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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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