Results 1 to 24 of 24

Thread: Nutrient Partitioning

  1. #1
    Senior Member
    Join Date
    Dec 2001
    Posts
    0

    Nutrient Partitioning

    I've been doing alot of research lately. From what I've been able to gather it seems that nutrient partitioning is key when it comes to a clean bulk. Being able to add a good amount of LBM w/o adding much or any BF. Plus there are so many methods of increasing nutrient partitioning, such as supplementing with Ephedrine/nicotine and green tea, also weight training or HIIT. Another thing that I've learned is that supplementing with fish oils can help steer fat storage away from the midsection(spare tire) in males, which is always a plus when bulking, especially for me. I hate having that fat on my abs.

    Does anybody have something to add to this?

  2. #2
    Do that voodoo that he do
    Join Date
    Apr 2002
    Location
    Bangor, ME, United States
    Posts
    4,173
    Read the refeed sticky if you haven't already.

    That should give you some more info, then you can get into more specific questions.
    Be a man. Be awesome at it. Be proud of it. Beyond the Barbell

    "Borris is correct. That sounds logical if you ask me."
    -galileo

  3. #3
    Senior Member Spartacus's Avatar
    Join Date
    Feb 2003
    Location
    Chicago
    Posts
    965
    isn't part of what makes hiit nutrient partition the fact that it depletes muscle glycogen, so nutirents entering the body after a workout go toward the muscle?

    so on the net is it helpful for bulking?

  4. #4
    Senior Member
    Join Date
    Dec 2001
    Posts
    0
    I read that ages ago when the thread was first started, but why would one need to refeed while bulking? I'll be eating excess calories so how would my leptin drop?

    Or are you refering to ST's dieting strategy?
    Last edited by Bryan; 09-29-2003 at 10:00 AM.

  5. #5
    $3n10r M3mb3r defcon's Avatar
    Join Date
    Jul 2003
    Location
    Canada
    Posts
    1,331
    hmm, i never heard of nutrient partitioning before.. can someone give me a link to a basic over view of it.. or explain it to me please. thanx

  6. #6
    confused by simplicity bradley's Avatar
    Join Date
    Aug 2002
    Location
    Alabama
    Posts
    5,467
    Originally posted by Spartacus
    isn't part of what makes hiit nutrient partition the fact that it depletes muscle glycogen, so nutirents entering the body after a workout go toward the muscle?

    so on the net is it helpful for bulking?
    Yes, HIIT will cause GLUT4 translocation, due to the effects of the muscles contracting, which will cause a nutrient partitioning effect. Glucose transporter (GLUT) receptors are responsible for glucose uptake into the cells, but they are also found in fat cells as well. If the GLUT receptors are not "available" on the muscle cell then the remaining glucose will be taken up by adipose tissue (fat).

    Note there are other types of GLUT receptors located throughout the body.

  7. #7
    confused by simplicity bradley's Avatar
    Join Date
    Aug 2002
    Location
    Alabama
    Posts
    5,467
    Originally posted by defcon
    hmm, i never heard of nutrient partitioning before.. can someone give me a link to a basic over view of it.. or explain it to me please. thanx
    Basically nutrient partitioning is the process of getting nutrients into the muscles cells and not into fat cells (positive partitioning).

  8. #8
    Senior Member Spartacus's Avatar
    Join Date
    Feb 2003
    Location
    Chicago
    Posts
    965
    so can nutrient partitioning cause muscle to grow at an accelerated rate compared to fat cell growth?

    so is muscle growth not necessarily limited by microtrama inflicted by excercise?

  9. #9
    Do that voodoo that he do
    Join Date
    Apr 2002
    Location
    Bangor, ME, United States
    Posts
    4,173
    Originally posted by Bryan
    I read that ages ago when the thread was first started, but why would one need to refeed while bulking? I'll be eating excess calories so how would my leptin drop?

    Or are you refering to ST's dieting strategy?
    Sort of. I just wanted to make sure you'd read the sticky. Partitioning is one of my main study hobbies.

    The general: "Anyone have something to add to this" was pretty vague. There's a lot more to add, I was just wondering which route you were going to go down.
    Be a man. Be awesome at it. Be proud of it. Beyond the Barbell

    "Borris is correct. That sounds logical if you ask me."
    -galileo

  10. #10
    confused by simplicity bradley's Avatar
    Join Date
    Aug 2002
    Location
    Alabama
    Posts
    5,467

    Re: Nutrient Partitioning

    Originally posted by Bryan
    I've been doing alot of research lately. From what I've been able to gather it seems that nutrient partitioning is key when it comes to a clean bulk. Being able to add a good amount of LBM w/o adding much or any BF. Plus there are so many methods of increasing nutrient partitioning, such as supplementing with Ephedrine/nicotine and green tea, also weight training or HIIT. Another thing that I've learned is that supplementing with fish oils can help steer fat storage away from the midsection(spare tire) in males, which is always a plus when bulking, especially for me. I hate having that fat on my abs.

    Does anybody have something to add to this?
    Alpha lipoic acid would also fall into this category, as well as the other insulin mimickers.

  11. #11
    Do that voodoo that he do
    Join Date
    Apr 2002
    Location
    Bangor, ME, United States
    Posts
    4,173
    Originally posted by Spartacus
    so can nutrient partitioning cause muscle to grow at an accelerated rate compared to fat cell growth?

    so is muscle growth not necessarily limited by microtrama inflicted by excercise?
    That's kind of a 'round-about explanation, but yeah, you can grow muscle at a faster rate than you gain fat.

    Of course, this can be done with a standard bulk (which has partitioning properties of course). Partitioning is becoming sort of a buzz word.

    What do you mean by not necessarily limited by microtrauma inflicted by exercise? Do you mean if someone sits around and in a caloric surplus will gain muscle? Yes, actually, they will. Their proportion of fat gain will be much higher than that of muscle, but being overfed is an anabolic stimulous.
    Be a man. Be awesome at it. Be proud of it. Beyond the Barbell

    "Borris is correct. That sounds logical if you ask me."
    -galileo

  12. #12
    confused by simplicity bradley's Avatar
    Join Date
    Aug 2002
    Location
    Alabama
    Posts
    5,467
    Originally posted by Spartacus
    so can nutrient partitioning cause muscle to grow at an accelerated rate compared to fat cell growth?
    Well by causing an increased amount of nutrients to enter the cell, then yes this would cause increase in muscle cell growth. Although this would be more of a "byproduct" of training.



    so is muscle growth not necessarily limited by microtrama inflicted by excercise?
    If there are not nutrients (glucose, aminos, etc.) to help rebuild the damaged muscle cell then you will not grow. You need muscle contraction to increase nutrient partitioning, and then you need nutrients to help rebuild the damaged muscle tissue. Hence the reason pre/post workout nutrition is so important. One follows the other, so to speak.
    Last edited by bradley; 09-29-2003 at 10:41 AM.

  13. #13
    Senior Member Spartacus's Avatar
    Join Date
    Feb 2003
    Location
    Chicago
    Posts
    965
    do you think that muscle would grow faster if nutirent partitioners are added, provided cals, pre and post workout shake, workout routine etc are all the same
    Last edited by Spartacus; 09-29-2003 at 10:44 AM.

  14. #14
    confused by simplicity bradley's Avatar
    Join Date
    Aug 2002
    Location
    Alabama
    Posts
    5,467
    Originally posted by Spartacus
    do you think that muscle would grow faster if nutirent partitioners are added, provided cals, pre and post workout shake, etc are all the same
    Supplements like fish oil have many benefits above and beyong that of being a nutrient partioner, but increased nutrient partitioning would be beneficial as far as maximizing muscle gain and minimizing fat gain. How much of a difference they will make is the real question.

    ALA has its benefits, but it is not for everyone. If you are an ectomorph then ALA might be of more benefit, but if you are an endomorph then ALA might not be your best bet.

    CLA would also be another supplement that could be considered a nutrient partioner.
    Last edited by bradley; 09-29-2003 at 10:48 AM.

  15. #15
    Senior Member
    Join Date
    Dec 2001
    Posts
    0
    The general: "Anyone have something to add to this" was pretty vague. There's a lot more to add, I was just wondering which route you were going to go down.
    Just anything to push the subject further, what other supplements do you know of that have partitioning characteristics? Bradley mentioned R-ALA.

    If I'm not mistaken ALCAR can be added to the list also.
    Last edited by Bryan; 09-29-2003 at 10:56 AM.

  16. #16
    confused by simplicity bradley's Avatar
    Join Date
    Aug 2002
    Location
    Alabama
    Posts
    5,467
    Originally posted by Bryan
    If I'm not mistaken ALCAR can be added to the list also.
    Yes L-carnitine and ALCAR have reported nutrient partioning effects, as well as vanadium and vinegar.

  17. #17
    Gonnabebig Member JuniorMint6669's Avatar
    Join Date
    Jun 2003
    Location
    Costa Mesa, CA
    Posts
    1,697
    Originally posted by bradley


    but if you are an endomorph then ALA might not be your best bet.

    Ive heard this a lot, but never really an explanation as to why not? Also, what about mesomorphs? (Im thinking that all this time I was just a lazy mesomorph, hiding in an endo's body)

    Also, what is your opinion on ALA vs. R-ALA?

  18. #18
    Senior Member
    Join Date
    Dec 2001
    Posts
    0
    ALA has two isomers(I think), S-ALA and R-ALA, R-ALA is the one you're after when you're supplementing with ALA. So companies started to extract(i guess) the R-ALA. R-ALA is more expensive generally than ALA but you dont need to take as many grams/day.

  19. #19
    confused by simplicity bradley's Avatar
    Join Date
    Aug 2002
    Location
    Alabama
    Posts
    5,467
    Originally posted by JuniorMint6669


    Ive heard this a lot, but never really an explanation as to why not? Also, what about mesomorphs? (Im thinking that all this time I was just a lazy mesomorph, hiding in an endo's body)
    An endomorph would run the risk of having too much glucose in the cells, since ALA works independant of insulin, which would cause more of a lipogenic state, via DNL. I am sure ALA would be more suited for a meso than an endo, since mesomorphs are somewhere "in between" endomorphs and ectomorphs.


    Also, what is your opinion on ALA vs. R-ALA?
    If I was just going by the what the literature states, then I would say R-ALA, but I have seen many anecdotal reports stating that the racemic is better than R-ALA. I think R-ALA is probably the better of the two, but it would depend on who you are asking. The study below might be of interest.

    ----------------

    Differential effects of lipoic acid stereoisomers on glucose metabolism in insulin-resistant skeletal muscle.

    Streeper RS, Henriksen EJ, Jacob S, Hokama JY, Fogt DL, Tritschler HJ.

    Department of Physiology, University of Arizona, Tucson 85721-0093, USA.

    The racemic mixture of the antioxidant alpha-lipoic acid (ALA) enhances insulin-stimulated glucose metabolism in insulin-resistant humans and animals. We determined the individual effects of the pure R-(+) and S-(-) enantiomers of ALA on glucose metabolism in skeletal muscle of an animal model of insulin resistance, hyperinsulinemia, and dyslipidemia: the obese Zucker (fa/fa) rat. Obese rats were treated intraperitoneally acutely (100 mg/kg body wt for 1 h) or chronically [10 days with 30 mg/kg of R-(+)-ALA or 50 mg/kg of S-(-)-ALA]. Glucose transport [2-deoxyglucose (2-DG) uptake], glycogen synthesis, and glucose oxidation were determined in the epitrochlearis muscles in the absence or presence of insulin (13.3 nM). Acutely, R-(+)-ALA increased insulin-mediated 2-DG-uptake by 64% (P < 0.05), whereas S-(-)-ALA had no significant effect. Although chronic R-(+)-ALA treatment significantly reduced plasma insulin (17%) and free fatty acids (FFA; 35%) relative to vehicle-treated obese animals, S-(-)-ALA treatment further increased insulin (15%) and had no effect on FFA. Insulin-stimulated 2-DG uptake was increased by 65% by chronic R-(+)-ALA treatment, whereas S-(-)-ALA administration resulted in only a 29% improvement. Chronic R-(+)-ALA treatment elicited a 26% increase in insulin-stimulated glycogen synthesis and a 33% enhancement of insulin-stimulated glucose oxidation. No significant increase in these parameters was observed after S-(-)-ALA treatment. Glucose transporter (GLUT-4) protein was unchanged after chronic R-(+)-ALA treatment but was reduced to 81 +/- 6% of obese control with S-(-)-ALA treatment. Therefore, chronic parenteral treatment with the antioxidant ALA enhances insulin-stimulated glucose transport and non-oxidative and oxidative glucose metabolism in insulin-resistant rat skeletal muscle, with the R-(+) enantiomer being much more effective than the S-(-) enantiomer.

  20. #20
    Gonnabebig Member JuniorMint6669's Avatar
    Join Date
    Jun 2003
    Location
    Costa Mesa, CA
    Posts
    1,697
    Ill try to tie this all in together at the end.



    Originally posted by bradley
    The racemic mixture of the antioxidant alpha-lipoic acid (ALA) enhances insulin-stimulated glucose metabolism in insulin-resistant humans and animals. We determined the individual effects of the pure R-(+) and S-(-) enantiomers of ALA on glucose metabolism in skeletal muscle of an animal model of insulin resistance, hyperinsulinemia, and dyslipidemia: the obese Zucker (fa/fa) rat. Obese rats were treated intraperitoneally acutely (100 mg/kg body wt for 1 h) or chronically [10 days with 30 mg/kg of R-(+)-ALA or 50 mg/kg of S-(-)-ALA]. Glucose transport [2-deoxyglucose (2-DG) uptake], glycogen synthesis, and glucose oxidation were determined in the epitrochlearis muscles in the absence or presence of insulin (13.3 nM). Acutely, R-(+)-ALA increased insulin-mediated 2-DG-uptake by 64% (P < 0.05), whereas S-(-)-ALA had no significant effect.
    Many people say the S isomer has a negative effect, that cancels out some of the R isomer. But here, it shows no significant effect.

    Although chronic R-(+)-ALA treatment significantly reduced plasma insulin (17%) and free fatty acids (FFA; 35%) relative to vehicle-treated obese animals, S-(-)-ALA treatment further increased insulin (15%) and had no effect on FFA.
    R isomer reduces plasma insulin, is this a good thing? However S isomer increases insulin, is this bad? Perhaps this is "canceling out" effect people sometimes refer to.

    Insulin-stimulated 2-DG uptake was increased by 65% by chronic R-(+)-ALA treatment, whereas S-(-)-ALA administration resulted in only a 29% improvement. Chronic R-(+)-ALA treatment elicited a 26% increase in insulin-stimulated glycogen synthesis and a 33% enhancement of insulin-stimulated glucose oxidation. No significant increase in these parameters was observed after S-(-)-ALA treatment.
    Again, I do not see a negative effect of the S isomer, but rather a 29% improvment in 2-DG uptake.

    Glucose transporter (GLUT-4) protein was unchanged after chronic R-(+)-ALA treatment but was reduced to 81 +/- 6% of obese control with S-(-)-ALA treatment. Therefore, chronic parenteral treatment with the antioxidant ALA enhances insulin-stimulated glucose transport and non-oxidative and oxidative glucose metabolism in insulin-resistant rat skeletal muscle, with the R-(+) enantiomer being much more effective than the S-(-) enantiomer.

    Well studies are just studies, but ive read others like this. It seems to me, cost wise, it would be much better to take a mix rather than R-ALA. 300mg of a mix is the cheaper than 100mg of R-ALA. If you had a 50/50 mix of the isomers, you are getting 150mg of R-ALA plus the slim benefits of the S isomer. However I am not sure if this is the typical makeup of the mix, as a 10/90 mix would likely yield much different results.

    I have also heard anectodal reports going both ways, yet most seem to favor R-ALA. I just am trying to understand why I have about 1 weeks worth of R-ALA left, at which point I will switch to racemic just to try it out for myself.

    Also, why would more glucose in the cells be more lipogenic than not using ALA and having it go to AT anyways? Or would it be the same, and just be a waste of money on a supplement that does nothing?

    Thankyou

  21. #21
    confused by simplicity bradley's Avatar
    Join Date
    Aug 2002
    Location
    Alabama
    Posts
    5,467
    Originally posted by JuniorMint6669
    Many people say the S isomer has a negative effect, that cancels out some of the R isomer. But here, it shows no significant effect.
    In that particular instance the S-isomer had no significant affect, while the R-isomer increased glucose uptake by 64%, which I agree is of no consequence other than the fact that you have to take more ALA as compared to R-ALA.

    R isomer reduces plasma insulin, is this a good thing? However S isomer increases insulin, is this bad? Perhaps this is "canceling out" effect people sometimes refer to.
    If the goal if ALA is to increase glucose uptake (insulin mimicker), you would not want to increase insulin, due to insulin's effect on lipolysis. If insulin is present you will not be burning fat, so in essence the S-isomer is detracting from the benefits associated with the R-isomer.

    Again, I do not see a negative effect of the S isomer, but rather a 29% improvment in 2-DG uptake.
    "Insulin-stimulated 2-DG uptake was increased by 65% by chronic R-(+)-ALA treatment, whereas S-(-)-ALA administration resulted in only a 29% improvement. Chronic R-(+)-ALA treatment elicited a 26% increase in insulin-stimulated glycogen synthesis and a 33% enhancement of insulin-stimulated glucose oxidation. No significant increase in these parameters was observed after S-(-)-ALA treatment. "

    If you read more closely you will see that the R-isomer caused a 65% increase in glucose uptake, as compared to 29% with the S-isomer. I am sure the S-isomer would cause some increase in glucose uptake, due to the fact that it increased plasma insulin levels.

    Well studies are just studies, but ive read others like this. It seems to me, cost wise, it would be much better to take a mix rather than R-ALA. 300mg of a mix is the cheaper than 100mg of R-ALA. If you had a 50/50 mix of the isomers, you are getting 150mg of R-ALA plus the slim benefits of the S isomer. However I am not sure if this is the typical makeup of the mix, as a 10/90 mix would likely yield much different results.
    Most racemic ALA is a 50/50 mixture of the two isomers, but I have yet to see where the S-isomer shows any benefit. Although I agree that if you take 900mg of ALA or 300mg of R-ALA, you are likely to see any significant difference.

    Also, why would more glucose in the cells be more lipogenic than not using ALA and having it go to AT anyways? Or would it be the same, and just be a waste of money on a supplement that does nothing?
    When overfeeding on carbs, then you are correct in that it probably would be better to overfill the muscle cells rather than have the glucose transported into adipose tissue. In other words ALA would be beneficial for the endomorph in periods of overfeeding, i.e. refeeds, etc.

    On the other hand if you cause the cells to be think they are in a fed state, then lipolysis will be halted. You can basically "trick" the cells into thinking they are in a fed state, when in actuality they are not, and this will disrupt homeostasis in the cell. If an endo is going to supplement with ALA then you would want to make sure that the nutrients are available to avoid sending a "false" fed signal.

    I hope that makes sense

  22. #22
    Gonnabebig Member JuniorMint6669's Avatar
    Join Date
    Jun 2003
    Location
    Costa Mesa, CA
    Posts
    1,697
    Originally posted by bradley
    [B]

    If the goal if ALA is to increase glucose uptake (insulin mimicker), you would not want to increase insulin, due to insulin's effect on lipolysis. If insulin is present you will not be burning fat, so in essence the S-isomer is detracting from the benefits associated with the R-isomer.
    Hmm, when I read this I thought "more insulin more anabolic more muscle". But of course less fat burning. But if taken with carbs, there will be insulin present anyways, I just wonder how much of a difference that would make if taken only around workout (which I am doing at the moment)


    If you read more closely you will see that the R-isomer caused a 65% increase in glucose uptake, as compared to 29% with the S-isomer. I am sure the S-isomer would cause some increase in glucose uptake, due to the fact that it increased plasma insulin levels.
    This was kind of my "more insulin = good" thinking, which I am still unclear on.

    Most racemic ALA is a 50/50 mixture of the two isomers, but I have yet to see where the S-isomer shows any benefit. Although I agree that if you take 900mg of ALA or 300mg of R-ALA, you are likely to see any significant difference.
    agreed, in theory. Ill let you know in a few weeks

    When overfeeding on carbs, then you are correct in that it probably would be better to overfill the muscle cells rather than have the glucose transported into adipose tissue. In other words ALA would be beneficial for the endomorph in periods of overfeeding, i.e. refeeds, etc.

    On the other hand if you cause the cells to be think they are in a fed state, then lipolysis will be halted. You can basically "trick" the cells into thinking they are in a fed state, when in actuality they are not, and this will disrupt homeostasis in the cell. If an endo is going to supplement with ALA then you would want to make sure that the nutrients are available to avoid sending a "false" fed signal.

    I hope that makes sense
    Actually, no, it doesnt I had no idea a "fed" state would halt lipolysis. I actually thought the opposite would be true... Perhaps I misunderstood, but I thought leptin levels drop when starving, and start preserving fat. But with a "fed" signal, leptin levels rise and fat is not considered such a precious commodity.

    Now if you were saying that more nutrients are in the muscle, and less are available elsewhere... so that no fed signal was being sent, leptin levels drop, lipolysis slows, that would make sense to me. But ??

  23. #23
    confused by simplicity bradley's Avatar
    Join Date
    Aug 2002
    Location
    Alabama
    Posts
    5,467
    Originally posted by JuniorMint6669

    Hmm, when I read this I thought "more insulin more anabolic more muscle". But of course less fat burning. But if taken with carbs, there will be insulin present anyways, I just wonder how much of a difference that would make if taken only around workout (which I am doing at the moment)
    Yes, although keep in mind that ALA will increase glucose transport, so therefore insulin levels should drop faster. This would cause one to enter into a "fat burninng' state faster.

    You bring up a good point, about what difference should one expect when using ALA only around a workout. If you are using high GI carbs, then I doubt the difference would be significant, due the increased insulin sensitivity that is associated with training.

    Actually, no, it doesnt I had no idea a "fed" state would halt lipolysis. I actually thought the opposite would be true... Perhaps I misunderstood, but I thought leptin levels drop when starving, and start preserving fat. But with a "fed" signal, leptin levels rise and fat is not considered such a precious commodity.
    You are correct in your definition of a fed signal, but when overfeeding there is spillover into fat cells, i.e de novo lipogenesis. If you cause this to occur when the cell is not actually in a fed state, you are causing the cell to store fat (lipogenic state) and not burn fat (lipolytic state). In other words, when the cell should be burning fat it will be storing fat, much the same way as when refeeding.

    I apologize if my first explanation was not clear.
    Last edited by bradley; 09-29-2003 at 06:17 PM.

  24. #24
    Gonnabebig Member JuniorMint6669's Avatar
    Join Date
    Jun 2003
    Location
    Costa Mesa, CA
    Posts
    1,697
    That makes more sense, thanks.

Bookmarks

Posting Permissions

  • You may not post new threads
  • You may not post replies
  • You may not post attachments
  • You may not edit your posts
  •