Thread: protein mix
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Old 08-30-2006, 01:46 PM
EricT EricT is offline
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Join Date: Jul 2005
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Quote:
Originally Posted by hrdgain
I still would rather be safe then sorry.


I don't blame you there, bro. I'm just talking about facts vs. perception of facts. The evidence simply goes both ways and lots of the hysteria about soy doing stuff like shrinking your testicles and making you hate girls is based on faulty and even mythological assumptions. One of those is that Asians eat a ton of soy everyday..which they don't. Hell I just read about a couple of studies suggesting that soy protects older men AGAINST the effects of estrogen (prob by by the weak phyto estrogens blocking estradiol). Pesonally I could care less whether someone eats soy or not and there are certainly a lot of reasons why someone might choose not to. I DEFINITELY say only in moderation. Just like most things...

One the glutamine thing I agree with you in general, verb. But I hate articles that take studies done on ENDURANCE training and pretending that is valid for resistance training. The bioavailibility thing is certainly misunderstood, as you pointed out, and glutamine has many benefits in the body. It's prob one of the most, if not the most, important aminos there is.

Quote:
In addition to restoring and elevating plasma glutamine levels, oral glutamine supplementation increases muscle glycogen storage to the same capacity as glucose (Bowtell, 1999).
To my knowledge this is not what the study said at all. It talked about stimulating WHOLE body carbohydrate storage. I.E. in other tissues not just muscle....like the live.


On the glycogen synthesis thing here is a good post from over at Mind and Muscle (not that it matters too much but you know I can't let this stuff go ):


Quote:
Originally Posted by dawza
There is some evidence (convincing) that glutamine will upregulate glycogen synthase. At the very least, in vivo human data regarding glutamine's glycogen storage potentiation is more promising than equivalent data evaluating anti-catabolic and/or anabolic effects.
Quote:
Originally Posted by dawza

I would not expect differences in this regard whether one used free form or peptides.

This is an excerpt from van Hall et al., 2000:

The failure of glutamine supplementation to enhance adaptations to resistance training may be due to the fact that resistance training is not stressful enough to benefit from glutamine supplementation. For example, glutamine has been shown to be beneficial for resynthesis of glycogen, by acting as a precursor for glycogen synthesis in the liver and muscle following severe endurance type exercise, where muscle glycogen has been depleted by approximately 90% (Varnier et al. 1995; Bowtell et al. 1999). Glycogen is depleted during resistance exercise; however, a typical session of similar volume to that used in the present study results in a glycogen depletion of only 36% (Roy & Tarnopolsky, 1998). This level of depletion may not be severe enough to benefit from glutamine supplementation. Whether glutamine supplementation enhances glycogen resynthesis following exercise is controversial, as recently it was demonstrated that oral glutamine supplementation had no effect on glycogen resynthesis following intense interval exercise that resulted in glycogen depletion.

This is a piece from a paper I wrote on glutamine earlier this year for a class:

In evaluating van Hall’s et al.’s study, we must consider that van Hall et al. included 0.8g/kg glucose (56g for a 70kg subject) in all three of their experimental drinks; therefore, any potentiation by glutamine may have been eclipsed by the large quantity of glucose. The dose of glutamine in van Hall et al.’ study was 21g for a 70kg subject (0.3g/kg); given 3x (immediately post, 1hr post, and 2 hrs post), this would be expected to have at least some effect, which it (and the protein hydrosylates) did, as far as attenuating the 20% postexercise decrease in plasma [glutamine] that was seen when only the control (0.8g/kg glucose) was ingested. Plasma glutamine levels were significantly affected by the glutamine + glucose drinks, more so that any of the other combos.

There is much evidence that after high-intensity exercise, glyconeogenesis from lactate and other glucogenic substances (amino acids) occurs, and this is the primary pathway of metabolism for these substrates in type IIb fibers. Therefore, we have to consider that van Hall et al. used short-duration, high-intensity intervals, which should have stimulated glyconeogenesis to a large degree. In addition, as little as 30% decrease in muscle glycogen content stimulated glyconeogenesis by 51% in exercised muscles in rats (Bonen & Homonko, 1994). Thus, we would expect to see substantial flux of lactate into glycogen. If the athletes were glycogen-depleted prior to onset of exercise, we would expect to see substantial gluconeogenesis from amino acids; the abstract implies that the athletes were not glycogen-depleted PRE-exercise; therefore, it would have been interesting to measure lactate kinetics post-exercise. It is very likely that there was enough lactate to prevent significant glutamine contribution to glycogen formation. Combined with the addition of glucose in a glycogen-depleted state, which would independently stimulate glycogen synthase (Halse et al. 2003), it is very likely that glutamine’s effects were shadowed by these factors.

We would need to see lactate and glutamine flux data to fully evaluate this study’s claims, as well as how well glycogen levels were standardized across subjects.

A study by Candow et al. (2001) estimates a depletion of glycogen (muscle) by 36%; this still should be enough to cause a marked increase in glyconeogenesis; however, as the authors postulated, this degree of depletion is probably not enough to hinder performance. Also, levels of muscle glycogen were not measured, so we cannot determine whether glutamine enhanced glycogen accumulation post-exercise. It is possible that it did, as the authors did not give glucose in addition to the glutamine, as van Hall et al. did; therefore, glutamine-induced synthase activation/cell-swelling may have enhanced flux of glyconeogenic precursors into glycogen, assuming that there is not an upstream step in conversion of the substrates to glycogen precursors (glucose, glucose-1P) that is rate-limiting.

Had van Hall et al. incorporated a control that gave glutamine ONLY, and another one that gave a placebo devoid of any substances, their results would be much more useful in determining glutamine’s value to glycogen repletion.

The authors also state:

To our knowledge, this is the first study to investigate the effect of oral glutamine supplementation during strength training. Glutamine supplementation has been shown to enhance glycogen resynthesis following endurance-type exercise (Varnier, et al. 1995; Bowtell et al. 1999).

Bowtell et al.’s study, Effect of oral glutamine on whole body carbohydrate storage during recovery from exhaustive exercise provides strong support for the use of glutamine as a stimulator of post-exercise replenishment after glycogen-depleting exercise. This study looked at the effects of glutamine (8g oral), glucose polymer (61g in 330mL water), or the glucose polymer + 8g glutamine, on glycogen synthesis after depletion. The glycogen-depletion approach Bowtell et al. used is very interesting, as they used high-intensity exercise to deplete glycogen in IIb fibers, then switched to low-intensity exercise to exhaustion to deplete type I and IIa fibers, as well as to reduce elevated plasma lactate levels to baseline levels. Therefore, lactate contributing to glycogen repletion is eliminated, and we are assured of complete glycogen depletion.

The results of Bowtell et al.’s study are as follows:

-Muscle glycogen stores were depleted in all trials to 13mmol glycosyl units/kg wet wt, compared to resting values of 110-170mmol glycosyl units/kg wet wt.
-The average rate of glycogen replenishment after exercise was not significantly different between trials.
-Plasma insulin and glucose were significantly elevated in both glucose trials, compared to glutamine-only.
-There was no difference in whole body glucose oxidation of glucose between trials; however, non-oxidative glucose disposal (a measure of carbohydrate storage), measured by isotopic glucose tracer infusion, was significantly higher in the glucose + glutamine compared to the glutamine-only trial at 52.5 minutes (4.22 +/- 0.22 vs. 1.97 +/- 0.45mmol/kg/hr), and even more so at 82.5 minutes (4.72 +/- 0.86 vs. 2.63 +/- 0.74mmul/kg/hr).
-The non-oxidative glucose disposal was also higher in the second hour in the glucose + glutamine trial compared to the glucose-only and glutamine-only trials (4.48 +/- 0.61 vs. 3.59 +/- 0.18 vs. 2.43 +/- 0.55mmol/kg/hr for glucose + glutamine, glucose only, and glutamine only, respectively).

The authors conclude, based on these results, that the glutamine + glucose trial resulted in a higher total body storage of carbohydrate; however, the total muscle storage of glucose tended to be higher for the glucose-polymer only trial compared to the glucose + glutamine and glutamine-only trials.

The most interesting finding of this study is that glutamine only at 8g orally stimulated glycogen repletion independent of other substrates, which is strong evidence for its ability to stimulate glycogen synthase. While the speed of resynthesis was elevated in the trials containing glucose, total repletion with glutamine was equal in terms of muscle glycogen. The authors state that glutamine-only caused 4.1 +/- 1.1 mmol/kg/hr glycogen synthesis, compared to 0.5-1.0mmol/kg/hr synthesis in a saline or alanine+glycine control from a study by Varnier et al., which used identical methodology. Considering that the authors depleted lactate to baseline values, and did not provide exogenous gluconeogenic or glyconeogenic substances, one must wonder where the substrate for glycogen replenishment is coming from.

In conclusion, from this study, it appears that glutamine only at 8g may be useful in stimulating glycogen storage in depleted skeletal muscle, while adding glutamine to glucose may cause increased total glucose storage, but in tissues other than skeletal muscle, possibly the liver


References:

Bonen, A. & Homonko, D. A. (1994) Effects of exercise and glycogen depletion on glyconeogenesis in muscle. Journal of Applied Physiology, 76(4):1753-1758.

Bowtell, J. L., Gelly, K., Jackman, M. L., Patel, A., Simeoni, M. & Rennie, M. J. (1999) Effect of oral glutamine on whole body carbohydrate storage during recovery from exhaustive exercise. Journal of Applied Physiology, 86: 1770-1777.

Candow, D. G., Chilibeck, P. D., Burke, D. G., Davison, S. K. & Palmer, T. S. (2001) Effect of glutamine supplementation combined with resistance training in young adults. European Journal of Applied Physiology, 86(2): 142-149.

van Hall, G., Saris, W. H., van de Schoor, P. A. & Wagenmakers, A. J. (2000) The effect of free glutamine and peptide ingestion on the rate of muscle glycogen resynthesis in man. Int J Sports Med, 21(1):25-30

Halse, R., Fryer, L. G., McCormack, J. G., Carling, D. & Yeaman, S. J. (2003) Regulation of glycogen synthase by glucose and glycogen: a possible role for AMP-activated protein kinase. Diabetes, 52(1):9-15.

Roy, B. D. & Tarnopolsky, M. A. (1998) Influence of differing macronutrient intakes on muscle glycogen resynthesis after resistance exercise. Journal of Applied Physiology, 76: 1247-1255.

Varnier, M., Leese, G. P., Thompson, J. & Rennie, M. J. (1995) Stimulatory effect of glutamine on glycogen accumulation in human skeletal muscle. American Journal of Physiology, 269: E309-E315.
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Does glutamine stimulate protein synthesis? The recent evidence says no...at least in rats. Does this mean it has no benefits to weight trainers? Of course not. I used to take lots of it and I noticed I got less colds in the cold and flu season....I thought. But I haven't taken it in quite a while and it's made no difference.
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If you act sanctimonious I will just list out your logical fallacies until you get pissed off and spew blasphemous remarks.

Last edited by EricT; 08-30-2006 at 02:21 PM.
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