathered from evidence in GH-deficient patients, burn patients, hypophysectomized animals, and animal models in which GH receptor and IGF-IR activity are lacking.(Figure 3).


This all seems very relevant in to the bigger picture.


Now if you could argue in an evidence based manner, I have no problem to continue this discussion in a decent manner.

 

[jornT]

Thats the pot calling the kettle black isn't it? Wasn't your initial post in this thread one word? Very scientific Jorn.

Like scientific data, I would like you to take forum posts into context as well. When I made that post, I was clearly just picking on Tim with as only goal to let him know he was wrong again which greatly annoys him as he likes to be a forum guru. Look at what I said:

Ironslave read that thesis so he can also vouch that Tim is wrong. I do not feel the need to tell you guys why (i'm the bad guy anyway), I'm just trying to get a message across to Tim.

I was just flaming (as I repeatedly pointed out), not presenting an argument so it has nothing to do with how scientific my arguments are in normal discussions.

Anyway, it looks like you at least tried to take some points I asked for into account (references and data instead of reasoning) in your last post, so I’m willing to continue in a normal manner again.

No, I do not think that behavior theories apply only to lower level IQ's. Inertia would apply to any person who attaches their emotions to their beliefs. I have taught my self to not attach my emotions to any of my beliefs for that exact reason. So when my beliefs are challenged

KEYWORDS: I THINK. Did I not ask you to not think and use logic which might or might not be wrong? Again, in science you do not think, use logic or extrapolate, but you use data that has been actually found. Any form of reasoning is done in the discussion to try to explain the data that have been found and for further hypotheses, NOT to prove anything. Therefore, your thinking has little to no value in a discussion when actual data is available.

It is funny that you start explaining me on the terms I just introduced and you probably googled to look up. Furthermore, I have had actual training in them, not my own interpretations and own ‘thinking’. And you want to know what example was used in my class about reactance? Sharon Brehm (a proffesor) wanted to find out why her husband always did the exact opposite of what she told him to do. Jack Brehm is not exactly low IQ: http://brehm.socialpsychology.org/ but high in the reactance trait.

See how your thinking is all wrong? That is why thinking, assuming, and extrapolating are very weak argument and not even close to evidence.

For someone so deeply rooted in scientific method you do an awful lot of guess work and assuming when making judgments on me.

First of all, I said: ‘I THINK this is going on:’ See how I don’t say anything absolute because I know better? Also, people who think they are smart are (as you demonstrated by saying ‘You can not seriously think that I would fall victim to such a simple theory on behavior’) are
higher in the reactance trait. So another argument can be added to the list I previously posted why I think you are being antagonistic. Nothing is proven, but I have a pretty damn strong case. Not that I care why you are antagonistic, if you are able to present a strong case it would be fine.

And for the record sociology is the science or study of the origin, development, organization, and functioning of human society.

Psychology, which inertia wold fall under, is the science of the mind or of mental states and processes, the science of human and animal behavior, the sum or characteristics of the mental states and processes of a person or class of persons, or of the mental states and processes involved in a field of activity, mental ploys or strategy.

Yeah, let’s get into semantics, that is really proving your point. You cannot fully isolate concepts between sociology and psychology. Also, I was thought about inertia and reactance in a course given by the sociological department. I’ll guess I have to go tell them to leave that out the course next year because it has nothing to do with their area of expertise.

What part of POST REFERENCES!!!! did you not get?

The part where you got emotionally attached to your scientific beliefs and are becoming very defensive when they are questioned.

LOL! Better leave the analysis to me dr Freud, I already explained you above that you do not understand that your talking about. Also, nice try to dodge the bullet, but your remark does not justify anything. Luckily you provided reference from this point on, so lets take a look at them.

GH has direct effects on most tissues, including skeletal muscle (d'Ercole et al., 1984; Gostelli-Peter et al., 1994; Jorgensen et al., 2006).

GH has direct effects on most tissues, including skeletal muscle (d'Ercole et al., 1984; Gostelli-Peter et al., 1994; Jorgensen et al., 2006).

GH stimulates the synthesis of IGF-I in most tissues (Figure 1Figure 1; d'Ercole et al., 1984; Gostelli-Peter et al., 1994).

There are two main mechanisms by which muscle mass may be increased: hypertrophy or an increase in myofibre size and hyperplasia or an increase in myofibre number.

GH regulates postnatal body growth.(Savage et al., 1993; Zhou et al., 1997; Efstratiadis, 1998)

Well at least you post some references now, however which of those are supposed to prove anything you claim? We are talking about increased skeletal muscle hypertrophy or hyperplasia induced by supraphysiological doses of GH and insulin. (and whether or not big infrequent spikes are more effective than regular small spikes with the same AUC). Which of those papers mentions those effects where?

Insulin rapidly activates protein synthesis by activating components of the translational machinery including eIFs (eukaryotic initiation factors) and eEFs (eukaryotic elongation factors). In the long term, insulin also increases the cellular content of ribosomes to augment the capacity for protein synthesis.Department of Biochemistry and Molecular Biology, University of British Columbia, 2350 Health Sciences Mall, Vancouver, Canada V6T 1Z3. cgpr@interchange.ubc.ca PMID: 16545079 [PubMed - indexed for MEDLINE

Protein synthesis also depends on the energy status in the muscle as it is an ATP-dependent process(Bolster et al., 2002)

ATP is most efficiently created out of glucose and oxygen. ATP is synthesized in the mitochondria. Mitochondria is located on the INSIDE of cells. Glucose must be transported to the inside of cells to be utilized by the mitchondria for ATP synthesis.

Glucose is transported by GLUT4 (a glucose transporter protein) to the plasma membrane of a muscle cell. The hormone insulin, on the outside of the cell binds, to a receptor on the plasma membrane. That binding then sends a signal to increase the amount of GLUT4 on the surface of the cell. This increases the amount of glucose taken from the outside of the cell to the inside.
Source(s):
The World of the Cell by Becker et. al

Again, what are you trying to prove with this? That insulin plays a role in skeletal muscle protein synthesis? When did I said it didn’t? Actually, I explained exactly when it does and does not and this changes nothing.

http://jcem.endojournals.org/cgi/content/full/88/6/2706
This investigation revealed that significantly enhanced incretin responses occurred in types 1 and 2 diabetic patients and in lean and obese healthy subjects during a large meal test vs. a small meal test.

Second, we found that the ß-cell sensitivity to glucose tended to increase in both type 2 diabetic patients (29%) and obese healthy subjects (22%) during the large meal, compared with the small meal. The change in ß-cell sensitivity was seen in spite of only a minor insignificant increase in plasma glucose. The increased insulin response during the large meal could, therefore, reflect an increased secretion of incretin hormones. I put the above information in my post b/c i did not want to take the bolded red text out of context. But you can see that as meal size increases so does the insulin response.

I agree that the insulin response to a big meal is larger than that to a small meal. However, with smaller but more frequent meals, you also have more frequent insulin pulses. Where in that paper (did not read the paper in full detail, might be in there, if so, plz show me where in the results) does it says the total AUC for insulin secretion is larger with a big meal compared with multiple small meals isocaloric with the big meal? Based on Table 3. Insulin secretion during the two meal tests, it appears to be the other way around.

Now I will say I should have more clearly defined fast. I mean a period of 3-4 hours between meals. That was a my mistake. Now what I did not include in my initial post intentionally was what i have the athletes do in between meals regarding supplementation of amino acids. I left that out on purpose b/c you did not share all of the information on a the topic that i wanted to know, so i did not share all of my information I had that you were interested in hearing.

OK. I think we both can agree that both issues change little about what we're discussing.

So with that understood. We can look at growth hormones relationship with IGF-1.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2439518/?tool=pmcentrez

Ben, this is a review. Plz tell which part(s) you think are relevant to our discussion.

Here is the discussion, note the bolded part:

Conclusion
The mechanisms that lead to muscle adaptation to overload are not completely understood. Neither are those that regulate muscle mass development and maintenance. GH and IGF-I clearly play a role in muscle development pre- and postnatally. In GHD adults, there is evidence that serum GH affects muscle mass maintenance, but in healthy adults neither GH nor IGF-I has or enhances the hypertrophic effects of exercise. In contrast, much evidence supports the hypertrophic effect of autocrine/paracrine IGF-I in animals and suggests that it may play a role in adaptation to overload in both animals and humans. Increased muscle expression of IGF-I also enhances the effects of training in animals. Local injection of GH or IGF-I protein or plasmids is effective in animal models and may eventually be used with therapeutic ends. There is evidence for an effect of GH on other performance parameters that is related to increased lean body mass as opposed to increased skeletal muscle mass.

Yeah I realize that your argument is that GH increases trigger skeletal muscle hyperplasia and not hypertrophy, so I did a search for hyperplasia and this is the only time it is mentioned in your own paper:

Mechanisms of muscle mass regulation
There are two main mechanisms by which muscle mass may be increased: hypertrophy or an increase in myofibre size and hyperplasia or an increase in myofibre number. It is generally accepted that the number of fibres within a muscle is fixed during the perinatal period (Stickland, 1981). It has been suggested, however, that myofibre splitting occurs if a myofibre becomes too large (Antonio and Gonyea, 1993), but this has not been reported in humans. New myofibres may also form as a result of fusion of satellite cells (see below) and small myotubes and myofibres expressing myogenic markers can be found in human muscle after training (Kadi and Thornell, 1999). Nevertheless, the consensus is that an increase in muscle cross-sectional area (CSA) is primarily due to an increase in myofibre CSA rather than myofibre number.

So in summery:
- you are likely high in reactance and inertia trait.
- you have not proved that physiological GH pulses result in hyperplasia in humans or other significant beneficial effects on skeletal muscle.
- you have not proved that physiological insulin pulses from large infrequent meals have beneficial effects on skeletal muscle compared to more infrequent smaller meals

 

[BigBen]

Like scientific data, I would like you to take forum posts into context as well. When I made that post, I was clearly just picking on Tim with as only goal to let him know he was wrong again which greatly annoys him as he likes to be a forum guru. Look at what I said:

You are clearly mistaken. Look back in this thread. Jorn your first post was "Wrong." just like i said one word. Stop trying to lie in favor of your argument.

I was just flaming (as I repeatedly pointed out), not presenting an argument so it has nothing to do with how scientific my arguments are in normal discussions.

Anyway, it looks like you at least tried to take some points I asked for into account (references and data instead of reasoning) in your last post, so I’m willing to continue in a normal manner again.



KEYWORDS: I THINK. Did I not ask you to not think and use logic which might or might not be wrong? Again, in science you do not think, use logic or extrapolate, but you use data that has been actually found. Any form of reasoning is done in the discussion to try to explain the data that have been found and for further hypotheses, NOT to prove anything. Therefore, your thinking has little to no value in a discussion when actual data is available.

Me saying "i think" was in context to what you said bud. You said :

Fall victim to a simply theory? Do you think this is only is something that applies to low IQ people or something (which would make it all the more relevant)

So in my reply i said:

No, I do not think that behavior theories apply only to lower level IQ's.

It is very clear and appropriate that i responded to you in the manner i did b/c it was in context to your original post. You are clearly allowing your emotions to enter into teh argument and you clearly have your self worth attached to your scientific beliefs. I will respond to the rest of this post but i do not care to continue with the discussion b/c their is nothing I can learn from you when you are so obviously in favor of what you have read and adopted as true that nothing can enter into your mind that does not first fit into those beliefs.



It is funny that you start explaining me on the terms I just introduced and you probably googled to look up. Furthermore, I have had actual training in them, not my own interpretations and own ‘thinking’. And you want to know what example was used in my class about reactance? Sharon Brehm (a proffesor) wanted to find out why her husband always did the exact opposite of what she told him to do. Jack Brehm is not exactly low IQ: http://brehm.socialpsychology.org/ but high in the reactance trait.


This whole paragraph assumes that i think inertia applies to low IQ people only. I clearly stated that i did not think that. I dont know what the purpose of this was other than to support what i said and that is that inertia does not apply to just low IQ persons.

See how your thinking is all wrong? That is why thinking, assuming, and extrapolating are very weak argument and not even close to evidence.

no i do not see how my thinking is wrong. I do see how you took an incorrect assumption you made about me, which i told you was incorrect and still continued to argue against a belief i do not posses.

First of all, I said: ‘I THINK this is going on:’ See how I don’t say anything absolute because I know better? Also, people who think they are smart are (as you demonstrated by saying ‘You can not seriously think that I would fall victim to such a simple theory on behavior’) are
higher in the reactance trait. So another argument can be added to the list I previously posted why I think you are being antagonistic. Nothing is proven, but I have a pretty damn strong case. Not that I care why you are antagonistic, if you are able to present a strong case it would be fine.

You are so adorably naive. I gave you a clear explanation as to what i meant when i said fall victim to the theory. You choose to ignore that post b/c if you ignore my explanation you can make an easier argument against me. The problem is that you are arguing against something that is imaginary b/c i do not exist in the manner you are trying to represent me. If i did i would be much easier to argue against i do agree with that and i also see that as being your motivation to keep ignoring me when i clarify my posts.

Yeah, let’s get into semantics, that is really proving your point. You cannot fully isolate concepts between sociology and psychology. Also, I was thought about inertia and reactance in a course given by the sociological department. I’ll guess I have to go tell them to leave that out the course next year because it has nothing to do with their area of expertise.





LOL! Better leave the analysis to me dr Freud, I already explained you above that you do not understand that your talking about. Also, nice try to dodge the bullet, but your remark does not justify anything. Luckily you provided reference from this point on, so lets take a look at them.

No you convinced yourself that you are correct b/c i dont think you have put forth an argument for anything other than supporting the fact that you twist events to benefit your points of view. It it utterly hilarious how smart you think you are and how little you notice the errors screaming from your arguments.



Well at least you post some references now, however which of those are supposed to prove anything you claim? We are talking about increased skeletal muscle hypertrophy or hyperplasia induced by supraphysiological doses of GH and insulin. (and whether or not big infrequent spikes are more effective than regular small spikes with the same AUC). Which of those papers mentions those effects where?

no no no. You are mistaken. I was talking about optimizing the levels of these hormones to keep an athlete from becoming catabolic. As a result of not force feeding the athlete every 2 hours the body is allowed to let these hormones function to their full potential rather than the mediums that would happen if they were force fed every two hours.

Again, what are you trying to prove with this? That insulin plays a role in skeletal muscle protein synthesis? When did I said it didn’t? Actually, I explained exactly when it does and does not and this changes nothing.

ok i will quote you again please do not ignore me this time:

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.

my reply:

Insulin rapidly activates protein synthesis by activating components of the translational machinery including eIFs (eukaryotic initiation factors) and eEFs (eukaryotic elongation factors). In the long term, insulin also increases the cellular content of ribosomes to augment the capacity for protein synthesis.Department of Biochemistry and Molecular Biology, University of British Columbia, 2350 Health Sciences Mall, Vancouver, Canada V6T 1Z3. cgpr@interchange.ubc.ca PMID: 16545079 [PubMed - indexed for MEDLINE

I agree that the insulin response to a big meal is larger than that to a small meal. However, with smaller but more frequent meals, you also have more frequent insulin pulses. Where in that paper (did not read the paper in full detail, might be in there, if so, plz show me where in the results) does it says the total AUC for insulin secretion is larger with a big meal compared with multiple small meals isocaloric with the big meal? Based on Table 3. Insulin secretion during the two meal tests, it appears to be the other way around.

but as you well know when insulin levels are high then GH levels are low. I choose to get the benefits from both hormones optimal function. With insulin secretion also comes seritonin secretion. Also why would you want to force feed an athlete every two hours when the athletes stmach does not really empty for 3-4 hours assuming they are eating whole food meals? You want your athlethes to walk around being stuffed all day and put the burden of digestion on them continually?


OK. I think we both can agree that both issues change little about what we're discussing.



Ben, this is a review. Plz tell which part(s) you think are relevant to our discussion.

Here is the discussion, note the bolded part:

Conclusion
The mechanisms that lead to muscle adaptation to overload are not completely understood. Neither are those that regulate muscle mass development and maintenance. GH and IGF-I clearly play a role in muscle development pre- and postnatally. In GHD adults, there is evidence that serum GH affects muscle mass maintenance, but in healthy adults neither GH nor IGF-I has or enhances the hypertrophic effects of exercise. In contrast, much evidence supports the hypertrophic effect of autocrine/paracrine IGF-I in animals and suggests that it may play a role in adaptation to overload in both animals and humans. Increased muscle expression of IGF-I also enhances the effects of training in animals. Local injection of GH or IGF-I protein or plasmids is effective in animal models and may eventually be used with therapeutic ends. There is evidence for an effect of GH on other performance parameters that is related to increased lean body mass as opposed to increased skeletal muscle mass.

Yeah I realize that your argument is that GH increases trigger skeletal muscle hyperplasia and not hypertrophy, so I did a search for hyperplasia and this is the only time it is mentioned in your own paper:

i did tell you what parts were relevant. but again they are below:
So with that understood. We can look at growth hormones relationship with IGF-1.
http://www.ncbi.nlm.nih.gov/pmc/arti...tool=pmcentrez


GH has direct effects on most tissues, including skeletal muscle (d'Ercole et al., 1984; Gostelli-Peter et al., 1994; Jorgensen et al., 2006).

GH stimulates the synthesis of IGF-I in most tissues (Figure 1Figure 1; d'Ercole et al., 1984; Gostelli-Peter et al., 1994).

In summary, normal GH/IGF-I function does have a role in the development and maintenance of muscle mass, as gathered from evidence in GH-deficient patients, burn patients, hypophysectomized animals, and animal models in which GH receptor and IGF-IR activity are lacking.(Figure 3).

My point is that i do not choose to ignore any factor that is involved in the end product. I may focus more on other factors than on this but i acknowledge it and manipulate it appropriately with meal size and meal timing.



So in summery:
- you are likely high in reactance and inertia trait.
- you have not proved that physiological GH pulses result in hyperplasia in humans or other significant beneficial effects on skeletal muscle.
- you have not proved that physiological insulin pulses from large infrequent meals have beneficial effects on skeletal muscle compared to more infrequent smaller meals

I think it is clear that you have misunderstood what really exists on my side of the argument. I have once again tried to clear this up for you. I will decide upon your reply if I will have any benefit from continuing this conversation with you. Probably not, but we will see. How do you not acknowledge that you are misrepresenting me when I clearly expressed my points in my post previous to this one? Then you quoted me and still misrepresented me. I honestly see nothing beneficial coming from this discussion.

 

[Justwonderin]

this reminds me a little of the scene in anchorman when they were yelling at the boss in his office after Veronica gets hired on and they're taking turns yelling and then Brick steps in and is like "I don't know what we're yelling about!"--- thats me right now

 

[jornT]

Weak strawmans and pulling stuff out of context. But you can try to pull that of as often as you want, I will recognize it everytime.

You are clearly mistaken. Look back in this thread. Jorn your first post was "Wrong." just like i said one word. Stop trying to lie in favor of your argument.

When did I claim that my first post was not one post? I said take it into context, and I'll explain the context again. That post was to make fun of Tim. 'Flaming' Tim has nothing to do with how scientific my discussions are, because there was not even a discussion. The discussion started when people, including you asked me to present my information.

It is very clear and appropriate that i responded to you in the manner i did b/c it was in context to your original post. You are clearly allowing your emotions to enter into teh argument and you clearly have your self worth attached to your scientific beliefs.

Uh dude, I have showed several times that your beliefs were flat out WRONG and other not proven. You on the other hand have not shown any of my beliefs wrong. Without showing that any of my 'beliefs' are wrong, it is impossible to conclude that I am attached to it and cannot admit I'm wrong.

I will respond to the rest of this post but i do not care to continue with the discussion b/c their is nothing I can learn from you when you are so obviously in favor of what you have read and adopted as true that nothing can enter into your mind that does not first fit into those beliefs.

Translation: I realize that I cannot win this argument, so I'll reframe it in a way that I can leave the discussion without admitting I'm wrong.

This whole paragraph assumes that i think inertia applies to low IQ people only. I clearly stated that i did not think that. I dont know what the purpose of this was other than to support what i said and that is that inertia does not apply to just low IQ persons.

Ok, sorry. I misread your paragraph. However, you claim to have taught yourself to not attach your emotions to any of your beliefs for that exact reason. Gimme a break. Strong claim. No one high in reactance is gonna admit: yeah I do the exact opposite of what people tell me to do. It doesn't work like that, don't act like your some Budha who has superion zen like control over his emotions.

So back to the issue at hand. You say that I cannot think such a simple behavior theory applies to you. I think it does. I think you are stupid for thinking you are 'above' them. I just explained what I think that is going on, it doesn't really have much use to continue about this as it cannot be proven.

no no no. You are mistaken. I was talking about optimizing the levels of these hormones to keep an athlete from becoming catabolic. As a result of not force feeding the athlete every 2 hours the body is allowed to let these hormones function to their full potential rather than the mediums that would happen if they were force fed every two hours.

I see your are back to 'logic' and assuming again. If you think this is how it works, show data.

ok i will quote you again please do not ignore me this time:

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.

my reply:

Insulin rapidly activates protein synthesis by activating components of the translational machinery including eIFs (eukaryotic initiation factors) and eEFs (eukaryotic elongation factors). In the long term, insulin also increases the cellular content of ribosomes to augment the capacity for protein synthesis.Department of Biochemistry and Molecular Biology, University of British Columbia, 2350 Health Sciences Mall, Vancouver, Canada V6T 1Z3. cgpr@interchange.ubc.ca PMID: 16545079 [PubMed - indexed for MEDLINE

Epic taking stuff out of context (very likely on purpose). Here is post that I made before the one you qouted:

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.

See how I recognised the rol of insulin on MPS, but point out that ADDITIONAL insulin has no benefits? The if somethng in the post you qoute = 'additional insulin', not insulin. Do you expect me to post 'insulin levels above 15 µU/ml ' everytime? I thought that was pretty obvious after that post, but if it was not, that is clearly what I was talking about. You still hav not have proven that insulin above 15 µU/ml has additional benefits wrt skeletal muscle protein synthesis, and therefore your theory is not proven.

but as you well know when insulin levels are high then GH levels are low. I choose to get the benefits from both hormones optimal function. With insulin secretion also comes seritonin secretion. Also why would you want to force feed an athlete every two hours when the athletes stmach does not really empty for 3-4 hours assuming they are eating whole food meals? You want your athlethes to walk around being stuffed all day and put the burden of digestion on them continually?

Claims and questions. Show me data that eating every 3-4h is optimal for hormone function and increase skeletal muscle protein synthesis/hypertrophy/hyperplasia or any relevant end point.
Show me (instead of shiften the burdun of proof) that being 'stuffed' all day is bad for the relevant end points mentions above. (BTW I could just as easily argue that multiple small meals are easier on the stomach than large infrequent meals)

i did tell you what parts were relevant. but again they are below:
So with that understood. We can look at growth hormones relationship with IGF-1.
http://www.ncbi.nlm.nih.gov/pmc/arti...tool=pmcentrez


GH has direct effects on most tissues, including skeletal muscle (d'Ercole et al., 1984; Gostelli-Peter et al., 1994; Jorgensen et al., 2006).

GH stimulates the synthesis of IGF-I in most tissues (Figure 1Figure 1; d'Ercole et al., 1984; Gostelli-Peter et al., 1994).

In summary, normal GH/IGF-I function does have a role in the development and maintenance of muscle mass, as gathered from evidence in GH-deficient patients, burn patients, hypophysectomized animals, and animal models in which GH receptor and IGF-IR activity are lacking.(Figure 3).

Ben those studies prove NOTHING. It appears you do not know what relevant endpoints are.

A surrogate endpoint is a measure of effect of a certain treatment that may correlate with a real endpoint but has no guaranteed relationship.

(do you agree with that, search the definition)

So GH might or might not increase IGF-1 (a surrogate endpoint), and IGF-1 might or might not correlate with the real endpoint. It does not matter, because the relationship between GH and the real endpoint has been studied and what was found? GH does not increase skeletal muscle hypertrophy or hyperplasia.

(again this is so insanely basic information)

Now keep whining that continueing this debate has no use for you and run like a coward. You cannot deny the fact that GH has been shown to be ineffective at the real endpoints and that you only posted about surrogate endpoints which is pretty much useless when real endpoint data is avaible.

 

[dilatedmuscle]

and here i was wondering whether i should put that extra tablespoon of whey

Yeah... so whats the deal, guys? More protein no matter what? less protein with more frequency? Regular masturbation to increase testosterone levels? tits or clits? live or die?

 

[BigBen]

Weak strawmans and pulling stuff out of context. But you can try to pull that of as often as you want, I will recognize it everytime.

Exactly what I expected from you. Something does not qualify as a straw man when I quote you and clearly keep you in context. It qualifies as the original garbage you posted thinking that noone would challenge you. You can not admit error. I have nothing more to gain from a discussion with you. You have proved clearly that you care more about your ego than you do the truth, at least the truth presented by anyone other than yourself. The sad part is that you actually believe what you are typing.

When did I claim that my first post was not one post? I said take it into context, and I'll explain the context again. That post was to make fun of Tim. 'Flaming' Tim has nothing to do with how scientific my discussions are, because there was not even a discussion. The discussion started when people, including you asked me to present my information.





Uh dude, I have showed several times that your beliefs were flat out WRONG and other not proven. You on the other hand have not shown any of my beliefs wrong. Without showing that any of my 'beliefs' are wrong, it is impossible to conclude that I am attached to it and cannot admit I'm wrong.

That was not the point at all of the paragraph you qquoted. You said:

KEYWORDS: I THINK. Did I not ask you to not think and use logic which might or might not be wrong? Again, in science you do not think, use logic or extrapolate, but you use data that has been actually found. Any form of reasoning is done in the discussion to try to explain the data that have been found and for further hypotheses, NOT to prove anything. Therefore, your thinking has little to no value in a discussion when actual data is available.

So i replied :

Me saying "i think" was in context to what you said bud. You said :


Quote:
Originally Posted by jornT
Fall victim to a simply theory? Do you think this is only is something that applies to low IQ people or something (which would make it all the more relevant)

So in my reply i said:

Quote:
Originally Posted by BigBen
No, I do not think that behavior theories apply only to lower level IQ's.

Showing you that me saying "i think" means " no the belief I hold" It is appropriate to the context of the argument. Your looking weaker by the minute.


Translation: I realize that I cannot win this argument, so I'll reframe it in a way that I can leave the discussion without admitting I'm wrong.

No, not at all. Actually I see the weakness of your argument and I am exposing it pargraph by paragraph in each and every reply and I know i am the stronger. The fact that i choose not to clarify after this post is proof that. The weakness represented by your arguement should offend the scienific side of you.


Ok, sorry. I misread your paragraph. However, you claim to have taught yourself to not attach your emotions to any of your beliefs for that exact reason. Gimme a break. Strong claim. No one high in reactance is gonna admit: yeah I do the exact opposite of what people tell me to do. It doesn't work like that, don't act like your some Budha who has superion zen like control over his emotions.


Actually Sir, and I say sir b/c i do respect you for what you desire to be, i respond b/c you need to be challenged. You have not presented anyinformation that would require me to change my belif other than your words backed by no studies shwoing the opposite of what I am saying. I would absolutley admit being wrong in front of the entire forum and anyone else for that matter if I was incorrect. The fact of the matter is that I do not desire to get glorified for my knowledge. I read all that I do b/c i do desire to understand, for myself. I do have total control over my emotions other than those that are initially reflexes. But Jorn if you show me that growth hormone, insulin, and IGF-1 are not relevant at the levels the occur at naturally then I would definitely reconsider. BUT how can i be expected to believe your word when it is not backed by studies when you would not accpet mine.

So back to the issue at hand. You say that I cannot think such a simple behavior theory applies to you. I think it does. I think you are stupid for thinking you are 'above' them. I just explained what I think that is going on, it doesn't really have much use to continue about this as it cannot be proven.

No, you think your argument is correct and in light of my antagonisic repsonses to you, you reason that I must be most easily explained by inertia. The fact of the matter is that could not be further from he truth. You have not presented any information other than your own word that i am wrong. I want you to post a study that says that growth hormone, insulin, and IGF-1 at naturally occuring levels or slightly above play a role small enough to ignore in muscle hypertrophy and/or growth and i will definately admit my error, glady.

I see your are back to 'logic' and assuming again. If you think this is how it works, show data.

i honestly do not want to waste my time trying to convince you of anything anymore as it is wasted effort, honestly.

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.



Epic taking stuff out of context (very likely on purpose). Here is post that I made before the one you qouted:



See how I recognised the rol of insulin on MPS, but point out that ADDITIONAL insulin has no benefits? The if somethng in the post you qoute = 'additional insulin', not insulin. Do you expect me to post 'insulin levels above 15 µU/ml ' everytime? I thought that was pretty obvious after that post, but if it was not, that is clearly what I was talking about. You still hav not have proven that insulin above 15 µU/ml has additional benefits wrt skeletal muscle protein synthesis, and therefore your theory is not proven.



Claims and questions. Show me data that eating every 3-4h is optimal for hormone function and increase skeletal muscle protein synthesis/hypertrophy/hyperplasia or any relevant end point.
Show me (instead of shiften the burdun of proof) that being 'stuffed' all day is bad for the relevant end points mentions above. (BTW I could just as easily argue that multiple small meals are easier on the stomach than large infrequent meals)



Ben those studies prove NOTHING. It appears you do not know what relevant endpoints are.

A surrogate endpoint is a measure of effect of a certain treatment that may correlate with a real endpoint but has no guaranteed relationship.

(do you agree with that, search the definition)

So GH might or might not increase IGF-1 (a surrogate endpoint), and IGF-1 might or might not correlate with the real endpoint. It does not matter, because the relationship between GH and the real endpoint has been studied and what was found? GH does not increase skeletal muscle hypertrophy or hyperplasia.

(again this is so insanely basic information)

Now keep whining that continueing this debate has no use for you and run like a coward. You cannot deny the fact that GH has been shown to be ineffective at the real endpoints and that you only posted about surrogate endpoints which is pretty much useless when real endpoint data is avaible.

Jorn what purpose do i have from 'running' from your weak arguing points. I feel like you are an utter waste of my time at this point. I choose to not cooment b/c you make the same errors in argument hat you are complaining i make. You make claims about my posts but then dont back then wiiith any thing, in one instance you put one study to back you, but that is hardly enough to be mind changing. You keep taking my points about GH out of context. I will repeat myself and then back it again with a study. GH and IGF-1 should not be ignored as a factor of muscle growth b/c of their anti catabolic effects even at normal physiologcal dosages.

In summary, normal GH/IGF-I function does have a role in the development and maintenance of muscle mass, as gathered from evidence in GH-deficient patients, burn patients, hypophysectomized animals, and animal models in which GH receptor and IGF-IR activity are lacking.(Figure 3).

So i suppose you will whine for a while then post weak counter arguments as you have been doing the last 3 posts since I backed my claims with evidance. Do not misrepresent my points of view then argue against me. At this point I have no benefit from continuing with you b/c you are in it for the glory of your ego. If not then ignore me, b/c I will certainly be ignoring you from this point forward. You add nothing other than stubbornedness to this thread and frustration b/c your weak counter arguments are not accepted.

/My pariciapation in the thread

Reason: I am beyond your emotion driven responses.

 

[jornT]

Nice try, and I fully expect you not to respond to this as must be pretty clear for you that you cannot win this argument (for the simple reason you are wrong).

What was your original post:

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.

Muscle cells do divide in the presence of Growth hormone

We discussed so far that GH does not increase skeletal muscle protein synthesis/hypertrophy/hyperplasia (your own review said so). And now all in a sudden you come with anti-catabolic shit? That is NOT what you said originally.

Do you even realize that you just admit I was right when I said that GH had no beneficial effects with relation to increasing MPS/hypertrophy/hyperplasia, and since that is what we were discussing....

In summary, normal GH/IGF-I function does have a role in the development and maintenance of muscle mass, as gathered from evidence in GH-deficient patients, burn patients, hypophysectomized animals, and animal models in which GH receptor and IGF-IR activity are lacking.(Figure 3). [/COLOR]

Yeah to bad none of those models are relevant. Your argument was that pulses of these hormones would have beneficial effects in your ATHLETES and now you come with deficiency models. Or do you not understand that deficiency models are not always relevant?

Being depleted in vitamins/minerals etc also lowers test. That does not mean that those vitamins/minerals increase test everytime you give it to them. (although the supplement industry tries to make you believe this) They only do when you are deficient. Deficiency models are not valid to support your original claims. Plz provide data about normal humans, where physiological pulses increase relevant endpoints.

 

[MrChewiebitums]

this is really getting annoying, its like watching two really smart babys fight over a rattle

 

[Big_Guns_Lance]

What the hells happened in here.

 

[BigBen]

Nice try, and I fully expect you not to respond to this as must be pretty clear for you that you cannot win this argument (for the simple reason you are wrong).

What was your original post:





We discussed so far that GH does not increase skeletal muscle protein synthesis/hypertrophy/hyperplasia (your own review said so). And now all in a sudden you come with anti-catabolic shit? That is NOT what you said originally.

So again. The benefits i mention of Growth hormone come from the fact that when growth hormone increases so does the stimulation of IGF-1 synthesis.



IGF-1 effect on skeletal muscle:

Insulin-like growth factor 1 (IGF-1) can induce skeletal muscle hypertrophy, defined as an increase in skeletal muscle mass. Hypertrophy occurs as a result of an increase in the size, as opposed to the number, of pre-existing skeletal muscle fibers. IGF-1's pro-hypertrophy activity comes predominantly through its ability to activate the Phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. Novartis Institutes for BioMedical Research Inc., 100 Technology Square room 4210, Cambridge, MA 02139, USA




Do you even realize that you just admit I was right when I said that GH had no beneficial effects with relation to increasing MPS/hypertrophy/hyperplasia, and since that is what we were discussing....

I should have been more specific about why growth hormone was beneficial for skeletal muscle growth b/c of its relationship with IGF-1 synthesis. I will give you that. I will also say that i was under the impression that IGF-1 caused skeletal muscle cell hyperplasia, but that does not appear to be the case. All recent studies I have read show IGF-1 positively effects muscle cell hypertrophy, not hyperplasia. One of those studies is quoted above.

Yeah to bad none of those models are relevant. Your argument was that pulses of these hormones would have beneficial effects in your ATHLETES and now you come with deficiency models. Or do you not understand that deficiency models are not always relevant?


http://www.pponline.co.uk/encyc/human-growth-hormone.html
What many athletes and coaches have failed to understand, however, is that athletes can employ specific training regimens and dietary strategies to optimise their natural secretion of human growth hormone (hGH)

Diet, exercise and sleep patterns all play a role in human growth hormone (hGH) secretion.

foods stimulate insulin secretion which, in turn, contributes to a reduction in human growth hormone (hGH)Metabolism 48(9): 1152-6

Part of the reason I allow longer periods between meals. I supplement amino acids in between meals also.

The reasoning:

http://74.125.95.132/search?q=cache:...&ct=clnk&gl=us

A study was carried out in 15 male volunteers to evaluate qualitatively the secretion of growth factors following stimulation by oral amino acids. the results showed that oral administration of a combination of two amino acids (1200 mg l-lysine plus 1200 mg l-Arginine Pyroglutamate) provoked a release of pituitary somatotrophin and insulin. This phenomenon was reproducible and the growth hormone secreted in response to this stimulation had biological activity (as demonstrated by radiorecepter assay and somatomedin induction).

We could demonstrate that the association of the two amino acids does result in the release of biological-active hormone able to affect peripheral cellar receptors and thus growth in general.

Insulin is, of course, an equally important factor in cell growth. Even if there are some uncertainties regarding the bioactivity of the substance assayed, there is no doubt the amino acids stimulated insulin as well as HGH: hence, both of the physiologically important growth factors are affected. It should also be noted that the hypoglycemia which follows the insulin peak is a further stimulus to HGH secretion.

Probably the most significant aspect of our findings is that these HGH responses have demonstrated following oral administration of the amino acid complex.

References

Cited References used in the above study can be obtained from Bio Corp., 204 East 2nd Avenue, Suite 408, San Mateo, California 94401, 1-800-246-9004
The above study clearly demonstrates the effectiveness of blending specific amino acids to achieve increased levels of growth hormone production.



Previous research has demonstrated that ingestion of essential amino acids and their metabolites induce anabolic effects with the potential to augment gains in lean body mass and strength after resistance exercise training.

The purpose of the present study was to examine the effects of an essential amino acid-based formula (Muscle Armor™ (MA); Abbott Laboratories, Abbott Park, IL) containing β-hydroxy-β-methylbutyrate (HMB) on hormonal and muscle damage markers in response to 12 wk of resistance exercise.


Results: Lean body mass, muscle strength, and muscle power significantly (P ≤ 0.05) increased in both groups after training; however, MA supplementation augmented these responses to a significantly greater extent when compared with the CON group. MA supplementation promoted increases in resting and exercise-induced testosterone and resting growth hormone concentrations. In addition, MA reduced preexercise cortisol concentrations. Throughout the training protocol, MA attenuated circulating creatine kinase and malondealdehyde compared with the CON group, suggesting that MA might have influenced a reduction in muscle damage.

Again more evidence to support amino acid supplementation for greater gains through hormone regulation: MA supplementation promoted increases in resting and exercise-induced testosterone and resting growth hormone concentrations. In addition, MA reduced preexercise cortisol concentrations.


Muscle Armor™ (MA) = essential amino acid-based formula
More evidence that suggests that increasing these levels of hormones does in fact make a difference in the composition of an athlete even if they are not supraphysiological increases.

 

[jornT]

I should have been more specific about why growth hormone was beneficial for skeletal muscle growth b/c of its relationship with IGF-1 synthesis. I will give you that. I will also say that i was under the impression that IGF-1 caused skeletal muscle cell hyperplasia, but that does not appear to be the case. All recent studies I have read show IGF-1 positively effects muscle cell hypertrophy, not hyperplasia. One of those studies is quoted above.

Great, you are admitting you were wrong on a couple of things. We are starting to get somewhere.

However, you are still making a couple of logical mistakes. The study where you bolded the effects of IGF-1 on protein synthesis says IGF-1 CAN induce skeletal muscle hypertophy. The same is through for insulin, however, at which doses, in what context etc? The effects of hormones on skeletal muscle hypertrophy are not YES or NO, but it depends on alot of factors including dose. I explained this before in the context of insulin.

However, what is more important is that you still use surrogate endpoints. You try to string studies together:
study A: GH increases IGF-1
study B: IGF-1 increases hypertrophy (again, look at the context including dose, have you done this? Because you can already guess what kind of specific claims I would like see referenced)

your conclusion (if we assume B in correct, which we can't based on the data you have provided): GH increases hypertrophy.

However, that is not how science works, data that looks DIRECTLY at real endpoints, in this case skeletal muscle hypertrophy have much more value. (Like a compare a meta-analyse has much more value than a cross sectional study, this is NOT a case of there is conflicting data so the truth must be somewhere in between).

Can you explain to me, why studies who examined the effect of GH on skeletal muscle hypertrophy, have found no results? If GH has significant effects on IGF-1 and IGF-1 has significant effects on skeletal muscle hypertrophy, why hasn't that process happend and resulted in hypertrophy in those studies?

Also, you make logical mistakes with your amino acid studies. Amino acids might influence hormones, and they might also influence lean body mass. But that does not prove that the effects of amino acids on lean body mass are because of the hormones. They might have other effects which are responsible for that.

 

[Natzo]

what happened to disagree with me equals gay??

 

[BigBen]

Great, you are admitting you were wrong on a couple of things. We are starting to get somewhere.

However, you are still making a couple of logical mistakes. The study where you bolded the effects of IGF-1 on protein synthesis says IGF-1 CAN induce skeletal muscle hypertophy. The same is through for insulin, however, at which doses, in what context etc? The effects of hormones on skeletal muscle hypertrophy are not YES or NO, but it depends on alot of factors including dose. I explained this before in the context of insulin.

Everything i have been reading leads me to believe that they are unsure or have not came to a definite conclusion beyond the fact that IGF-1 DOES play a role in skeletal muscle hypertrophy and acts as an anti catabolic agent as well.

Can you explain to me, why studies who examined the effect of GH on skeletal muscle hypertrophy, have found no results? If GH has significant effects on IGF-1 and IGF-1 has significant effects on skeletal muscle hypertrophy, why hasn't that process happend and resulted in hypertrophy in those studies?



Post a few studies please, i am not saying i dont believe you I would just like to read them. But what you are saying is that you do not believe that the relationship between GH and IGF-1 is important and that IGF-1 is not a relevant enough factor to consider when looking at prevention of skeletal muscle wasting, skeletal muscle maintenance, and skeletal muscle hypertrophy. That is what I am getting form you and that is why I keep arguing with you. I read things like the studies below and see that IGF-1 and GH are relevant to skeletal muscle mass. Maybe they are not the most important factor but why should they be over looked in light of these:

IGF-1 LOCALLY

GH stimulates the synthesis of IGF-I in most tissues(Figure 1Figure 1; d'Ercole et al., 1984; Gostelli-Peter et al., 1994)

In conclusion, the mechanisms of load-induced muscle hypertrophy are still not fully understood, but increasing evidence suggests a role for locally expressed IGF-I in this process.J Physiol. 2003 February 15; 547(Pt 1): 247–254.



IGF-1 IN BLOOD PLASMA
GH increases hepatic IGF-1-mRNA and the plasma IGF-1 level.PMID: 8887900 [PubMed - indexed for MEDLINE]

IGF-1 does not bind to hepatocytes or adipocytes, and therefore its primary insulin-sensitizing action is believed to be mediated through skeletal muscle.J Clin Invest. 2004 January 1; 113(1): 25–27.
doi: 10.1172/JCI200420660.


IGF-1 ON SKELETAL MUSCLE
(IGF-1) is a promising anti-atrophy agent2, 3, 4, 5 because of its ability to promote hypertrophy. IGF-1 stimulates the proliferation of satellite cells. Skeltal muscle hypertrophy is regulated by at least three major molecular processes; (1) satellite cell activity; (2)gene transcription; (3) protein translation. IGF-1 can influence the activity of all these mechanisms including increase in proliferation in satellite cells, skeletal actin mRNA expression and protein synthesis. (Florini et al. 1996; Chakravarthy et al. 2000a). Thus, increased IGF-1 expression plays an important role in mediating muscle hypertrophy induced by mechanical loading (Adams & Haddad, 1996; Adams & McCue,1998).


Results indicate that a single bout of mechanical loading in humans alters activity of the muscle IGF-I system, and the enhanced response to ECC suggests that IGF-I may somehow modulate tissue regeneration after mechanical damage.Am J Physiol Endocrinol Metab 280: E383-E390, 2001;
0193-1849/01

Insulin-like growth factor-1 (IGF-1) is known to have anabolic effects on skeletal muscle cells.Journal of Applied Physiology
Vol. 81, No. 6, pp. 2509-2516, December 1996
EXERCISE AND MUSCLE




Also, you make logical mistakes with your amino acid studies. Amino acids might influence hormones, and they might also influence lean body mass. But that does not prove that the effects of amino acids on lean body mass are because of the hormones. They might have other effects which are responsible for that.

Does not prove that they were not from that either i posted that study b/c as lean mass increased as hormone levels were higher. The purpose of me positing the study was to say hormones increased along with and increase of skeletal muscle. I know it does prove a cause and effect relationship but their is a positive correlation. But i agree you cant be sure and i was not trying to say that for sure.


I have another question why are you arguing so strongly against doing things to increase GH production and IGF-1 production when you appear to be in favor of milk bc of its ability to increase plasma igf-1 in this thread?

http://www.musclemecca.com/showthread.php/most-underrated-protein-carb-fat-sources-46426p2.html

First off Ben, I'm not out to flame you like I used to. Having said that, your approch to nutrition is still flawed. You presume to many things.

Milk has been shown to raise plasma IGF-1 in humans. Even if you do not know this, this is something you can look up within seconds, you should not do guess work.

Flex posted that people who drink milk have higher IGF-1.You posted that IGF-1 in milk gets destroyed in the stomach. This is corrected, BUT, not a logical point to make. Milk still raises plasma IGF-1, so your addition that the IGF-1 in milk gets destroyed in the stomach doesn't add anything, except possible confusion for people who might think that you're trying to say that milk ingestion does not raise IGF-1. See my problem with it?

Having made sure to say that milk affects plasma IGF-1 you must have some positive belief in IGF-1 and its effects on skeletal muscle. But maybe your not in favor of milk for that reason, but it does look that way. Im sure you will clear that up though.

 

[remnant]

Its a miscalculation to consume too much protein. The fact remains that excess proteins are shed by use body through the process of deamination. Therefore consuming excess proteins does not yield any tangible dividends.

 

[Alexandoy]

Its a miscalculation to consume too much protein. The fact remains that excess proteins are shed by use body through the process of deamination. Therefore consuming excess proteins does not yield any tangible dividends.

I know that anything excessive in our intake is usually just a waste but not much of an issue. I asked a doctor about Vitamin C and excessive intake will just result in temporary loose bowel movement so the body can shed off the excess Vitamin C. But with protein, I'm sure there is no benefit when taken in excess. But does it really have a very bad effect on the body?