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ALA for athletes
- Thread starter swimmar
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If you are are working out for several hours you are relying on lipid oxidation for your energy, not glycogen. One thing that the ever-running ALA infomercials don't tell you is that in type 2 diabetics, the only humans in which ALA has ever been shown to have a benefit, ALA shifts substrate utilization away from fats toward carbs (1), obviously a bad thing if you are trying to conserve glycogen stores or burn fat. I would download that whole article referenced below and read it if you are a serious athlete considering ALA.
One way ALA improves glucose utilization is by burning it at the expense of fat. Glucose is partially oxidized by glycolysis before the end product, pyruvate, enters the citric acid cycle for complete burning. The enzyme pyruvate dehydrogenase, which converts pyruvate to acetyl coenzyme A which enters the citric acid cycle for complete oxidation, is defective in type 2 diabetes. This creates a roadblock in the glucose utilization pathway, resulting in elevated plasma glucose and insulin resistance. ALA in some way stimulates pyruvate dehydrogenase, allowing more glucose to be burned, in turn allowing more glucose to enter cells.
This explains part of ALA's antidiabetic action. The downside is you are burning more carbs and glycogen instead of fat. This shift in substrate utilization is a feature of several different antidiabetic drugs, including the popular Avandia. It has been suggested that this is at least partly responsible for the weight gain associated with Avandia. It may be the case with ALA as well.
(1) Diabetes Care 1999 Feb;22(2):280-7
alpha-Lipoic acid treatment decreases serum lactate and pyruvate concentrations and improves glucose effectiveness in lean and obese patients with type 2 diabetes.
Konrad T, Vicini P, Kusterer K, Hoflich A, Assadkhani A, Bohles HJ, Sewell A, Tritschler HJ, Cobelli C, Usadel KH
One way ALA improves glucose utilization is by burning it at the expense of fat. Glucose is partially oxidized by glycolysis before the end product, pyruvate, enters the citric acid cycle for complete burning. The enzyme pyruvate dehydrogenase, which converts pyruvate to acetyl coenzyme A which enters the citric acid cycle for complete oxidation, is defective in type 2 diabetes. This creates a roadblock in the glucose utilization pathway, resulting in elevated plasma glucose and insulin resistance. ALA in some way stimulates pyruvate dehydrogenase, allowing more glucose to be burned, in turn allowing more glucose to enter cells.
This explains part of ALA's antidiabetic action. The downside is you are burning more carbs and glycogen instead of fat. This shift in substrate utilization is a feature of several different antidiabetic drugs, including the popular Avandia. It has been suggested that this is at least partly responsible for the weight gain associated with Avandia. It may be the case with ALA as well.
(1) Diabetes Care 1999 Feb;22(2):280-7
alpha-Lipoic acid treatment decreases serum lactate and pyruvate concentrations and improves glucose effectiveness in lean and obese patients with type 2 diabetes.
Konrad T, Vicini P, Kusterer K, Hoflich A, Assadkhani A, Bohles HJ, Sewell A, Tritschler HJ, Cobelli C, Usadel KH
swimmar
New member
I'm not talking about cross-country running or distance cycling or anything. My sport, for example, is swimming. I'm a sprinter, so for comparison, I pretty much train like a track athlete who specializes in the 200m and 400m.
Since sprint training is heavily geared towards glycogen consumption, I'm not sure how much that study would shed any light.
On the flip side, say instead of being in a ketogenic diet for fat loss, how would ALA help for someone who wanted to bulk about a little bit and still train pretty intensely?
Since sprint training is heavily geared towards glycogen consumption, I'm not sure how much that study would shed any light.
On the flip side, say instead of being in a ketogenic diet for fat loss, how would ALA help for someone who wanted to bulk about a little bit and still train pretty intensely?
After sprinting your muscles are depleted in glycogen and need to replenish their stores. In order to do this they have to stop burning glycogen and burn fat. Numerous studies have shown that fatty acid oxidation continues for quite a while after exercise ceases. During this time glycogen from your liver is broken down into glucose and transported to your muscles where it is reincorporated into glycogen there.
A compound called malonyl-CoA controls to a large degree how much fatty acid enters your cell's mitochondria for burning. After sprinting, levels of malonyl-CoA are depressed, allowing more fat to be used as fuel in the citric acid cycle. The reason the malonyl-CoA is depressed is because you have lowered cellular glucose by spriniting. This is how the body regulates the ratio of fat to glucose burned. An increase in glucose has the opposite effect: it increases malonyl-CoA, slowing fat utilization and promoting glucose burning.
What is the role of ALA in all this? Well, ALA has not been studied as thoroughly as other antidiabetic drugs. The thiazolidinediones like Avandia have. It turns out they increase dramatically the activity of the enzyme that creates malonyl-CoA. This is all part of their strategy to lower blood sugar. They are causing the glucose that would have otherwise been incorporated into glycogen to be burned. If ALA had this effect as part of its ability to lower blood glucose it would impair your recovery.
We already know ALA has the thiazolidinedione like effect on pyruvate dehydrogenase. It is possible although not shown that it has a similar effect on malonyl-CoA
A compound called malonyl-CoA controls to a large degree how much fatty acid enters your cell's mitochondria for burning. After sprinting, levels of malonyl-CoA are depressed, allowing more fat to be used as fuel in the citric acid cycle. The reason the malonyl-CoA is depressed is because you have lowered cellular glucose by spriniting. This is how the body regulates the ratio of fat to glucose burned. An increase in glucose has the opposite effect: it increases malonyl-CoA, slowing fat utilization and promoting glucose burning.
What is the role of ALA in all this? Well, ALA has not been studied as thoroughly as other antidiabetic drugs. The thiazolidinediones like Avandia have. It turns out they increase dramatically the activity of the enzyme that creates malonyl-CoA. This is all part of their strategy to lower blood sugar. They are causing the glucose that would have otherwise been incorporated into glycogen to be burned. If ALA had this effect as part of its ability to lower blood glucose it would impair your recovery.
We already know ALA has the thiazolidinedione like effect on pyruvate dehydrogenase. It is possible although not shown that it has a similar effect on malonyl-CoA
nhbgorilla
New member
so is ALA good for athletes? i unfortunately dont understand a word of that post or what it means for athletes. can anyone translate?
Studly Hungwell
New member
ALA does not sound good for atheletes from the above statement. If you deplete your muscle glycogyn stores, you will inhibit recovery.
It's impossible to tell a priori whether any particular antidiabetic will cause weight loss because of a decrease in insulin, or a weight gain from substrate shifting or some other factor. Some people lose weight on thiazolidinediones from all the anecdotal discussion of the drug I have come across. Metformin is another drug that does not induce weight gain in many people; in others it does.
There is also no research to suggest ALA will "shuttle more nutrients into the muscles for a faster recovery" For starters it has no demonstrated effect on amino acid transport, nor would one be expected from its mode of action. Second, glycogen synthase levels limit the rate that glycogen can be stored in muscle. As glycogen accumulates, it shuts off this synthase, blocking any more glycogen deposition. Any additional glucose that enters the cell will be used as fuel rather than stored. And this glucose is burned at the expense of fat that would otherwise have been burned to maintain cell function.
Insulin is a potent stimulator of glycogen synthase. By lowering insulin with ALA (remember, ALA has never been shown to do anything in people that are not insulin resistant; about 75% of the population) you will lose out on the increase in glycogen synthase caused by the insulin and possibly reduce the amount of glycogen stored in muscle.
Antidiabetic drugs like ALA have one purpose: to lower blood sugar levels and hence insulin levels in type 2 diabetics, and restore glucose homeostasis. They are not designed to improve athletic performance in normal people; they are designed to help the symptoms and stave off the health risks of type 2 diabetes. An improvement in athletic performance in obese or diabetic people using ALA or another such drug come about becuase these people are unable to use glucose like other people.
There is also no research to suggest ALA will "shuttle more nutrients into the muscles for a faster recovery" For starters it has no demonstrated effect on amino acid transport, nor would one be expected from its mode of action. Second, glycogen synthase levels limit the rate that glycogen can be stored in muscle. As glycogen accumulates, it shuts off this synthase, blocking any more glycogen deposition. Any additional glucose that enters the cell will be used as fuel rather than stored. And this glucose is burned at the expense of fat that would otherwise have been burned to maintain cell function.
Insulin is a potent stimulator of glycogen synthase. By lowering insulin with ALA (remember, ALA has never been shown to do anything in people that are not insulin resistant; about 75% of the population) you will lose out on the increase in glycogen synthase caused by the insulin and possibly reduce the amount of glycogen stored in muscle.
Antidiabetic drugs like ALA have one purpose: to lower blood sugar levels and hence insulin levels in type 2 diabetics, and restore glucose homeostasis. They are not designed to improve athletic performance in normal people; they are designed to help the symptoms and stave off the health risks of type 2 diabetes. An improvement in athletic performance in obese or diabetic people using ALA or another such drug come about becuase these people are unable to use glucose like other people.
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fhg43
New member
BigDog60 said:
It may be coincidence, but I had been carrying a few extra lbs and was having hard time getting rid of them. I was doing tons of cardio (thats what I do so my lack of weight loss confused me), eating well, and using ALA with my ECA. I noticed I couldn't lose some stubborn fat. However I kept everything the same and removed ALA (ran out) and the weight (fat) flew off! Makes sense my metabolism shifted more towards fat for fuel!
nandi's info makes sense for me, an endurance athlete. I'll probably quit using ALA. Will save me some money too!
FHG
swimmar
New member
BigDog60 said:
The amount of fat that's burned during exercise is pretty insignificant, unless you're Lance Armstrong. Most of us don't train hard for six hours a day though. So just because ALA shifts energy sources away from fat and towards glycogen doesn't have to mean that ALA will not let you lose fat.
swimmar
New member
nandi12 said:
Hm.. I've just recently found out about this ALA stuff. From what I've been able to gather from the archives, I thought that ALA raised insulin levels at a time when there was no glycogen to be transported to muscles (assuming that the muscle glycogen stores are full). This is usually a good thing, right? Or am I way off base here?
(why is this stupid body so damn complex? my head hurts)
swimmar
New member
Re: Re: Re: Re: ALA for athletes
You sure?
I was under the impression that glycogen first is sent off to muscles, then when they are filled, then the liver stocks up on glycogen.
Here's a quote from Lyle McDonald:
"Without exercise to deplete muscle glycogen (a misunderstanding of the ketogenic state is that muscle glycogen is depleted. All that's important for ketosis to occur is that blood glucose be lowered and all that requires is for liver glycogen to be empty. You could have full muscle glycogen and still be in ketosis. Using insulin would do just that), a carb-up would fill up muscle glycogen (moreso since it wasn't depleted in the first place) and then spill way over (I mean more than I get with my pig outs on the weekend) to fat cells."
Taken from http://groups.google.com/groups?hl=...es+group%3Amisc.fitness.weights+author%3Alyle
serge said:
You sure?
I was under the impression that glycogen first is sent off to muscles, then when they are filled, then the liver stocks up on glycogen.
Here's a quote from Lyle McDonald:
"Without exercise to deplete muscle glycogen (a misunderstanding of the ketogenic state is that muscle glycogen is depleted. All that's important for ketosis to occur is that blood glucose be lowered and all that requires is for liver glycogen to be empty. You could have full muscle glycogen and still be in ketosis. Using insulin would do just that), a carb-up would fill up muscle glycogen (moreso since it wasn't depleted in the first place) and then spill way over (I mean more than I get with my pig outs on the weekend) to fat cells."
Taken from http://groups.google.com/groups?hl=...es+group%3Amisc.fitness.weights+author%3Alyle
swimmar
New member
Re: Re: Re: Re: Re: Re: Re: Re: ALA for athletes
I don't believe it is.
Anyways, I thought the big deal about ALA was that you could eat a whole bunch of carbs and still remain in ketosis, as it gets more glycogen from the liver to muscles than would happen if you were not on ALA.
serge said:
I don't believe it is.
Anyways, I thought the big deal about ALA was that you could eat a whole bunch of carbs and still remain in ketosis, as it gets more glycogen from the liver to muscles than would happen if you were not on ALA.
Actually, neither muscle or liver glycogen need be zero for ketogenesis to occur. There is simply an inverse correlation between liver glycogen and ketones. Whenever the liver is producing glucose via gluconeogenesis, which happens almost all the time, except when insulin levels are high right after a meal, ketone bodies are formed. They are an inevitable byproduct of gluconeogenesis. The greater the demand for glucose, whether from starvation, exercise, or hypoglycemia, or whatever, the more ketones are produced. For instance, when hypoglycemia is induced with insulin, the liver generates glucose both by breaking down its own glycogen, and by forming new glucose from amino acids and fat derived glycerol. Ketone bodies are formed during that gluconeogenesis, even though there is still plenty of glycogen left in the liver.
What lead you to believe this? Marketing hype. Where are "the whole bunch of carbs" going to go?
Skeletal muscle uses primarily fat as its fuel, so they won't be burned there. Glycogen synthase levels determine how much glucose that is taken up by muscle is turned into glycogen. ALA does not elevate glycogen synthase; on the contrary by lowering insulin it lowers glycogen synthase. So all that glucose won't be turned into glycogen and stored in muscle. That leaves uptake by fat cells and conversion to fat, or uptake by the liver for storage as glycogen, or uptake by the liver and conversion to fat which is then transported to fat cells for storage. Do those sound like attractive options?
swimmar
New member
nandi12 said:
Woah. I thought glycogen was the prefered fuel for skeletal muscles (for intensive work).
Anyways, a quick medline search shows that most research on ALA has been done on type-2 diabetics, as you probably know by now. So I realize that there's no PROOF that ALA will do all these amazing things in a normal human. However, most people on this board seem to report somewhat good results with taking ALA before a meal with carbs, some people have reported being able to take in amounts in excess of 200 carbs a day and still remain in ketosis. Even though there are no studies to prove that this is correct, I don't think there's any studies that prove that this is incorrect.
That's why fonz made the textbook statement.Unfortunately,science isn't always 100% dead on when it comes to real world results,particularly in respect to athletes.For how many years did we see abstracts from the scientific community supporting 'supposed facts' that anabolics did not increase muscular performance/size?Sometimes it becomes important to not stand so rigidly behind what is on paper,and listen to what is occurring from real life experience.I think the wisest policy is to use both as your finale weighing scale.Too many athletes have reported remarkable results with various ALA products to discount what they're saying based on what a particular research paper or two has concluded.Science is constantly shifting and evolving,and what may be law at one moment can completely change in the next.
What, that ALA increases glycogen synthase and glycogen storage? Did they perform muscle biopsies on themselves and then do an assay for those two things?
If people want to spend their money on ALA and they think it works I think that's great. My objective here is to add a little science to the nonstop ALA hype that swamps this board. Hopefully some people might be able to use that science to help weigh the undocumented claims about ALA, and learn a little about how the body works in the process.
swimmar
New member
nandi12 said:
But you are saying that since there has been no studies that show that ALA improves glycogen synthase and glycogen storage, that ALA does not improve glycogen synthase and glycogen storage.
Yes, it has never been shown. That's no reason to then state, without any reservation, that it...
Again, the absence of proof of a statement does not lead to the statement being false. Something along the lines of "If ALA decreases .... and increases ...., then this would happen" would be appropriate.
quartermiler
New member
nandi12, not to flame or anything... but some people here cant break down what all your saying because it is too complicated, like you copy and pasted it from a book or something. You are very knowledgable, but try to break it down into lamen's (spelling?) terms for some of us, lol. Once again, dont mean to flame or anything.
macrophage69alpha
New member
1. ala and r-ala increase glycogen stores.. if you wish to dispute show some CONCLUSIVE evidence otherwise... because ALL evidence, both clinical and anecdotal, use points to this.
2. ala is not an "anti-diabetic" drug.. it is a naturally occuring vitamin and produced in vivo by humans (well at least r-ala is)..
3. reduction of plasma insulin is GOOD.... note that the person above who was having trouble using fat was using ala (if from an older batch was likely proportionately higher in s-ala).. increased plasma insulin is VERY BAD for fat loss.. from several stand points.. including gh and LPL..
4. Nandi.. your research is good but your application shows limited experience.. as well as gross underestimation of both insulin resistance in the population and effects of higher plasma insulin levels.
5. to address the ketotic issue..
ALA, among other things, will give FALSE POSITIVES with sodium nitroprusside (the reagent in ketostix)
2. ala is not an "anti-diabetic" drug.. it is a naturally occuring vitamin and produced in vivo by humans (well at least r-ala is)..
3. reduction of plasma insulin is GOOD.... note that the person above who was having trouble using fat was using ala (if from an older batch was likely proportionately higher in s-ala).. increased plasma insulin is VERY BAD for fat loss.. from several stand points.. including gh and LPL..
4. Nandi.. your research is good but your application shows limited experience.. as well as gross underestimation of both insulin resistance in the population and effects of higher plasma insulin levels.
5. to address the ketotic issue..
ALA, among other things, will give FALSE POSITIVES with sodium nitroprusside (the reagent in ketostix)
Quartermiler, one thing I seldom do is cut and paste. I may quote passages from relevant studies or post abstracts, but if you spent some time on the boards where I am either a mod or administrator, you would see how I lash into people who cut and paste.
Would you be happier if instead of trying to explain things using what I consider minimal terminology from basic physiology and metabolism I said simply "IMO ALA sucks and all the crap you read about it here is just that: crap". If I simply said "There is no evidence that it works except in type 2 diabetics" members like swimmar would say "the absence of proof of a statement does not lead to the statement being false".
Is there proof that creatine will increase my IQ, make me rich, and make me more attractive to women? No. To quote once again swimmar's logic: "the absence of proof of a statement does not lead to the statement being false". So should I assume creatine may actually do these things until proven otherwise? I don't think so. That is not how science works.
If a person has type 2 diabetes I have no doubt that by improving overall glucose uptake by increasing the effectiveness of the GLUT 4 transport system, both oxidative (burning for fuel) and nonoxidative (storage as glycogen) glucose disposal will increase. Is there evidence that ALA has this effect in the estimated 75% of the population that is not insulin resistant or has type 2 diabetes? No. As swimmar pointed out, this does not mean it doesn't happen. Should I assume it works and spend my money on it. No, but that is me.
My original point in this whole thread was that in people for whom ALA works, namely type 2 diabetics, by virtue of increasing pyruvate dehydrogenase there is a substrate shift from fat burning to carb burning by increasing the flux of pyruvate into the citric acid cycle.
Swimmar also was wondering about using ALA to induce ketosis. As I pointed out earlier, ketosis and the production of ketone bodies are a byproduct of gluconeogenesis, your liver's attempt to increase the supply of blood glucose for the brain. Another way ALA works to lower blood sugar is to slow gluconeogenesis (1). The liver powers the gluconeogenesis process by burning fat. Less gluconeogenesis means less fat burning. All this is part of ALA's strategy to more effectively use the carbs you eat.
But as Fonz and Huck would say, sometimes you have to ignore the science and go with your feelings.
And as far as my limited experience goes, I have been doing science both in academia and the private sector for almost 25 years now. As far as evidence goes that ALA does not work, here is an abstract showing no effect no non diabetic rats. Macro, Huck, or Fonz, can you produce a study showing that ALA works in those who do not have type 2 diabetes?
J Appl Physiol 2002 Jan;92(1):50-8
Effects of exercise training and antioxidant R-ALA on glucose transport in insulin-sensitive rat skeletal muscle.
Saengsirisuwan V, Perez FR, Kinnick TR, Henriksen EJ.
Muscle Metabolism Laboratory, Department of Physiology, University of Arizona, College of Medicine, Tucson, Arizona 85721-0093, USA.
We have recently demonstrated (Saengsirisuwan V, Kinnick TR, Schmit MB, and Henriksen EJ, J Appl Physiol 91: 145-153, 2001) that exercise training (ET) and the antioxidant R-(+)-alpha-lipoic acid (R-ALA) interact in an additive fashion to improve insulin action in insulin-resistant obese Zucker (fa/fa) rats. The purpose of the present study was to assess the interactions of ET and R-ALA on insulin action and oxidative stress in a model of normal insulin sensitivity, the lean Zucker (fa/-) rat. For 6 wk, animals either remained sedentary, received R-ALA (30 mg. kg body wt(-1). day(-1)), performed ET (treadmill running), or underwent both R-ALA treatment and ET. ET alone or in combination with R-ALA significantly increased (P < 0.05) peak oxygen consumption (28-31%) and maximum run time (52-63%). During an oral glucose tolerance test, ET alone or in combination with R-ALA resulted in a significant lowering of the glucose response (17-36%) at 15 min relative to R-ALA alone and of the insulin response (19-36%) at 15 min compared with sedentary controls. Insulin-mediated glucose transport activity was increased by ET alone in isolated epitrochlearis (30%) and soleus (50%) muscles, and this was associated with increased GLUT-4 protein levels. Insulin action was not improved by R-ALA alone, and ET-associated improvements in these variables were not further enhanced with combined ET and R-ALA. Although ET and R-ALA caused reductions in soleus protein carbonyls (an index of oxidative stress), these alterations were not significantly correlated with insulin-mediated soleus glucose transport. These results indicate that the beneficial interactive effects of ET and R-ALA on skeletal muscle insulin action observed previously in insulin-resistant obese Zucker rats are not apparent in insulin-sensitive lean Zucker rats.
(1) Biochem J 1984 May 1;219(3):773-80
Inhibition of gluconeogenesis in rat liver by lipoic acid. Evidence for more than one site of action.
Blumenthal SA.
Would you be happier if instead of trying to explain things using what I consider minimal terminology from basic physiology and metabolism I said simply "IMO ALA sucks and all the crap you read about it here is just that: crap". If I simply said "There is no evidence that it works except in type 2 diabetics" members like swimmar would say "the absence of proof of a statement does not lead to the statement being false".
Is there proof that creatine will increase my IQ, make me rich, and make me more attractive to women? No. To quote once again swimmar's logic: "the absence of proof of a statement does not lead to the statement being false". So should I assume creatine may actually do these things until proven otherwise? I don't think so. That is not how science works.
If a person has type 2 diabetes I have no doubt that by improving overall glucose uptake by increasing the effectiveness of the GLUT 4 transport system, both oxidative (burning for fuel) and nonoxidative (storage as glycogen) glucose disposal will increase. Is there evidence that ALA has this effect in the estimated 75% of the population that is not insulin resistant or has type 2 diabetes? No. As swimmar pointed out, this does not mean it doesn't happen. Should I assume it works and spend my money on it. No, but that is me.
My original point in this whole thread was that in people for whom ALA works, namely type 2 diabetics, by virtue of increasing pyruvate dehydrogenase there is a substrate shift from fat burning to carb burning by increasing the flux of pyruvate into the citric acid cycle.
Swimmar also was wondering about using ALA to induce ketosis. As I pointed out earlier, ketosis and the production of ketone bodies are a byproduct of gluconeogenesis, your liver's attempt to increase the supply of blood glucose for the brain. Another way ALA works to lower blood sugar is to slow gluconeogenesis (1). The liver powers the gluconeogenesis process by burning fat. Less gluconeogenesis means less fat burning. All this is part of ALA's strategy to more effectively use the carbs you eat.
But as Fonz and Huck would say, sometimes you have to ignore the science and go with your feelings.
And as far as my limited experience goes, I have been doing science both in academia and the private sector for almost 25 years now. As far as evidence goes that ALA does not work, here is an abstract showing no effect no non diabetic rats. Macro, Huck, or Fonz, can you produce a study showing that ALA works in those who do not have type 2 diabetes?
J Appl Physiol 2002 Jan;92(1):50-8
Effects of exercise training and antioxidant R-ALA on glucose transport in insulin-sensitive rat skeletal muscle.
Saengsirisuwan V, Perez FR, Kinnick TR, Henriksen EJ.
Muscle Metabolism Laboratory, Department of Physiology, University of Arizona, College of Medicine, Tucson, Arizona 85721-0093, USA.
We have recently demonstrated (Saengsirisuwan V, Kinnick TR, Schmit MB, and Henriksen EJ, J Appl Physiol 91: 145-153, 2001) that exercise training (ET) and the antioxidant R-(+)-alpha-lipoic acid (R-ALA) interact in an additive fashion to improve insulin action in insulin-resistant obese Zucker (fa/fa) rats. The purpose of the present study was to assess the interactions of ET and R-ALA on insulin action and oxidative stress in a model of normal insulin sensitivity, the lean Zucker (fa/-) rat. For 6 wk, animals either remained sedentary, received R-ALA (30 mg. kg body wt(-1). day(-1)), performed ET (treadmill running), or underwent both R-ALA treatment and ET. ET alone or in combination with R-ALA significantly increased (P < 0.05) peak oxygen consumption (28-31%) and maximum run time (52-63%). During an oral glucose tolerance test, ET alone or in combination with R-ALA resulted in a significant lowering of the glucose response (17-36%) at 15 min relative to R-ALA alone and of the insulin response (19-36%) at 15 min compared with sedentary controls. Insulin-mediated glucose transport activity was increased by ET alone in isolated epitrochlearis (30%) and soleus (50%) muscles, and this was associated with increased GLUT-4 protein levels. Insulin action was not improved by R-ALA alone, and ET-associated improvements in these variables were not further enhanced with combined ET and R-ALA. Although ET and R-ALA caused reductions in soleus protein carbonyls (an index of oxidative stress), these alterations were not significantly correlated with insulin-mediated soleus glucose transport. These results indicate that the beneficial interactive effects of ET and R-ALA on skeletal muscle insulin action observed previously in insulin-resistant obese Zucker rats are not apparent in insulin-sensitive lean Zucker rats.
(1) Biochem J 1984 May 1;219(3):773-80
Inhibition of gluconeogenesis in rat liver by lipoic acid. Evidence for more than one site of action.
Blumenthal SA.
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swimmar
New member
quartermiler, the concepts aren't terribly difficult, it helps to have another web browser open so you can do a google search on any familar terms.
But "The enzyme pyruvate dehydrogenase, which converts pyruvate to acetyl coenzyme A which enters the citric acid cycle for complete oxidation, is defective in type 2 diabetes" was just a little too much. Yeah, it's great that you can throw all these technical terms around. Impressive. It's also akin to walking into a high school calculus class and start spouting off stuff on Irrotational and Solenoidal Fields if they are just beginning integration. If nandi12 were on sci.med, it would be different.
But "The enzyme pyruvate dehydrogenase, which converts pyruvate to acetyl coenzyme A which enters the citric acid cycle for complete oxidation, is defective in type 2 diabetes" was just a little too much. Yeah, it's great that you can throw all these technical terms around. Impressive. It's also akin to walking into a high school calculus class and start spouting off stuff on Irrotational and Solenoidal Fields if they are just beginning integration. If nandi12 were on sci.med, it would be different.
serge
New member
READ AND LEARN
KETOSIS FOR NEWBIES
by Beowulf
Even if you are just taking up this ridiculous hobby, you know doubt have heard of a ketogenic diet. It should be noted that ketogenic diets are, well, an unrelenting bitch from hell intent on destroying you and stealing your newly acquired rocket car (typically reserved for "gold" level AE writers). So, since you are familiar with ketogenic diets do you really know how they work? Do you know what to expect? The intent of this article is to answer these, no doubt, burning questions.
If you are uninterested in the science of things this is not section for you. However, if you want to learn the "why" in addition to the "how" part of the equation, I would recommend that you keep reading. In a normal dietary situation (in the presence of carbohydrates) your body uses glucose as its primary fuel source. Every one is happy. Your brain has sufficient glucose to function at 100%, your muscles have bountiful glycogen stores, and your kidneys are not having to put in overtime to remove urea from your blood. The body only requires 50 grams of carbohydrates per day to avoid going into ketosis. That is only two hundred kcalories a day from carbs (one gram of carbs = four kcalories). This is rather remarkable considering that your brain all by its lonesome utilizes 140-150 grams of carbohydrate in a day.
In the absence of carbohydrates, or with a very restricted carbohydrate intake, your body thinks it is starving to death. You could even be hypercaloric (more calories consumed than spent) and your body would still think that it is starving. In reality, your brain is starving. Did you ever wonder why bodybuilders who misuse insulin die? Failure to consume adequate carbohydrate and the usage of insulin will result in the effective removal of all the glucose in the bloodstream. The insulin drives it into muscle and fat. The end result is that the brain just runs out of gas and one goes into a coma or dies.
Enter your friend and mine: ketosis. In the absence of carbohydrates the body still has to have glucose to operate. This is because the CNS (Central Nervous System) prefers to use glucose for fuel. It will only use ketone bodies for fuel once blood plasma concentrations are extremely high, primarily because ketone bodies don't pass through the blood brain barrier all that well. There are two substances in the body that we will be concerned with that can convert to glucose: glycerol and protein. Lactate can also be converted to glucose, but this is not of terrible importance for our purposes.
Glycerol has a three-carbon skeleton and that is what the krebs cycle is looking for. Once protein is broken down into its constituent amino acids it enters the krebs cycle at different places. Some of these intermediaries are three carbon molecules and some will eventually become pyruvate itself. You see, pyruvate has a three carbon skeleton as well so by stripping off all the crap and starting from the three carbon skeleton up, two glycerols or pyruvates can be run essentially backwards through glycolisis (the formation of two three carbon pyruvates from one six carbon glucose) to form one six carbon molecule of glucose.
Where does the gycerol come from? A fat is constructed from three fatty acids and, you guessed it, a gycerol. Since fatty acids cannot be run backwards through glycolisis, something has to be done with them when they are stripped of their glycerol. The fatty acids are chemically modified into acetyl CoA (trust me, this process far outreaches the scope of this article) which progresses through the Krebs cycle, or citric acid cycle. A good number of these acetyls are metabolized completely and produce ATP. However, a considerable portion of these do not proceed all the way through the krebs cycle. There is excess acetyl CoA generated from the oxidation of fat because the Krebs cycle only works so fast (however, it really is remarkably fast). This extra acetyl CoA is packaged by the liver as ketones. The liver is the only place in the body that produces ketones.
Ketones are funny things. Their primary purpose is, of course, to serve as a fuel source. Ketones feed what glucose would ordinarily feed. The thing is that once blood ketone concentrations rise to a certain point they can no longer be efficiently utilized by the body and certain cells in your body just don't use them all that well. The end result is that they are removed from the bloodstream and end up in your urine. You are essentially peeing calories. This is a novel theme because your body is an ancient and incredibly efficient machine. It almost never wastes anything.
Another interesting thing to note is most nutritional experts will tell you that a ketogenic diet WILL cause muscle wasting. However, as bodybuilders we know that ketogenic diets are notorious for their muscle sparing properties. What gives here? In the author's humble opinion it all has to do with weight training. Compare a normal sedentary individual with resistance trainee. Are they both going to use protein for fuel? You bet. Are they going to equal amounts of protein for fuel? Doubtful. A sedentary individual will never need as much dietary protein to repair the microtrauma incurred from everyway events like walking and standing upright as a trained person would require to repair the catastrophic (by comparison) microtrauma resulting from a hard day of squats. Bodybuilders simply need that protein for things other than fuel. I concede the fact that protein is going to be used to make glucose. The brain absolutely positively must have glucose and we should be glad to spare some protein so that we don't slip into a coma or die. However, I simply don't buy the notion that a disproportionate amount of protein to fat is going to be utilized. The body will do what it has to do to stay alive first, but after that, it has a miracullous way of healing itself.
It is important to note that in order for protein to be used as a fuel source, its constituent amino acids must be deaminated. This means that the amino group is cleaved off of the amino acid. The problem arises because this amino group contains a nitrogen and that nitrogen reacts to form ammonia in your cells. Needless to say, ammonia in your cells is some serious shit. This ammonia makes its way to the liver, where it is converted to urea. Urea is toxic as well and excess levels can lead to gout (uric acid poisoning), however, it is not as toxic as it predecessor. Urea is eventually filtered out of the blood by the kidneys and excreted in urine. This is important because when urea concentrations rise you must urinate more in order to expel the potentially toxic product. Also, due to the higher concentration of urea in the blood you have to urinate much more frequently. This, in combination with the fact that glycogen stored in muscles actually exists in a 1:3 ratio with water and when the glycogen leaves so does the water, can spell trouble. .If you do not drink an increased amount of water, you will become dehydrated.
Part of the reason that the Atkins diet became so popular so quickly in the mainstream is because dieters can lose weight very rapidly during the first week of the diet. They could also lose weight very rapidly if we were to administer a diuretic and they didn't diet. Essentially the same thing is happening.
While ketosis is a really nifty trick, it is important to remember that energy expenditure is the real determinant in weight loss. If you cut carbs and are still in a hypercaloric state, guess what, you are going to gain weight. If you are in ketosis and you are in a hypercaloric state, you will more than likely gain weight. Ketosis is not a ticket to eat all you want. You are still subject to the law of energy conservation.
Another consideration should be that your body really does prefer glucose as a fuel source to ketones (I am can't stress this point enough). Being as such, the tissues that don't use ketones for fuel well are going to give you problems in the form of decreased performance. This is a major problem because two of the tissues that don't fare well on ketones are the brain and skeletal muscle.
The brain will find a way to function, let there be no doubt, but it will not function at full capacity. Things will seem a little hazy. You will more than likely not notice this because everything slows down, even the conscious perception which would enable you to notice it. While potentially troubling, this is not a huge problem. Reaction times will be longer for certain, but probably not to the point of compromising safety in most situations.
The inability to use ketones as a fuel source of skeletal muscles will get your attention. You will go to the gym and perform like shit. You will miss your heaviest lifts and you will feel shame. Obviously, the rules are altered a considerable deal by simultaneous usage of AAS and implementation of a ketogenic diet but if you are training clean, you will have to fight through some piss poor training sessions. This is the beauty of diets such as Bodyopus, The Anabolic Diet, and Animabolics. They allow for a carb up period after a given time and, as a result, you won't feel, for lack of a better term, so flat.
While most of the other side effects primarily afflict special populations with either liver or kidney damage, another side effect is universal. You see, fiber has a way of hiding itself in foods that contain carbohydrates. Fiber is the primary reason for peristalisis, or the contraction of your bowel to move food toward the toilet. This is a very nice way of saying that you will more than likely become very very badly constipated if you don't use a fiber supplement to keep the plumbing flowing. I can speak from personal experience on this one. You will find yourself in the bathroom making deals with the almighty. Sayings like, "Dear Lord, if you let me take this dump I swear that I will bake cookies for the church bake sale" or "Dear Lord, if I don't make it through this, give the paramedics the intelligence to come up with a good story to tell my mother like I died saving a bus full of orphans or something like that....." will become part of your daily restroom regimen.
I have never met anyone who was not completely miserable while on a ketogenic diet. You are starving your body and it is really, really pissed at you. You will experience carb cravings the lacks of which no one but Oprah has experienced. It will be entirely unpleasant. The smell of bread will instantly transform you into a frothing rabid beast. It will be bad. However, if you stay the course you will be rewarded with body recomposition that is more radical than any other nutrition plan known to man. Is it possible to lose weight with carbs? You bet. Remember, caloric expenditure is the key to weight loss. Do I think that ketogenic diets are more effective at striping off adipose and sparing muscle? I do.
KETOSIS FOR NEWBIES
by Beowulf
Even if you are just taking up this ridiculous hobby, you know doubt have heard of a ketogenic diet. It should be noted that ketogenic diets are, well, an unrelenting bitch from hell intent on destroying you and stealing your newly acquired rocket car (typically reserved for "gold" level AE writers). So, since you are familiar with ketogenic diets do you really know how they work? Do you know what to expect? The intent of this article is to answer these, no doubt, burning questions.
If you are uninterested in the science of things this is not section for you. However, if you want to learn the "why" in addition to the "how" part of the equation, I would recommend that you keep reading. In a normal dietary situation (in the presence of carbohydrates) your body uses glucose as its primary fuel source. Every one is happy. Your brain has sufficient glucose to function at 100%, your muscles have bountiful glycogen stores, and your kidneys are not having to put in overtime to remove urea from your blood. The body only requires 50 grams of carbohydrates per day to avoid going into ketosis. That is only two hundred kcalories a day from carbs (one gram of carbs = four kcalories). This is rather remarkable considering that your brain all by its lonesome utilizes 140-150 grams of carbohydrate in a day.
In the absence of carbohydrates, or with a very restricted carbohydrate intake, your body thinks it is starving to death. You could even be hypercaloric (more calories consumed than spent) and your body would still think that it is starving. In reality, your brain is starving. Did you ever wonder why bodybuilders who misuse insulin die? Failure to consume adequate carbohydrate and the usage of insulin will result in the effective removal of all the glucose in the bloodstream. The insulin drives it into muscle and fat. The end result is that the brain just runs out of gas and one goes into a coma or dies.
Enter your friend and mine: ketosis. In the absence of carbohydrates the body still has to have glucose to operate. This is because the CNS (Central Nervous System) prefers to use glucose for fuel. It will only use ketone bodies for fuel once blood plasma concentrations are extremely high, primarily because ketone bodies don't pass through the blood brain barrier all that well. There are two substances in the body that we will be concerned with that can convert to glucose: glycerol and protein. Lactate can also be converted to glucose, but this is not of terrible importance for our purposes.
Glycerol has a three-carbon skeleton and that is what the krebs cycle is looking for. Once protein is broken down into its constituent amino acids it enters the krebs cycle at different places. Some of these intermediaries are three carbon molecules and some will eventually become pyruvate itself. You see, pyruvate has a three carbon skeleton as well so by stripping off all the crap and starting from the three carbon skeleton up, two glycerols or pyruvates can be run essentially backwards through glycolisis (the formation of two three carbon pyruvates from one six carbon glucose) to form one six carbon molecule of glucose.
Where does the gycerol come from? A fat is constructed from three fatty acids and, you guessed it, a gycerol. Since fatty acids cannot be run backwards through glycolisis, something has to be done with them when they are stripped of their glycerol. The fatty acids are chemically modified into acetyl CoA (trust me, this process far outreaches the scope of this article) which progresses through the Krebs cycle, or citric acid cycle. A good number of these acetyls are metabolized completely and produce ATP. However, a considerable portion of these do not proceed all the way through the krebs cycle. There is excess acetyl CoA generated from the oxidation of fat because the Krebs cycle only works so fast (however, it really is remarkably fast). This extra acetyl CoA is packaged by the liver as ketones. The liver is the only place in the body that produces ketones.
Ketones are funny things. Their primary purpose is, of course, to serve as a fuel source. Ketones feed what glucose would ordinarily feed. The thing is that once blood ketone concentrations rise to a certain point they can no longer be efficiently utilized by the body and certain cells in your body just don't use them all that well. The end result is that they are removed from the bloodstream and end up in your urine. You are essentially peeing calories. This is a novel theme because your body is an ancient and incredibly efficient machine. It almost never wastes anything.
Another interesting thing to note is most nutritional experts will tell you that a ketogenic diet WILL cause muscle wasting. However, as bodybuilders we know that ketogenic diets are notorious for their muscle sparing properties. What gives here? In the author's humble opinion it all has to do with weight training. Compare a normal sedentary individual with resistance trainee. Are they both going to use protein for fuel? You bet. Are they going to equal amounts of protein for fuel? Doubtful. A sedentary individual will never need as much dietary protein to repair the microtrauma incurred from everyway events like walking and standing upright as a trained person would require to repair the catastrophic (by comparison) microtrauma resulting from a hard day of squats. Bodybuilders simply need that protein for things other than fuel. I concede the fact that protein is going to be used to make glucose. The brain absolutely positively must have glucose and we should be glad to spare some protein so that we don't slip into a coma or die. However, I simply don't buy the notion that a disproportionate amount of protein to fat is going to be utilized. The body will do what it has to do to stay alive first, but after that, it has a miracullous way of healing itself.
It is important to note that in order for protein to be used as a fuel source, its constituent amino acids must be deaminated. This means that the amino group is cleaved off of the amino acid. The problem arises because this amino group contains a nitrogen and that nitrogen reacts to form ammonia in your cells. Needless to say, ammonia in your cells is some serious shit. This ammonia makes its way to the liver, where it is converted to urea. Urea is toxic as well and excess levels can lead to gout (uric acid poisoning), however, it is not as toxic as it predecessor. Urea is eventually filtered out of the blood by the kidneys and excreted in urine. This is important because when urea concentrations rise you must urinate more in order to expel the potentially toxic product. Also, due to the higher concentration of urea in the blood you have to urinate much more frequently. This, in combination with the fact that glycogen stored in muscles actually exists in a 1:3 ratio with water and when the glycogen leaves so does the water, can spell trouble. .If you do not drink an increased amount of water, you will become dehydrated.
Part of the reason that the Atkins diet became so popular so quickly in the mainstream is because dieters can lose weight very rapidly during the first week of the diet. They could also lose weight very rapidly if we were to administer a diuretic and they didn't diet. Essentially the same thing is happening.
While ketosis is a really nifty trick, it is important to remember that energy expenditure is the real determinant in weight loss. If you cut carbs and are still in a hypercaloric state, guess what, you are going to gain weight. If you are in ketosis and you are in a hypercaloric state, you will more than likely gain weight. Ketosis is not a ticket to eat all you want. You are still subject to the law of energy conservation.
Another consideration should be that your body really does prefer glucose as a fuel source to ketones (I am can't stress this point enough). Being as such, the tissues that don't use ketones for fuel well are going to give you problems in the form of decreased performance. This is a major problem because two of the tissues that don't fare well on ketones are the brain and skeletal muscle.
The brain will find a way to function, let there be no doubt, but it will not function at full capacity. Things will seem a little hazy. You will more than likely not notice this because everything slows down, even the conscious perception which would enable you to notice it. While potentially troubling, this is not a huge problem. Reaction times will be longer for certain, but probably not to the point of compromising safety in most situations.
The inability to use ketones as a fuel source of skeletal muscles will get your attention. You will go to the gym and perform like shit. You will miss your heaviest lifts and you will feel shame. Obviously, the rules are altered a considerable deal by simultaneous usage of AAS and implementation of a ketogenic diet but if you are training clean, you will have to fight through some piss poor training sessions. This is the beauty of diets such as Bodyopus, The Anabolic Diet, and Animabolics. They allow for a carb up period after a given time and, as a result, you won't feel, for lack of a better term, so flat.
While most of the other side effects primarily afflict special populations with either liver or kidney damage, another side effect is universal. You see, fiber has a way of hiding itself in foods that contain carbohydrates. Fiber is the primary reason for peristalisis, or the contraction of your bowel to move food toward the toilet. This is a very nice way of saying that you will more than likely become very very badly constipated if you don't use a fiber supplement to keep the plumbing flowing. I can speak from personal experience on this one. You will find yourself in the bathroom making deals with the almighty. Sayings like, "Dear Lord, if you let me take this dump I swear that I will bake cookies for the church bake sale" or "Dear Lord, if I don't make it through this, give the paramedics the intelligence to come up with a good story to tell my mother like I died saving a bus full of orphans or something like that....." will become part of your daily restroom regimen.
I have never met anyone who was not completely miserable while on a ketogenic diet. You are starving your body and it is really, really pissed at you. You will experience carb cravings the lacks of which no one but Oprah has experienced. It will be entirely unpleasant. The smell of bread will instantly transform you into a frothing rabid beast. It will be bad. However, if you stay the course you will be rewarded with body recomposition that is more radical than any other nutrition plan known to man. Is it possible to lose weight with carbs? You bet. Remember, caloric expenditure is the key to weight loss. Do I think that ketogenic diets are more effective at striping off adipose and sparing muscle? I do.
swimmar
New member
nandi12 said:
No, of course you shouldn't assume that creatine does those things. I never said the opposite of my statement, which would be "The absence of proof of a statement does lead to the statement's truth." The thing is, you can't assume that an unproven thing is true or not. But you did state that ALA did decrease insulin levels. No "maybe it will"s or "assuming this is true"s or any other qualifications.
macrophage69alpha
New member
nandi..
do you really want to compare insulin sensitive lean zucker rats with the general population.. you will find that there is little similarity...
% of pop with some form of insulin resistance MUCH higher than you indicate.. especially among the AS using population.. as well as BC for women
will discuss this more fully with you (with studies, which while they do have value are often micro as opposed to macro oriented) when have time..
do you really want to compare insulin sensitive lean zucker rats with the general population.. you will find that there is little similarity...
% of pop with some form of insulin resistance MUCH higher than you indicate.. especially among the AS using population.. as well as BC for women
will discuss this more fully with you (with studies, which while they do have value are often micro as opposed to macro oriented) when have time..
Re: Re: Re: ALA for athletes
And then Ketones are turned into glycogen. So then what do you go out of ketosis? NO! ALA makes me lose BF. No doubt about it. Nandi12, One thing you have to remember is that these studies more than likely did not use 2000-3000mg of ALA. A high Dose changes things often in many drugs. ALA at this dose mimics Insulin. It often puts me in hypoglycemia as a matter of fact.
Quad
swimmar said:
And then Ketones are turned into glycogen. So then what do you go out of ketosis? NO! ALA makes me lose BF. No doubt about it. Nandi12, One thing you have to remember is that these studies more than likely did not use 2000-3000mg of ALA. A high Dose changes things often in many drugs. ALA at this dose mimics Insulin. It often puts me in hypoglycemia as a matter of fact.
Quad
swimmar
New member
Another good summary is at http://groups.google.com/groups?hl=...hts&hl=en&lr=&ie=UTF-8&oe=UTF-8&start=10&sa=N
And then Ketones are turned into glycogen. So then what do you go out of ketosis? NO! ALA makes me lose BF. No doubt about it. Nandi12, One thing you have to remember is that these studies more than likely did not use 2000-3000mg of ALA. A high Dose changes things often in many drugs. ALA at this dose mimics Insulin. It often puts me in hypoglycemia as a matter of fact.
Quad
--------------------------------------------------------------------------------
I did not know that ketones were converted to glycogen... I've looked around, but can't find anything that supports that. Should go re-read that Keto book.
I want to correct myself. Ketones do not convert to glycogen they are an alternative fuel source. but ALA does lower insulin insensitivity and it does mimic insulin at high doses.
Quad
--------------------------------------------------------------------------------
I did not know that ketones were converted to glycogen... I've looked around, but can't find anything that supports that. Should go re-read that Keto book.
I want to correct myself. Ketones do not convert to glycogen they are an alternative fuel source. but ALA does lower insulin insensitivity and it does mimic insulin at high doses.
Ahhh, kick ass point Quadsweep. If you go to GNC or local vitamin shop they will usually tell you to only take a handfull of ALA pills each day. Thats why i would assume these scientists are only testing with low amounts of ALA. If you read what people's results on this board you will hear a lot of"when i upped my ALA dosage to 3000mg a day the fat flew off", so maybe science is just slacking behind again and we need some new tests before anyhting is conclusive.
As for saying "X amount of people that are not insulin resistant....." I don't think any of us know how many people are. Over half of americans are obese (wasn't that the latest bit of "fat people" news?) so that makes me think its more people than you think.
quartermiler
New member
Did I say you cut and paste? No i didnt, i said thats what it seems like because it is so precise... and I wasnt asking for me either... I undertstood what you were saying but it looked like the person who originally started this post had difficulty understanding what you were saying. Not everyone here is as "educated" as you, and may not understand all that Anatomy and physiology mumbo jumbo.
luto199 said:
I think the number I read was Obesity is up 700% in the US and Type 2 adult onset diabetes is up 400% in the last 10 years. It is thought to be linked to fat free foods. The removal of fat caused the sugar in these foods to be digested much more quickly since fat is difficult to break down. This increased absorption rate causes larger blood sugar spikes which in turn causes larger insulin secretion by the pancreas. Over time this causes insulin insensitivity which can lead to Type 2 adult onset diabetes.
Quad
Been there, done that, nautica. Waste of money. As for the Zucker rats, the point was to keep as many variables controlled as possible. The insulin sensitive Zucker rats showed no benefit from ALA. I'm still waiting for you to post the study showing ALA has any benefit in insulin sensitive people, Macro.
This discussion has essentially turned into science arguing against religion. The high priests tell the masses to worship the god of ALA and everyone bows and scrapes accordingly. I find debating science much more rewarding than debating religion. The latter is always a lose-lose situation.
As for the doses Quadsweep, read the abstract. How much do you weigh? The rats were given 30mg/kg/BW/day. If you weigh 100kg, or 220lb, that is 3000mg equivalent.
It is true that AAS can cause insulin resistance. What is the mechanism for this? In the studies I have read it is at the level of glycogen synthase, an enzyme ALA has never been shown to increase. Obesity is the biggest risk factor for NIDDM. I don't see too many morbidly obese guys at the squat rack at my gym.
Like I said, its religion vs. science. Utterly pointless.
it's just that i don't think the science is conclusive enough yet to make any kind of decision.
Nandi, mind giving us a little info about yourself. Since your posting against ALA you are prob now the least popular person here, maybe some credentials behind your name will get you some respect here.
I'll go look again but i thought i have read some studies that are done on non diabetic rats.
Nandi, mind giving us a little info about yourself. Since your posting against ALA you are prob now the least popular person here, maybe some credentials behind your name will get you some respect here.
I'll go look again but i thought i have read some studies that are done on non diabetic rats.
Do you seriously think I care about gaining your respect, luto? I don't even know you. If you want to learn something by reading my posts and contrasting my ideas with those of other people that is fine. I post because writing forces me to clarify my thoughts and put together a coherent picture of what is going on. ( That and making macro resort to his big, supersize font; that always makes my day). I do this for my own benefit. It is purely selfish. It is like sitting down and preparing for a presentation, trying to anticipate responses.
www.catie.ca/pdf/alpha-lipoic.pdf
Here check this out, it talks about ALA to treat "Lipidystrophy" in people that have HIV, but NOT diabetics. Says MANY people experienced decreased insulin sensitivity. It then talks about another study with diabetic people, using 6mg-1.6g a day saying they had improved insulin sensitivity.
P.S. Search for thiotic acid, not just ALA when doing research on ALA.
Here check this out, it talks about ALA to treat "Lipidystrophy" in people that have HIV, but NOT diabetics. Says MANY people experienced decreased insulin sensitivity. It then talks about another study with diabetic people, using 6mg-1.6g a day saying they had improved insulin sensitivity.
P.S. Search for thiotic acid, not just ALA when doing research on ALA.
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macrophage69alpha
New member
nandi12 said:
btw- dont take credit for "supersizing" unless it was for you.. which it wasn't.
btw2- will get back to you.. but am a little busy right now.. just have time for quips
monkeyballs
New member
I want to chime in here....
My guess is that the whole purpose of this thread is that "swimmar" want to swim faster.
So the essence of your question is this, will ALA supplementation help my times.
The anecdotal evidence that I can provide- not at all.
I'm not a swimmer, but I am an athlete who is only concerned with the bottom line of moving as fast as I can from point A to point B. As for my own experience, ALA will not help the bottom line, and contrary to many people's experience, I gained a small ammount of bodyfat during the course of my use. All other variables in my training were identical, so I'm virtually convinced that ALA was the culprit. Yes...I could be wrong. I'm open to suggestions, but I feel fairly certain that ALA is not usefull in helping the athlete achieve the bottom line. Every national sports machine agrees with me as well. Not one (none) uses ALA as a team sponsered supplement. Athetes, like BB's, are concerned with the "real world" results that everyone here is raving about, and In the "real world", ALA has not been shown to help athletes.
Now as for a ketogenic diet, I can't imagine a worse Idea for an athlete than to deplete his body of fuel in an attempt to get rid of fat. You are a sprinter, so am I. Your training will go to shit pronto if you follow a ketogenic diet. Even though your a sprinter, your body will still need carbs for a whole slew of reasons in order to function at its peak ability. While in ketosis your recovery will suck, therefore you training volume will suffer, and ultimatly your training intensity has gone to the shitter as well. The end result is slower times. Bottom line.
You mentioned Lance Armstrong earlier...he consumes up to 5000 calories a day, 60% of which is carbohydrates, many of them simple. Yes, it has been shown that his body uses fat for fuel more efficently than just about anyone on the planet, but the word "ketosis" isn't anywhere in his vocabulary. Nor is it in that of just about any elite athlete. Elite is the key word here. I'm sure high school sprinters can get away with a ketogenic diet, and depending on what level your swimming at, you may too.
That's my .2$.
I'd also like to add that this is a great post with a very healthy debate going on; A debate which I would like to see stay as constructive as possible. And for those of you who think that this thread is has too much "fancy book learnin", there are plenty of other posts for you to read, let the text nerds enjoy this one.
My guess is that the whole purpose of this thread is that "swimmar" want to swim faster.
So the essence of your question is this, will ALA supplementation help my times.
The anecdotal evidence that I can provide- not at all.
I'm not a swimmer, but I am an athlete who is only concerned with the bottom line of moving as fast as I can from point A to point B. As for my own experience, ALA will not help the bottom line, and contrary to many people's experience, I gained a small ammount of bodyfat during the course of my use. All other variables in my training were identical, so I'm virtually convinced that ALA was the culprit. Yes...I could be wrong. I'm open to suggestions, but I feel fairly certain that ALA is not usefull in helping the athlete achieve the bottom line. Every national sports machine agrees with me as well. Not one (none) uses ALA as a team sponsered supplement. Athetes, like BB's, are concerned with the "real world" results that everyone here is raving about, and In the "real world", ALA has not been shown to help athletes.
Now as for a ketogenic diet, I can't imagine a worse Idea for an athlete than to deplete his body of fuel in an attempt to get rid of fat. You are a sprinter, so am I. Your training will go to shit pronto if you follow a ketogenic diet. Even though your a sprinter, your body will still need carbs for a whole slew of reasons in order to function at its peak ability. While in ketosis your recovery will suck, therefore you training volume will suffer, and ultimatly your training intensity has gone to the shitter as well. The end result is slower times. Bottom line.
You mentioned Lance Armstrong earlier...he consumes up to 5000 calories a day, 60% of which is carbohydrates, many of them simple. Yes, it has been shown that his body uses fat for fuel more efficently than just about anyone on the planet, but the word "ketosis" isn't anywhere in his vocabulary. Nor is it in that of just about any elite athlete. Elite is the key word here. I'm sure high school sprinters can get away with a ketogenic diet, and depending on what level your swimming at, you may too.
That's my .2$.
I'd also like to add that this is a great post with a very healthy debate going on; A debate which I would like to see stay as constructive as possible. And for those of you who think that this thread is has too much "fancy book learnin", there are plenty of other posts for you to read, let the text nerds enjoy this one.
Can you post how much you took, your age, bf, weight, height, what you ate, your routine, and where you got the ALA form. These things would be helpful.
You mentioned you run, and swimmar says he swimms. Maybe ALA for some reason would only have a posotive effect on those who weightlift???
And as far ALA not being sport team sponsors, well not a whole lot of people have even thought of ALA as a weight loss supplement until just recently. I mean r-ala JUST came out like a month and a half or 2 months ago. Dont judge it based on that.
You mentioned you run, and swimmar says he swimms. Maybe ALA for some reason would only have a posotive effect on those who weightlift???
And as far ALA not being sport team sponsors, well not a whole lot of people have even thought of ALA as a weight loss supplement until just recently. I mean r-ala JUST came out like a month and a half or 2 months ago. Dont judge it based on that.
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monkeyballs
New member
luto199 said:
No, sorry I'm not going to give you all of those stats. Too much time. I guess I'm just too selfish at the moment. It's late.
All I will say, is that my variables were in controll. My diet has been regimened for the past four years, and so has my training schedule.
Okay, next topic. No. I don't run. But if I did, then anything that would have a benifit on weightlifting would also have a benifit on running. Creatine is perfect example. Weightlifting and running (sprinting) aren't all that different in terms of kinesiology. Also, every anerobic athlete weightlifts, so the idea that ALA would only help weightlifters doesn't have much merit...
As for the issue of sports team sponsership, let me clarify-
I'm not talking about the denver broncos and EAS here, I'm talking about the dutch or north koreans...etc. State funded sports machines. And whatever we know about, they have studied and used for a good decade or so. Creatine was used by amature athletes as early as the late 70s. The earliest I saw it on our shelves was in the early 90's (could have been earlier...I don't know). Chances are nobody here has used (or maybe even heard of) gene therapy to augment their training.
ALA is known about by these various institutions, and to my knowledge, none use it.
I would like to add this. I'm about to hit up a 17aa cycle if my source issues ever work themselves out...I will use ALA as an anti-oxidant and liver protectant. So in this case, yes, ALA does help athletes.
me sleep now
well get back to me on that, i'm really interested in ala and would like to know everything about you since you say it didn't work.
BTW, just found this article at bodybuilding.com stating "Scientific evidence CLA burns fat" http://www.bodybuilding.com/fun/david22.htm Whats the relation between CLA and ALA?
BTW, just found this article at bodybuilding.com stating "Scientific evidence CLA burns fat" http://www.bodybuilding.com/fun/david22.htm Whats the relation between CLA and ALA?
fhg43
New member
monkeyballs said:
I have to agree with monkeyballs. Like I posted earlier I specifically used ALA w/ECA and killer diet to reduce fat-I got nothing. But as soon as I quit the ALA I lost my stubborn fat. I used very good ALA as well; Jarrows pharm grade, 900mg/day, one before each meal. Jarrows is probably 50+% r-ALA. Bottomline like MB said ALA didn't make me faster. That is the gold standard by which atletes measure supplements-does it make me faster, stronger, or increase endurance?
Anyway, like MB, I to am a highly trained athlete (not to say that nobody else is but...) and my diet is 60% carb, 25% pro, 15% fat. No way I want to go into ketosis! Each athlete has different needs. BB'ers definitely have different dietary needs than swimmar, monkeyballs, and myself. ALA may be beneficial for BB'ers and not endurance (or sprinter) athletes. Thats what our discussion is pointing to.
FHG
macrophage69alpha
New member
FHG,
difference between ala and r-ala is significant.. the increase in plasma insulin that a racemic will cause is probably not beneficial for atheletic performance..
though cannot say conclusively that r-ala would be either.. merely that they are different in several aspects with respect to physiology..
btw- when using racemic during bulking.. definitely noticed greater fat gains as well.. have not used r-ala thus (at least not with such high cals) so cannot comment.. yet..
difference between ala and r-ala is significant.. the increase in plasma insulin that a racemic will cause is probably not beneficial for atheletic performance..
though cannot say conclusively that r-ala would be either.. merely that they are different in several aspects with respect to physiology..
btw- when using racemic during bulking.. definitely noticed greater fat gains as well.. have not used r-ala thus (at least not with such high cals) so cannot comment.. yet..
fhg43
New member
luto199 said:
r-ALA isn't anything new. Plenty of really good ALA supps have existed. The fact that someone is marketing it maybe new.
BB'ers and lifters have a totally different standard for a supplement and if it works-does it make me skinny, does it make my muscles bigger, does it make me look good? There's nothing wrong with this criteria if your goals are low BF and big muscles. And ALA may help fat loss if you are engaged in a keto diet. Anecdotal evidence seems to support this. But the above criteria doesn't really apply to aerobic/anaerobic athletes.
FHG
macrophage69alpha
New member
fhg43 said:
yes... it is.. never before has the pure R enantiomer been available for anything but research.
all of those "prettygood" ALA sups were RACEMIC.. the cheaper manufacturing process used creates chiral enantiomers (mirror images) one with a right orientation and one with a left orientation .. half of each.. the left oriented molecule does not exist in nature (the right oriented one is produced by the human body).. the response in many aspects is considerably different
but again as far as athletic performance.. cant say definitively that r-ala will improve performance (at least directly).. obviously some of the anti-ox effects over time will affect performance..
there probably should be some improvement in fine motor control.. especially in older atheletes..
Lumberg
New member
Here is my reasoning (sort of an educated guess I have formulated after reading a lot, both studies and anecdotal evidence) about how ALA can help people lose fat.
Many people have questioned just how ALA can help BURN fat. Well, it doesn't.
Most fat deposition occurs when more carbs than the body can burn are consumed in one meal. The excess glucose circulating, along with the high insulin levels, cause the fat cells to store the excess energy as fat.
Well what ALA does is reduce or even prevent this from happening. The body goes through its usual cycles of burning and sotring fat. However the storage cycle is attenuated, and the time it takes to get into fat burning mode is decreased (ie blood glucose levels fall faster when a meal is taken with ALA).
JC
Many people have questioned just how ALA can help BURN fat. Well, it doesn't.
Most fat deposition occurs when more carbs than the body can burn are consumed in one meal. The excess glucose circulating, along with the high insulin levels, cause the fat cells to store the excess energy as fat.
Well what ALA does is reduce or even prevent this from happening. The body goes through its usual cycles of burning and sotring fat. However the storage cycle is attenuated, and the time it takes to get into fat burning mode is decreased (ie blood glucose levels fall faster when a meal is taken with ALA).
JC
monkeyballs
New member
macrophage69alpha said:
Perhaps it has never been available so easilly to the public, but I don't think that the guys at AF are in on the ground floor here. I'm sure that there has been some supplement available that is relativly close the R-ala that is sold here. Maybe not identical, but close.
swimmar
New member
Wow, some good discussion here.
Monkeyballs, yes, a ketogenic diet for an elite athlete is not a good idea. Personally, I follow a fairly low-carb diet, except for about two hours before and after each workout. Seems to work well for me. As far as eliteness goes, I'm not exactly sure what the criteria would be for that. Only Olympic caliber? Nationally ranked?
Anyways, what got me thinking about ALA is I read some stuff about it possibly increasing the amount of glycogen reserves in muscles, and I went, "Hey, that sounds like a good thing for athletics." Though apparently, it's not that great. Thanks for the response.
Monkeyballs, yes, a ketogenic diet for an elite athlete is not a good idea. Personally, I follow a fairly low-carb diet, except for about two hours before and after each workout. Seems to work well for me. As far as eliteness goes, I'm not exactly sure what the criteria would be for that. Only Olympic caliber? Nationally ranked?
Anyways, what got me thinking about ALA is I read some stuff about it possibly increasing the amount of glycogen reserves in muscles, and I went, "Hey, that sounds like a good thing for athletics." Though apparently, it's not that great. Thanks for the response.
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fhg43
New member
joncrane said:
I was under the impression that ALA helped users lean out by increasing glucose uptake i.e. cells can take in more glucose with ALA than without. So less excess carbs are stored as fat.
Well ALA doesn't replace insulin. So insulin will still be present post meal, and some excess carbs will still get stored as fat
At lower intensity your body burns less fat and more glucose. So post-meal your body is still burning carbs and continues to use available glucose. You can't really get back into fat (as primary fuel source) burning mode because you were never in that mode. Your body prefers to use carbs for energy because they breakdown easier than fat and protein. They are also used to create fuel for your brain-your body uses glucose (or another byproduct of carb metabolism) to make neurotransmitters. Your body doesn't need much energy to wander around or sit behind a computer and type an email. As activity level increase the percentage of fat you burn increases-the body is demanding more fuel so it must tap into fat stores to get that energy. There is a "Fat burning" zone BUT the intensity is higher than most people think. Anyway thats a whole new thread....
My point is your body is still storing fat on ALA and there is anecdotal evidence to support this point. As well your body wil always attempt to store some fat-that is a facet of our physiology that is near impossible to override. And yes you do burn fat at low activity levels but less than you think. Glucose is the fuel of choice because it is easy to use.
IMO ALA is going to affect everyone in different ways. The level of insulin one releases can vary from person to person. So ALA may exert a greater effect on insulin resistant individuals like AAS users.
FHG
serge
New member
monkeyballs said:
one must consider the doses used in the studies involving human subjects (not fucking rats), i have yet to see one abstract evaluating effects of ALA at a dose higher then 600mg/ed, not to mention 3g/ed; untill such a study is done we have nothing to go on but the anecdotal evidence
macrophage69alpha
New member
monkeyballs said:
NOPE...
Lumberg
New member
fhg43 said:
Thanks FHG for helping me understand a bit better. HOwever I have some issues:
1) If we are to believe ulter, while ALA does not replace insuling completely, it does in effect supplant it to a great degree. basically with ALA you will need significantly less insulin to shuttle your dietary carbs into your muscles.
2) isn't there a fat burning zone at rest? meaning when the body has consumed all the carbs from the previous meal? also a lot of bbers recognize the fact that lower-intensity cardio actually burns more fat than high-intensity cardio. how do you reconcile this?
JC
swimmar
New member
joncrane said:
? I didn't think that was the case. There was a study done some number of years ago that showed that more glycogen than fat was burned at high intensity work, while more fat than glycogen was burned at low intensity work. However, people didn't understand the difference between proportions and absolute amounts, and thought that low intensity was the way to go for fat loss.
monkeyballs said:
Why don't you think the guys at AF are on the ground floor here? You're gonna hurt their feelings. Why wouldn't they be on the ground floor, do you see anyone else selling NYC or Tyler's Liver Detox here?
AF was first and right now AF is the ONLY r-ALA there is in America.
As Macro has said repeatedly you can't compare ALA to r-ALA.
"We're finding - and others are, too - that the R(+)-form - the natural form - is much more powerful than the racemic mixture ... Hopefully ... companies are going to be producing on more of a clinical scale the R(+)-form of lipoic acid, because we're finding very significant effects using this, as opposed to the racemic mixture."
Dr. Tory Hagen, in Mitochondrial Decay in Aging.
"We have presented in this study new information indicating that this enhancement of glucose metabolism is sterospecific, with the R(+)-enantiomer being much more effective than the S(-)- enantiomer."
Dr. Ryan Streeper and colleagues, in The American Journal of Physiology.
"Lipoic acid sold in a health food store is a synthetic mixture, a racemic mixture. And R[+]- is the natural form and S[-]- is an unnatural one ... And in our hands R[+]- works and S[-]- doesn't."
Dr. Bruce Ames, in Strategies for Engineered Negligible Senescence.
"R[+]-LA [that is, R(+)-lipoic acid], and not a racemic mixture of R[+]-and S[-]- LA, should be considered a choice for therapeutic applications."
Dr. Lester Packer and colleagues, in Free Radical Biology and Medicine.
"The S[-]-enantiomer … part of the racemate, which is present as about a 50% impurity, needs to be eliminated."
Dr. Guido Zimmer and colleagues, in Methods in Enzymoogy.
THeMaCHinE
New member
Nandi12 -- thanks for your perspective on this thread. In my experience, your thinking has always been very solid.
swimmar
New member
Well, shit, I already bought 100 grams from BAC (it was pretty cheap). I'm not sure if it's r-ALA or what.
So uh, any recommendations on what to do with it? Will it make me gain 20 lbs of fat if I sign the UPS packing slip for it? Save it for a bulking cycle? Give it to my cat?
So uh, any recommendations on what to do with it? Will it make me gain 20 lbs of fat if I sign the UPS packing slip for it? Save it for a bulking cycle? Give it to my cat?
fhg43
New member
JC and swimmar-
Fuels sources and when the body chooses them are controversial and somewhat misunderstood topics. It is dependent on exercise intensity and duration as well as the type of exercise and athlete-so we have a lot of variables. But let's use Lance Armstrong since he was mentioned previously and I'll talk about how it works for him. Bear with me-I will use pretty simple concepts and indices
'Low intensity' from an energy system standpoint is APPROXIMATELY an intensity ~50-88% percent of max HR (depending on who you ask-in all actuality HR is just a rough index of workload-to actually determine the workload of Lance in our theoretical model you would have to look at his wattage output, lactate clearance, energy system/metabolic processes and the efficiency of those processes-however HR has been proven as a 'reasonable' index of athletic workload-HR is your body's response to work being done-this could be a whole new thread). This could vary somewhat from athlete to athlete. In this zone a majority of calories burned come from fat, meaning your body is choosing fat as its primary fuel source (60-70% energy comes from fat). As well glucose and protein is used as well. Well-trained aerobic/endurance athletes will have a wider 'zone' for using fat as the primary fuel source.
Your body converts fat down to ATP-same thing happens with glucose and protein. Fat molecules convert to ~ 3 or 4 times as much ATP as a glucose molecule-this is why when conditions allow your body prefers fat. In the "zone" your body still needs glucose as part of the fat breakdon process. Look at available glucose as the igniter of the fat breakdown reaction. Protein gets broken down too, but this is the hardest substance for your body to breakdown to ATP. However some protein breakdown is necessary and part of the energy system/aerobic respiration process.
So Lance is riding along at a HR of 160 which is, say, 80% of max HR (and for our purposes 80% intensity level). His metabolism has been trained very well to use fat for fuel so most of his caloric expenditure comes from fat being burned. After 3hrs, Lance comes to a mountain and accelerates up the climb. His HR increases to 170 which is about 87% percent (close to aerobic/lactic threshold). At this point his body begins to move away from fat a little and demand more glucose. The energy system/aerobic respiration process is speeding up and the body needs ATP ASAP and it is easier to breakdown glucose. Now Lance has been on this mountain for :30min. He is still burning fat but he is burning quite a bit of available glucose too. Lance is near the top and decides to ride all out to the top. He accelerates and his HR goes up to 188 or 95%. Now his body needs energy on demand. The energy system/aerobic respiration process is now making most of its energy from glucose (this could have been released by the liver or taken from food or a sports drink). Most of calories are coming from glucose. At the top Lance relaxes and coasts down the other side. At this point I am kinda fuzzy. I am sure he is gradually burning more fat. When he rests for the day though I believe his energy demands will be low enough they can be met by glucose in the blood or from the liver. At rest I believe the body derives energy from carbs and fat. It isn't fat entirely-otherwise we wouldn't have obese or overweight individuals-everyone would be 15% BF. if their body only burned fat at sedentary workloads (ie get up, go to work, drive home, watch TV, go to mall, movies-do you know what I mean).
So higher intensity does burn more calories and burns much of them from glucose. Low intensity (which you can see really isn't that low-try maintaining 160bpm for 3hrs and then 175bpm for :30min) burns more calories from fat. The higher intensity will raise metabolism for longer post workout. After a lower intensity workout metabolism will return to normal sooner. Metabolism rises in response to the bodies need to refuel/rebuild itself post workout. So it makes sense that after a harder workout your body will take longer to repair.
In well trained endurance athletes they can get into fat burning mode/zone quicker than a poorly trained individual. As well their zone is wider and they may need less fat (converted to ATP) to do the same amount of work as a poorly trained athlete. As well their energy system/aerobic respiration process is much more efficient so they can produce more power from lower amounts of energy (i.e. Lance might only need 500kcal to complete a 30mile race in 1hr; whereas a poorly trained cyclist may need 1500cal to complete the same race in 1:15)
There are a ton of opinions and studies done re: energy system metabolism so you can get somewhat conflicting info here and there.
Currently, BB'ers feel they can burn more calories by doing HIIT, short high intensity interval workouts, rather than longer low intensity workouts. The theory goes like this: after accounting for all calories burned post workout from raised metabolism-they'll burn more calories, thus more fat, from an HIIT workout than from a low intensity workout. During the the low intensity workout they may burn a higher percentage of fat. However since metabolism isn't raised as long post-workout, overall calories burned is less; therefore less overall fat is burned. The flaw with low intensity workouts is often people don't work hard enough-they think 'oh if I just walk at 130bpm for :30min on the treadmill that'll be okay' when really it won't burn much fat at all. They need to get the HR closer to 150 for :45 to really see any fat burning benefit. Either way you burn fat-in general people need to cardio a little harder, a little longer to see results they want (this is a general observation made from posts on the board).
This site had some interesting tidbits (I think ALL their figures are low though-but goes to show the discrepancies in specifics of energy system function).
http://teaching.ucdavis.edu/nut111/carb/carb.html
So there is an energy system primer. Now how ALA affects this...let me regroup and think about that a moment.
FHG
Fuels sources and when the body chooses them are controversial and somewhat misunderstood topics. It is dependent on exercise intensity and duration as well as the type of exercise and athlete-so we have a lot of variables. But let's use Lance Armstrong since he was mentioned previously and I'll talk about how it works for him. Bear with me-I will use pretty simple concepts and indices
'Low intensity' from an energy system standpoint is APPROXIMATELY an intensity ~50-88% percent of max HR (depending on who you ask-in all actuality HR is just a rough index of workload-to actually determine the workload of Lance in our theoretical model you would have to look at his wattage output, lactate clearance, energy system/metabolic processes and the efficiency of those processes-however HR has been proven as a 'reasonable' index of athletic workload-HR is your body's response to work being done-this could be a whole new thread). This could vary somewhat from athlete to athlete. In this zone a majority of calories burned come from fat, meaning your body is choosing fat as its primary fuel source (60-70% energy comes from fat). As well glucose and protein is used as well. Well-trained aerobic/endurance athletes will have a wider 'zone' for using fat as the primary fuel source.
Your body converts fat down to ATP-same thing happens with glucose and protein. Fat molecules convert to ~ 3 or 4 times as much ATP as a glucose molecule-this is why when conditions allow your body prefers fat. In the "zone" your body still needs glucose as part of the fat breakdon process. Look at available glucose as the igniter of the fat breakdown reaction. Protein gets broken down too, but this is the hardest substance for your body to breakdown to ATP. However some protein breakdown is necessary and part of the energy system/aerobic respiration process.
So Lance is riding along at a HR of 160 which is, say, 80% of max HR (and for our purposes 80% intensity level). His metabolism has been trained very well to use fat for fuel so most of his caloric expenditure comes from fat being burned. After 3hrs, Lance comes to a mountain and accelerates up the climb. His HR increases to 170 which is about 87% percent (close to aerobic/lactic threshold). At this point his body begins to move away from fat a little and demand more glucose. The energy system/aerobic respiration process is speeding up and the body needs ATP ASAP and it is easier to breakdown glucose. Now Lance has been on this mountain for :30min. He is still burning fat but he is burning quite a bit of available glucose too. Lance is near the top and decides to ride all out to the top. He accelerates and his HR goes up to 188 or 95%. Now his body needs energy on demand. The energy system/aerobic respiration process is now making most of its energy from glucose (this could have been released by the liver or taken from food or a sports drink). Most of calories are coming from glucose. At the top Lance relaxes and coasts down the other side. At this point I am kinda fuzzy. I am sure he is gradually burning more fat. When he rests for the day though I believe his energy demands will be low enough they can be met by glucose in the blood or from the liver. At rest I believe the body derives energy from carbs and fat. It isn't fat entirely-otherwise we wouldn't have obese or overweight individuals-everyone would be 15% BF. if their body only burned fat at sedentary workloads (ie get up, go to work, drive home, watch TV, go to mall, movies-do you know what I mean).
So higher intensity does burn more calories and burns much of them from glucose. Low intensity (which you can see really isn't that low-try maintaining 160bpm for 3hrs and then 175bpm for :30min) burns more calories from fat. The higher intensity will raise metabolism for longer post workout. After a lower intensity workout metabolism will return to normal sooner. Metabolism rises in response to the bodies need to refuel/rebuild itself post workout. So it makes sense that after a harder workout your body will take longer to repair.
In well trained endurance athletes they can get into fat burning mode/zone quicker than a poorly trained individual. As well their zone is wider and they may need less fat (converted to ATP) to do the same amount of work as a poorly trained athlete. As well their energy system/aerobic respiration process is much more efficient so they can produce more power from lower amounts of energy (i.e. Lance might only need 500kcal to complete a 30mile race in 1hr; whereas a poorly trained cyclist may need 1500cal to complete the same race in 1:15)
There are a ton of opinions and studies done re: energy system metabolism so you can get somewhat conflicting info here and there.
Currently, BB'ers feel they can burn more calories by doing HIIT, short high intensity interval workouts, rather than longer low intensity workouts. The theory goes like this: after accounting for all calories burned post workout from raised metabolism-they'll burn more calories, thus more fat, from an HIIT workout than from a low intensity workout. During the the low intensity workout they may burn a higher percentage of fat. However since metabolism isn't raised as long post-workout, overall calories burned is less; therefore less overall fat is burned. The flaw with low intensity workouts is often people don't work hard enough-they think 'oh if I just walk at 130bpm for :30min on the treadmill that'll be okay' when really it won't burn much fat at all. They need to get the HR closer to 150 for :45 to really see any fat burning benefit. Either way you burn fat-in general people need to cardio a little harder, a little longer to see results they want (this is a general observation made from posts on the board).
This site had some interesting tidbits (I think ALL their figures are low though-but goes to show the discrepancies in specifics of energy system function).
http://teaching.ucdavis.edu/nut111/carb/carb.html
So there is an energy system primer. Now how ALA affects this...let me regroup and think about that a moment.
FHG
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macrophage69alpha
New member
swimmar said:
you should be able to still get decent results with cutting..(though to achieve similar.. not same.. effects you will need higher doses 2-4g a day)
as for bulking.. probably not a good idea
macrophage69alpha
New member
serge said:
with racemic ala there is an increase in plasma insulin as well as (at least from studies with s-ala) preferential adipose storage..
My man Clarance Bass wrote a great article on High Intensity Cardio Trainging, where he experimented with speed skaters. His findings were that low intensity burned about double the calories, but the calories burned in HITT training were 9 times more effecient in fat burning.
Do a search on elite and look for it, or try google, its a good read.
myasshurts
New member
It doesn't suck balls, it just isn't as convenient as capsules. Other than that it is exactly the same.
monkeyballs
New member
macrophage69alpha said:
Okay.
I can see that this is not a debate that either of us stands a chance of winning.
I have my opinion, and you have yours. So be it.
I respect yours, as I'm sure it is an informed one from your perspective.
However I don't believe that R-ala is as new, or as remarkable as you have indicated. Somewhere in the lexicon of supplements used by elite athletes, surely R-ala has been considered carfully by someone with far more expertise than any of us, and conciously excluded. Obvioulsly, if the research exists (which you and ulter have regurally cited) then R-ala is no secret. If it is a potent as you say, then i'm sure some former east german would have had the shit for breakfast.
This is really a moot discussion...
Sure, the AF version is probably the only 100 percent R version readilly available.
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macrophage69alpha
New member
MB,
no one said that it would be of great benefit to "elite atheletes".. as they typically are A. younger and B. have great insulin sensitivity. but that does not describe 99% of the people on this forum.. bodybuilders and strength atheletes.. while perhaps "elite" rarely have the insulin sensitivity of endurance atheletes.. few of them even do cardio to a great extent..
many of the drugs used in these sports impair insulin sensitivity.... not to mention the fact that most here are amateurs as well as people just getting into the sport.. insulin sensitivity is an issue for many of these people.. as well as older atheletes (even elite ones)..
with older athletes.. the use of r-ala may be important to maintaining/restoring fine motor control.. as well as overall cns response..
pure r-ala has not been available, even for research, until the last decade (at least in significant amounts).. and this will likely continue to be the case to a certain extent due to certain patents..
no one said that it would be of great benefit to "elite atheletes".. as they typically are A. younger and B. have great insulin sensitivity. but that does not describe 99% of the people on this forum.. bodybuilders and strength atheletes.. while perhaps "elite" rarely have the insulin sensitivity of endurance atheletes.. few of them even do cardio to a great extent..
many of the drugs used in these sports impair insulin sensitivity.... not to mention the fact that most here are amateurs as well as people just getting into the sport.. insulin sensitivity is an issue for many of these people.. as well as older atheletes (even elite ones)..
with older athletes.. the use of r-ala may be important to maintaining/restoring fine motor control.. as well as overall cns response..
pure r-ala has not been available, even for research, until the last decade (at least in significant amounts).. and this will likely continue to be the case to a certain extent due to certain patents..
30% huh? It would funny if it wasn't someone who is actually supposed to know what he's talking about. If he doesn't know where it comes from then he doesn't know what it costs to make so how can he know what it should sell for? You gotta love how these people pick numbers like 30% out the sky and quote them like data from the Mayo Clinic.\
jc I can't tell you what's in the Fonz report. But I think that 300% number being thrown around may be, and I say may be, a pretty good number.
jc I can't tell you what's in the Fonz report. But I think that 300% number being thrown around may be, and I say may be, a pretty good number.
macrophage69alpha
New member
BAC does not carry it becuase they source out of india.. take that as you will..
monkeyballs
New member
macrophage69alpha said:
Fair enough...
But the athletes that I'm speaking of are not endurance athletes. I'm an anerobic athlete, and the athletes that I train with are as well. As for "elite" strength athlets, olympic lifters fall into this category, and none that I know of are using ALA (in any form) at their training table as per a recomendation by their coach. Also, anything that significantly improves strength is a benifit to an anerobic athlete. Powerlifters and sprinters have similiar training methods.
BB's are another lot altogether, as athletic performance is secondary to physique appearance. For their training goals, R-ala may be ideal. I have no idea.
I do agree with you on points A and B.
