Competition Diet Advice

Sparty2QP

New member
Ok, I am doing my first show April 24th (6 weeks out). I have been meeting with a guy that I work with, who has preped a lot of people for shows, I am not sure how many "natrual" bodybuilders he has worked with. Anyway, just looking for some good overall advice.

I am very lean, and am eating around 2800-3000 cals a day (42% p 38% c 20% f). Protein is chicken, eggs, tuna, whey powder. Carbs are whole wheat bread, (only 4 pcs 6:00 AM), brown rice, and oatmeal. (Eat like this year round, just more calories). I have a pre-wo shake, about 30-45 min before, and spike my insulin with yogurt immediately post-wo. I would say I am about 8-9%, but would like to get to 3-5%. Looking at 2 wks Clen, 2 weeks ECA, 2 more clen. Any advice? I currently weigh about 210, but would like to compete 198.
Also any pre contest advice such as supplements, etc. I currently use Glutamine w/Arganine, Whey powder, mv, and C. Any other suggestions? I have a zinc, mag, K supplement I will start 3 weeks before show.

Seeking advice on best way to cycle water and any basic (or advanced) advice you can give a first timer! THANKS!
 
Sounds like a great diet overall,the biggest problem I found was timing the carb load carb deplete...I would not limit water until the day before a show...Avoid sodium loading and depleting while it can be effective, if you miss your in deep Poo Poo.Try to eat up to a show so diet down to contest level one week before a contest..Then increase calories so showtime you look full and ripped instead of depleted and flat...
 
You spike your insulin by taking yogurt PW??? Nooooooooo. Whey with simple carbs is what you need. You want nutrients absorbed ASAP to counteract catabolism following your training. Use a Whey shake with water and use dextrose, maltodextrin, or a 50/50 mix of the 2.
 
No you don't. Yogurt is just fine or just plain skim milk. You do not need a high GI source or simple carbs to replenish glyocgen becuase its the saem over a 24 hour peroid whether you use low GI or High GI. THe rate of resynthesis is the saem and the rate of protein synthesis is the same. The whole "i needd something quick to eliminate catabolism" is blown out of proportion because of a lack of understanding.
 
RaRa - or Spary2QP - go read up on many of Bobo's posts, he has an exorbitant amount if very valuable info.
 
Bobo said:
No you don't. Yogurt is just fine or just plain skim milk. You do not need a high GI source or simple carbs to replenish glyocgen becuase its the saem over a 24 hour peroid whether you use low GI or High GI. THe rate of resynthesis is the saem and the rate of protein synthesis is the same. The whole "i needd something quick to eliminate catabolism" is blown out of proportion because of a lack of understanding.
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I know what a debatable topic this is, but I still hold strong to the High GI PW nutrition (more so when a following a ketogenic diet), so I'm not discrediting the low-gi standpoint, just having a different opinion.
I'm curious to your input Bobo though, as to a comparison between the GI's insulin responses and the use of exogenous slin (in terms of a normal individual, not in the condition of diabetes). I've had this discussion before with others, but maybe you could give better insight to it from a Low-GI advocate perspective. I do understand that the total amount of insulin released is the same, and to my understanding the only difference is the peak level of release at certain times. With that said, I use Rolled Oats (Low GI) vs. Dextrose (High-GI) and compare the peak activity times of released insulin. Now in comparison I compare Humalog slin vs. Regular-R slin. The activity timing of the Humalog I believe will have its' peak rate approx 1.5 hours after introduction where as the R will be as late as 4 hours after introduction. Now in a Bodybuilding perspective we optimally would want the shortest acting when using this post-training. I think comparing Nor-L slin PW is irrelevant as I believe it can have it's peak activity as high as 15 hours after introduction. But if we look at the Dextrose vs. Oats parallel with Humalog vs. Regular-R, wouldn't the same insulin response theory hold true that the higher GI Dextrose would be a more optimal choice over a slower GI carb source? I just see advocating a lower GI source as an argument againt the productivity of exogenous slin PW.
 
The whole problem is that the results from an exogneous source is so much different even if the amount (compared total release to total injected) is about the same. Nobody knows why and it is the same with many diufferent peptides (GH, IGF-1). I wish I could answer your questions but nodoy knows this one. The comparisons between the two just doesn't exist because even in many studies exogenous insulin causes a drastic increase in protein synthesis by itself whereas a normal physiological response does not. So logically your arguement would be valid if your premises were true. Unfortunetly they are not and it doesn't work that way and the differences between exogenous and endogenous insulin are worlds apart.


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.
 
Bouncer79 said:
I know what a debatable topic this is, but I still hold strong to the High GI PW nutrition (more so when a following a ketogenic diet), so I'm not discrediting the low-gi standpoint, just having a different opinion.
.
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Traditional ketogenic diets (high fat) reduce gluconeogensis so the role of glucose and high GI carbs post workout is even less important.
 
Extreme hyperinsulinemia unmasks insulin's effect to stimulate protein synthesis in the human forearm

Teresa A. Hillier, David A. Fryburg, Linda A. Jahn, and Eugene J. Barrett

Insulin clearly stimulates skeletal muscle protein synthesis in vitro. Surprisingly, this effect has been difficult to reproduce in vivo. As in vitro studies have typically used much higher insulin concentrations than in vivo studies, we examined whether these concentration differences could explain the discrepancy between in vitro and in vivo observations. In 14 healthy volunteers, we raised forearm insulin concentrations 1,000-fold above basal levels while maintaining euglycemia for 4 h. Amino acids (AA) were given to either maintain basal arterial (n = 4) or venous plasma (n = 6) AA or increment arterial plasma AA by 100% (n = 4) in the forearm. We measured forearm muscle glucose, lactate, oxygen, phenylalanine balance, and [3H]phenylalanine kinetics at baseline and at 4 h of insulin infusion. Extreme hyperinsulinemia strongly reversed postabsorptive muscle's phenylalanine balance from a net release to an uptake (P < 0.001). This marked anabolic effect resulted from a dramatic stimulation of protein synthesis (P < 0.01) and a modest decline in protein degradation. Furthermore, this effect was seen even when basal arterial or venous aminoacidemia was maintained. With marked hyperinsulinemia, protein synthesis increased further when plasma AA concentrations were also increased (P < 0.05). Forearm blood flow rose at least twofold with the combined insulin and AA infusion (P < 0.01), and this was consistent in all groups. These results demonstrate an effect of high concentrations of insulin to markedly stimulate muscle protein synthesis in vivo in adults, even when AA concentrations are not increased. This is similar to prior in vitro reports but distinct from physiological hyperinsulinemia in vivo where stimulation of protein synthesis does not occur. Therefore, the current findings suggest that the differences in insulin concentrations used in prior studies may largely explain the previously reported discrepancy between insulin action on protein synthesis in adult muscle in vivo vs. in vitro.

I think this kinda shows that in vitro tests are similarly applicable to in vivo.
 
No it doesn't. The study was only done on the forearms and does not even take into account that excess glucose would be taken up by other tissues other than the exercised muscle not to mention skeletal muscle glyocgen replenishment is biphasic.

"In 14 healthy volunteers, we raised forearm insulin concentrations 1,000-fold above basal levels while maintaining euglycemia for 4 h"


Right.....So we should raise our insulin concentrations by 1000 fold.


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. [email protected]

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). 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.



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.
 
Forgot to mention that the study you posted was done in 1998 and the one I posted was from 2000 so it is not one of the sutdies that was referred to in the one you posted.


Here is another one from 2000


Amino acids regulate skeletal muscle PHAS-I and p70 S6-kinase phosphorylation independently of insulin.

Long W, Saffer L, Wei L, Barrett EJ.

Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908, USA.

Refeeding reverses the muscle protein loss seen with fasting. The physiological regulators and cellular control sites responsible for this reversal are incompletely defined. Phosphorylation of phosphorylated heat-acid stabled protein (PHAS-I) frees eukaryotic initiation factor 4E (eIF4E) and stimulates protein synthesis by accelerating translation initiation. Phosphorylation of p70 S6-kinase (p70(S6k)) is thought to be involved in the regulation of the synthesis of some ribosomsal proteins and other selected proteins with polypyrimidine clusters near the transcription start site. We examined whether phosphorylation of PHAS-I and p70(S6k) was increased by feeding and determined the separate effects of insulin and amino acids on PHAS-I and p70(S6k) phosphorylation in rat skeletal muscle in vivo. Muscle was obtained from rats fed ad libitum or fasted overnight (n = 5 each). Other fasted rats were infused with insulin (3 microU x min(-1) x kg(-1), euglycemic clamp), amino acids, or the two combined. Gastrocnemius was freeze-clamped, and PHAS-I and p70(S6k) phosphorylation was measured by quantifying the several phosphorylated forms of these proteins seen on Western blots. We observed that feeding increased phosphorylation of both PHAS-I and p70(S6k) (P < 0.05). Infusion of amino acids alone reproduced the effect of feeding. Physiological hyperinsulinemia increased p70(S6K) (P < 0.05) but not PHAS-I phosphorylation (P = 0.98). Addition of insulin to amino acid infusion was no more effective than amino acids alone in promoting PHAS-I and p70(S6k) phosphorylation. We conclude that amino acid infusion alone enhances the activation of the protein synthetic pathways in vivo in rat skeletal muscle. This effect is not dependent on increases in plasma insulin and simulates the activation of protein synthesis that accompanies normal feeding.



Here's the full study to the one you posted and you can check the references. They mostly were done on diabetic rats.

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Some observations from the FULL study:

"This insulin infusion lowers circulating amino acids (23), an effect not seen in vitro in perfused tissues. We prevented hypoaminoacidemia by simultaneous systemic infusion of a balanced amino acid mixture at one of three rates selected to either replace or augment plasma amino acids and then examined the separate effect of amino acid supply on the response to marked hyperinsulinemia. "

Hardly realistic in the real world and in no way would reperesent a normal physiological response.


"Likewise, combining tracer and regional catheterization methods, most (27, 30, 38, 40, 41) but not all (9) laboratories have demonstrated that insulin specifically retards muscle proteolysis in humans, findings in accord with insulin's effect on proteolysis seen in vitro. Strikingly, in these studies, insulin did not stimulate protein synthesis either in the whole body or with one exception (9) in skeletal muscle. Thus insulin's protein anabolic action in vivo appeared to only partially parallel that which was seen in isolated muscle preparations. "

In other words, they can only mimic the action in isolated muscle preparations like in your study (forearm). They could not increase overall bulk protein synthesis as the study I posted showed.


"As IGF-I receptors can be stimulated by high concentrations of insulin, the present results together with findings from in vitro studies raise the possibility that some or all of insulin's action to stimulate protein synthesis may be mediated by pathways other than the insulin receptor."

That was the last sentence in the study. It is by another pathway that is mediated by amino acids as many studies now show. Thats the beauty of science.
 
Thanks bobo for providing me with some very intriguing info and data.. but, is there anything wrong with the pro dex shake (1:2 ratio) that has been preached about for so long?

True, the paper posted "In 14 healthy volunteers, we raised forearm insulin concentrations 1,000-fold above basal levels while maintaining euglycemia for 4 h". But what exactly is 1000 fold above our basal level? Would it be similar to the insulin spike caused by ingestion of simple carbs?
 
It depends. If your older, natural insulin resistance can be a major factor and you would end up addiing more fat that you would if you used a lower GI source.

High GI works, nobody is saying it doesn't, but Low GI works just as well with less risk of adipose storage.
 
Bobo, first, thanks for the informative reply... that's the first insight I've gotten to my argument that actually helped me understand why my comparison hasn't been proven. I Appreciate it.

Bobo said:
High GI works, nobody is saying it doesn't, but Low GI works just as well with less risk of adipose storage.
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I feel that why following a carb/protein based diet in the likes of a 40-40-20 ratio, yes, this statement seems more logical to me (in light of your last response to me). However, I don't see Low-GI being the optimal choice for a ketogenic dieter. Now again, I realize the fact that insulin amounts released are equal between the GI sources, but again, their peak activity timing will vary. This being said, a ketogenic dieting BBer will be ingesting their next real food meal approx 1-1.5 hours after training, and this meal will follow the keto guidelines of high fat. If using a High-GI carb source, insulin levels have passed their peak release times thus making for a more welcoming environment for high fat intake. A low-GI source will have a higher activity rate of the insulin released at the time of this meal. Assuming the meal is followed according to the keto plan we are introducing a high amount of fat when insulin is still present at a higher amount thus fueling adipose tissue. So would you agree with me that for a CKD diet the high GI source would be the better option in this case? The only argument I can see being made against this in terms of the diet would be to consume a modified meal of lower fat and higher protein in this time. The problem I see with this is that by lowering fat intake for this meal would mean less ketone production and risk of protein being the next energy source being used. Looking at the CKD purpose for the BBer it is generally seen as muscle maintenence with fat burning, however, we slow this progress if we follow that idea of low-GI use PW. So I'm basically asking now if a High-GI carb-source is seen as being the optimal choice for a CKD? Not to say that Low-GI wouldnt work, but that we risk greater spillover with it.
 
Nice thread......I'll comment when I have more time.

LOL....Bobo and Bouncer. ;) Two of my favorite bros :D

-- Chi
 
Bouncer79 said:
Bobo, first, thanks for the informative reply... that's the first insight I've gotten to my argument that actually helped me understand why my comparison hasn't been proven. I Appreciate it.


I feel that why following a carb/protein based diet in the likes of a 40-40-20 ratio, yes, this statement seems more logical to me (in light of your last response to me). However, I don't see Low-GI being the optimal choice for a ketogenic dieter. Now again, I realize the fact that insulin amounts released are equal between the GI sources, but again, their peak activity timing will vary. This being said, a ketogenic dieting BBer will be ingesting their next real food meal approx 1-1.5 hours after training, and this meal will follow the keto guidelines of high fat. If using a High-GI carb source, insulin levels have passed their peak release times thus making for a more welcoming environment for high fat intake. A low-GI source will have a higher activity rate of the insulin released at the time of this meal. Assuming the meal is followed according to the keto plan we are introducing a high amount of fat when insulin is still present at a higher amount thus fueling adipose tissue. So would you agree with me that for a CKD diet the high GI source would be the better option in this case? The only argument I can see being made against this in terms of the diet would be to consume a modified meal of lower fat and higher protein in this time. The problem I see with this is that by lowering fat intake for this meal would mean less ketone production and risk of protein being the next energy source being used. Looking at the CKD purpose for the BBer it is generally seen as muscle maintenence with fat burning, however, we slow this progress if we follow that idea of low-GI use PW. So I'm basically asking now if a High-GI carb-source is seen as being the optimal choice for a CKD? Not to say that Low-GI wouldnt work, but that we risk greater spillover with it.
Click to expand...

You looking at things in a linear fashion and it doesn't work that way. The results form a natural insulin spike go well beyond the pekk levels sometimes up to 7 hours (give or take 3 hours depeding on diet). Its alters HSL and LPL levels dramatically, especially high spikes. The additions of fats during this time is a bad idea because depending on what type of fat used, they can circulate for up to 9 hours and when HSL levels are inactivated and LPL levels are increased the increased chance of free fatty acid storage is increased. You keep thinking that its just the peak times of insulin are the focus and its not. Insulin causes a cascade type effect that effects many different metabolic pathways, mainly lipoprotein levels. A low GI source does not effect LPL/HSL levels nearly as much as Dextrose would so levels would not go up nearly as much. The mere presence of tryglycerides inactivated HSL levels further so its not just insulin. What you want to do is limit the amount these enymes are effected therefore low GI source is much more favorable. Bacially when Insulin levels are high as with a high GI source, cAMP levels are low, HSL is low and fat breakdown is low. THe use of a high GI source only amplifies this condition and the addition of dietary fat amplifies it even more. So its always better for Low GI, Low fat meal post exercise for up to 3 hours depending on the diet. If you must use fats use MCT's as they are broken down more as carbs and will have less effect on HSL, LPL and cAMP.
 
The above explantion is also the reaosn you NEVER include fat after injecting insulin.
 
Plus ketosis is way overated anyway. Its more of a side effect than anything of low carbohydrate diet. You don't need to stay in constant ketosis. You can even ask Lyle than one and he will agree.
 
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