[AldrichAStern]

I don't mean to be beating a dead horse, but some guys on abcbodybuilding.com brought up your claim on low-GI carbs pw and are ripping on it pretty harshly. I don't know if you want to respond, but if you do...

http://www.abcbodybuilding.com/forum...page=0#1094259

It'd be interesting to see how the debate turns out.

[cry0smate]

I think that there are always going to be stuides that disprove studies that disprove other studies, etc. I'm a believer in Dex/Whey PWO, some are not. But when you look at both me and someone else who follows a different path-- we both inevitably reach our goals. That's why I don't stay close minded and dismiss other's outlooks. Those who do that are too close minded and ignorant to see a bigger picture and to realize that there is more than one way to skin a cat. Unfortunate yes, but people are people.

IMO the only good thing about abc is the lists of exercises.

[AldrichAStern]

The thing that I found especially funny though is that they said that Bobo has 0 science to back up his claims

[Matthew D]

Actually if you do a search, you will find Bobo's old thread on this and his science that is used to back it up.. trust me, the man knows his nutrition..

[AldrichAStern]

yeah, no doubt.

[Matthew D]

I doubt he will even go over to that hole.. No need, you can educate someone that does not or will not listen to what is being said.. just the amount of personal bullshit remarks made by the admin over there makes the whole thing totally subjective.. and I didn't see one thing he quoted that was scientific or even common knowledge

[AldrichAStern]

haha, one thing I've noticed about Bobo is that he knows his **** so well, that he'll frequently say things like "You can look it up in any nutritional textbook", rather than sit there and explain what, to him, is basic nutrition. I guess someone looking from the outside who doesn't know about Bobo's reputation would definitely take that as getting out of the debate... but anyone who knows Bobo like people here on AM knows that he has so much credibility on what he says that he really doesn't go into things.

[cry0smate]

If I were him, I wouldn't waste my time. Even though I go a different route in comparsion to his plans of attack (from what little I know) there is no doubt that they are effective otherwise his client base wouldn't continue to grow nor would he have the success that he has had. Based on that who am I to argue? Nobody, that's why I don't. You gotta do what works for YOU.. So few people seem to understand that.

Results speak for themselves, backed up by science or not.

People are so damn close minded.. ugh....

[Sticks]

If i were him I wouldn't bother either, but personally I would love to see him go over there and bury them.

[Kruger]

I could rip that guy apart so easily that I would feel guilty.

"No matter what he is bashing, he still gives no actual argument(science) for his claim, because thats all he is doing is making a claim. "

I guess they didn't read the Avant thread.


" All he keeps talking about is the fat gain issue with a high GI carb but if he actually knew the physiology of post workout he would know that you wouldn't gain fat if you were taking the propor amounts of carbohydrates in your specified pwo coctail.

He doesn't use any science so he has no argument. "

Wrong again.

Determinants of post-exercise glycogen synthesis during short-term recovery.

Jentjens R, Jeukendrup A.

Human Performance Laboratory, School of Sport and Exercise Sciences, University of Birmingham, Edgbaston, Birmingham, UK.

The pattern of muscle glycogen synthesis following glycogen-depleting exercise occurs in two phases. Initially, there is a period of rapid synthesis of muscle glycogen that does not require the presence of insulin and lasts about 30-60 minutes. This rapid phase of muscle glycogen synthesis is characterised by an exercise-induced translocation of glucose transporter carrier protein-4 to the cell surface, leading to an increased permeability of the muscle membrane to glucose. Following this rapid phase of glycogen synthesis, muscle glycogen synthesis occurs at a much slower rate and this phase can last for several hours. Both muscle contraction and insulin have been shown to increase the activity of glycogen synthase, the rate-limiting enzyme in glycogen synthesis. Furthermore, it has been shown that muscle glycogen concentration is a potent regulator of glycogen synthase. Low muscle glycogen concentrations following exercise are associated with an increased rate of glucose transport and an increased capacity to convert glucose into glycogen.The highest muscle glycogen synthesis rates have been reported when large amounts of carbohydrate (1.0-1.85 g/kg/h) are consumed immediately post-exercise and at 15-60 minute intervals thereafter, for up to 5 hours post-exercise. When carbohydrate ingestion is delayed by several hours, this may lead to ~50% lower rates of muscle glycogen synthesis. The addition of certain amino acids and/or proteins to a carbohydrate supplement can increase muscle glycogen synthesis rates, most probably because of an enhanced insulin response. However, when carbohydrate intake is high (>/=1.2 g/kg/h) and provided at regular intervals, a further increase in insulin concentrations by additional supplementation of protein and/or amino acids does not further increase the rate of muscle glycogen synthesis. Thus, when carbohydrate intake is insufficient (<1.2 g/kg/h), the addition of certain amino acids and/or proteins may be beneficial for muscle glycogen synthesis. Furthermore, ingestion of insulinotropic protein and/or amino acid mixtures might stimulate post-exercise net muscle protein anabolism. Suggestions have been made that carbohydrate availability is the main limiting factor for glycogen synthesis. A large part of the ingested glucose that enters the bloodstream appears to be extracted by tissues other than the exercise muscle (i.e. liver, other muscle groups or fat tissue) and may therefore limit the amount of glucose available to maximise muscle glycogen synthesis rates. Furthermore, intestinal glucose absorption may also be a rate-limiting factor for muscle glycogen synthesis when large quantities (>1 g/min) of glucose are ingested following exercise.


Notice where it says FAT. Maybe this guy should read a bit more and stop relying on abcbodybuilding articles which are clearly lacking.


"He fails to pay attention to the necessity for cortisol execution, enhancing protein synthesis"

Enhancing protein synthesis? Hmm...wonder what the substrate and nutrient signal is for enchancing protein synthesis. Oh I know...

Amino acids stimulate translation initiation and protein synthesis through an Akt-independent pathway in human skeletal muscle.

Liu Z, Jahn LA, Wei L, Long W, Barrett EJ.

Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908, USA. zl3e@virginia.edu

Studies in vitro as well as in vivo in rodents have suggested that amino acids (AA) not only serve as substrates for protein synthesis, but also as nutrient signals to enhance mRNA translation and protein synthesis in skeletal muscle. However, the physiological relevance of these findings to normal humans is uncertain. To examine whether AA regulate the protein synthetic apparatus in human skeletal muscle, we infused an AA mixture (10% Travesol) systemically into 10 young healthy male volunteers for 6 h. Forearm muscle protein synthesis and degradation (phenylalanine tracer method) and the phosphorylation of protein kinase B (or Akt), eukaryotic initiation factor 4E-binding protein 1, and ribosomal protein S6 kinase (p70(S6K)) in vastus lateralis muscle were measured before and after AA infusion. We also examined whether AA affect urinary nitrogen excretion and whole body protein turnover. Postabsorptively all subjects had negative forearm phenylalanine balances. AA infusion significantly improved the net phenylalanine balance at both 3 h (P < 0.002) and 6 h (P < 0.02). This improvement in phenylalanine balance was solely from increased protein synthesis (P = 0.02 at 3 h and P < 0.003 at 6 h), as protein degradation was not changed. AA also significantly decreased whole body phenylalanine flux (P < 0.004). AA did not activate Akt phosphorylation at Ser(473), but significantly increased the phosphorylation of both eukaryotic initiation factor 4E-binding protein 1 (P < 0.04) and p70(S6K) (P < 0.001). [/b]We conclude that AA act directly as nutrient signals to stimulate protein synthesis through Akt-independent activation of the protein synthetic apparatus in human skeletal muscle.


Look like amino acids are repsonsible for increasing protein synthesis rates, not insulin. Oh but I guess he has those OLD studies stating insulin increases protein sysnthesis. Well if he actually did a little digging he would actually understand the difference between in vitro and in vivo. Something along the lines of this...

Physiological hyperinsulinemia stimulates p70(S6k) phosphorylation in human skeletal muscle.

Hillier T, Long W, Jahn L, Wei L, Barrett EJ.

Department of Internal Medicine, Division of Endocrinology, University of Virginia School of Medicine, Charlottesville, Virginia 22908, USA.

Using tracer methods, insulin stimulates muscle protein synthesis in vitro, an effect not seen in vivo with physiological insulin concentrations in adult animals or humans.To examine the action of physiological hyperinsulinemia on protein synthesis using a tracer-independent method in vivo and identify possible explanations for this discrepancy, we measured the phosphorylation of ribosomal protein S6 kinase (P70(S6k)) and eIF4E-binding protein (eIF4E-BP1), two key proteins that regulate messenger ribonucleic acid translation and protein synthesis. Postabsorptive healthy adults received either a 2-h insulin infusion (1 mU/min.kg; euglycemic insulin clamp; n = 6) or a 2-h saline infusion (n = 5). Vastus lateralis muscle was biopsied at baseline and at the end of the infusion period. Phosphorylation of P70(S6k) and eIF4E-BP1 was quantified on Western blots after SDS-PAGE. Physiological increments in plasma insulin (42 +/- 13 to 366 +/- 36 pmol/L; P: = 0.0002) significantly increased p70(S6k) (P: < 0.01), but did not affect eIF4E-BP1 phosphorylation in muscle. Plasma insulin declined slightly during saline infusion (P: = 0.04), and there was no change in the phosphorylation of either p70(S6k) or eIF4E-BP1. These findings indicate an important role of physiological hyperinsulinemia in the regulation of p70(S6k) in human muscle. This finding is consistent with a potential role for insulin in regulating the synthesis of that subset of proteins involved in ribosomal function. The failure to enhance the phosphorylation of eIF4E-BP1 may in part explain the lack of a stimulatory effect of physiological hyperinsulinemia on bulk protein synthesis in skeletal muscle in vivo.

In other words there is a major difference in effect from injecting insulin than normal physiological levels of insulin. Seems some people over there are basing there opinions on the WRONG studies. Talk about not backing up anything with science. THey wouldn't know how to interpret a study correctly if I showed them how.

Bottom line, what increases levels of protein synthesis and is the main nutrient signal? AMINO ACIDS, NOT INSULIN.


Oh and if they want to talk about glycogen storage, they can read this one too.

Carbohydrate nutrition before, during, and after exercise.

Costill DL.

The role of dietary carbohydrates (CHO) in the resynthesis of muscle and liver glycogen after prolonged, exhaustive exercise has been clearly demonstrated. The mechanisms responsible for optimal glycogen storage are linked to the activation of glycogen synthetase by depletion of glycogen and the subsequent intake of CHO. Although diets rich in CHO may increase the muscle glycogen stores and enhance endurance exercise performance when consumed in the days before the activity, they also increase the rate of CHO oxidation and the use of muscle glycogen. When consumed in the last hour before exercise, the insulin stimulated-uptake of glucose from blood often results in hypoglycemia, greater dependence on muscle glycogen, and an earlier onset of exhaustion than when no CHO is fed. Ingesting CHO during exercise appears to be of minimal value to performance except in events lasting 2 h or longer. The form of CHO (i.e., glucose, fructose, sucrose) ingested may produce different blood glucose and insulin responses, but the rate of muscle glycogen resynthesis is about the same regardless of the structure.



Those assclowns couldn't buy a clue.

[AldrichAStern]

Hahahaha... there we go

[Kruger]

As a couple people have stated who actually understand what I am talking about:

"This entire thread is marred by the simple fact that weight training is not a glycogen-depleting form of exercise. Sure, there will be some loss of glycogen stores, but nowhere near what is found from the type of glycogen-depleting protocols used in refeeding experiments. The type of high-intensity, rest-between-sets of weight lifting taxes the ATP-CP system heavily, but only has a small to moderate effect on glycogen reserves unless training volume is extremely high and/or there is little or no rest between sets and exercises.

Not that this automatically invalidates everything that's been said, but it seems to me that we may well be comparing apples to oranges here. I know of no published studies which look at the effect of the post-workout meal on protein synthesis/degradation or glycogen synthesis after weight training.

Janet Rankin did such a study two years ago in our department, and found no effect. Such an "unexciting" finding meant that it didn't get published, unfortunately.

In another thread a while back, we discussed at length a human study which looked at the effects of insulin infusion, both at reast and post-exercise, on muscle protein synthesis. The bottom line was that insulin infusion increased muscle protein syntheses via its effects on vasodilation, which in turn caused a greater rate of amino acid deliver to muscle tissue under resting conditions.

Post-exercise, when blood flow to muscles was already enhanced, insulin infusion had no further effect on protein synthesis. Thus, the idea that insulin spikes are anabolic in during post-workout conditions appears to be a myth, although there is still room for the anti-catabolic effects of insulin in the post workout state; however, the real-world significance of this for weight trainers is questionable.

More important for anabolism would seem to be a high level of circulating amino acids both during the workout and post-workout, in addition to a high level of blood flow to the muscles."

In other words, they are trying to create an enviroment with high GI carbs that is already present due to exercise. Maybe the guy who said I dind't understand physiology during post exercise should do a bit more reading.

Ok, now I feel guilty.


That about sums it up.

[Kruger]

You can lead a horse to water......

[ryansm]

For the billionth time.

[Kruger]

"He also makes these authors out to be the authority on the matter"

This guy was referring to Ivy, Tipton, Jentjens, Jeukendrup. Then he quotes Costill. Well guess who Costill, Groff, Gropper, etc...base their texts on.

You guessed it (Ivy, Tipton, Jentjens, Jeukendrup, etc..). This guy is lost.

"Alright, I have some time on my hands so I will destroy his arguements."

Well since I had time on my hands, I decided to do it back.