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  #21  
Unread 12-21-2010, 12:30 AM
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Originally Posted by cyclist View Post
Lactic acid threshold is not related to oxygen availability per se. Oxygen is not limiting at the so-called "anaerobic" threshold. This is a common mistake in textbooks.
Actually that is primarily how it is related in muscle. Lack of oxygen consumption causes an increase of lactate as the body is breaking down Glucose from stored glycogen for energy. Glucose to Pyruvate and then to oxidize the excess NADH generated from glycolysis you go to lactate BECAUSE you CAN'T use the electron transport chain due to the lack of oxygen.

Basically, low levels of 02 are associated with high levels of NADH and as a result High levels of lactate. That is the relation.

So, in a nut shell:
low o2 in the muslce tissues as a result of exercise=higher levels of lactate and lower levels of citric acid cycle intermediates, and you also have higher levels of NADH--which inhibits fatty acid oxidation (it's like the 3rd step where NAD is used as cofactor)

All of Lyle's stuff makes sense and is definitely backed up by all the biochem I've taken in med school. So, just follow his ideas and your solid. He's never really been wrong.
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  #22  
Unread 12-21-2010, 01:23 AM
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Originally Posted by Zé Apelido View Post
I don't have the answer, which is why I am asking a question. Maybe I should simplify it.

Stage 1

10 min of intervals (30 s on, 30 off)

OR

10 min "race" (reach near VO2max)

Stage 2

Rest 5 min

Stage 3

40 min steady cardio just below LT threshold

The question is: Is there a different effect between the two Stage 1 options on fat oxidation in Stage 3?
Yes there is.

Stage 1 will allow you to essentially couple aerobic and anaerobic metabolism to the best extent as to both release and burn more fat. You're getting the best of both worlds. You will allow your body to somewhat metabolize the lactate that you have made. AND you get the fat out by reducing glycogen.

Stage 2. Is really hard and you are generating a lot of lactate with no hope to metabolize it quickly. It's not that it won't work, but I don't think it's necessarily ideal.
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  #23  
Unread 12-21-2010, 09:18 AM
Zé Apelido Zé Apelido is offline
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Thanks.

So in fat burning stage 3, the steady 10 min stage 1 will cause less fat to be burned than the 10 min intervals. What is being increasingly metabolized, glycogen?
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  #24  
Unread 12-21-2010, 09:30 AM
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Originally Posted by dresden View Post
Higher intensity exercise tends to always be a better option for adaptations...
Really? Always?
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  #25  
Unread 12-21-2010, 09:34 AM
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Originally Posted by dresden View Post
Higher intensity exercise tends to always be a better option for adaptations,
Yet the best endurance athletes do 80% of their volume at low intensities.

Explain.
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  #26  
Unread 12-21-2010, 11:01 AM
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Originally Posted by kimbosliced View Post
Actually that is primarily how it is related in muscle. Lack of oxygen consumption causes an increase of lactate as the body is breaking down Glucose from stored glycogen for energy. Glucose to Pyruvate and then to oxidize the excess NADH generated from glycolysis you go to lactate BECAUSE you CAN'T use the electron transport chain due to the lack of oxygen.

Basically, low levels of 02 are associated with high levels of NADH and as a result High levels of lactate. That is the relation.

So, in a nut shell:
low o2 in the muslce tissues as a result of exercise=higher levels of lactate and lower levels of citric acid cycle intermediates, and you also have higher levels of NADH--which inhibits fatty acid oxidation (it's like the 3rd step where NAD is used as cofactor)

All of Lyle's stuff makes sense and is definitely backed up by all the biochem I've taken in med school. So, just follow his ideas and your solid. He's never really been wrong.
As I said, most textbooks get this wrong. If you actually measure oxygen levels at lactate threshold, you find that they're ten times higher than they would need to be to be limiting (10 Torr vs. 1 Torr). I just took an exercise physiology class and could dig up the lecture slides if you would like.

I am not disagreeing that fat oxidation goes down with increasing intensity, and I am sure Lyle's protocols work great. I just wanted to clarify the mechanism for any interested.
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  #27  
Unread 12-21-2010, 11:29 AM
Zé Apelido Zé Apelido is offline
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Originally Posted by cyclist View Post
As I said, most textbooks get this wrong. If you actually measure oxygen levels at lactate threshold, you find that they're ten times higher than they would need to be to be limiting (10 Torr vs. 1 Torr). I just took an exercise physiology class and could dig up the lecture slides if you would like.

Yeah the energy systems used are based on the rate of energy needed. Anaerobic glycolysis produces ATP at a faster rate than aerobically (but at a much higher cost in glycogen) and both produce energy at a faster rate than fat oxidation. Higher workloads demand more anaerobic glycolysis and oxygen is not the limiting factor. At altitude, however, lack of oxygen pressure could induce anaerobic mechanisms at lower workloads.
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  #28  
Unread 12-22-2010, 12:18 AM
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Quote:
Originally Posted by cyclist View Post
As I said, most textbooks get this wrong. If you actually measure oxygen levels at lactate threshold, you find that they're ten times higher than they would need to be to be limiting (10 Torr vs. 1 Torr). I just took an exercise physiology class and could dig up the lecture slides if you would like.

I am not disagreeing that fat oxidation goes down with increasing intensity, and I am sure Lyle's protocols work great. I just wanted to clarify the mechanism for any interested.
It depends on where the oxygen measurements are occurring--in anaerobic conditions as occurs in skeletal muscle--fat oxidation is greatly, greatly impaired and this is because not only do you not have enough oxygen but you also do not have enough NAD.

Tell me, where is your acetly coa going that you produced from fatty acids/carbs/aminos?

That is the mechanism.
An exercise physiology course cannot overcome basic biochemical mechanisms--which as to the one I'm pointing out is correct.

Reduced o2=reduced ETC=increased glycolysis and glycogenolysis=increased NADH=increased lactate.

I don't really care how exercise physiologist are determining what lactate threshold truly is (as measured in the laboratory). The basic mechanism I just elucidated explains why the stuff happens. The term "lactate threshold" and all that jargon is something Lyle can argue...I'm more concerned with the actual mechanism, which you are saying is incorrect--which it is not.
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  #29  
Unread 12-22-2010, 12:25 AM
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Originally Posted by Zé Apelido View Post
Thanks.

So in fat burning stage 3, the steady 10 min stage 1 will cause less fat to be burned than the 10 min intervals. What is being increasingly metabolized, glycogen?
Yes, glycogen.

The problem comes with too much lactate and inhibition of beta oxidation of fatty acids as a result of this 10 minute burst and you have way too much NADH in the muscle (which inhibits like everything we are trying to do as far as energy metabolism)

Lactate will dissipate in muscle and RBCs by the Cori Cycle (converts it back to glucose) in the liver and by being converted to pyruvate, but this takes time.

Soo....
Listen to Lyle, while he may not like nerding out on the biochemical mechanisms anymore (or atleast not like explaining it), his basic ideas and principles are definitely correct and are founded on scientific principles.

If you want to make your own plan, at least formulate it from his stuff.
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  #30  
Unread 12-22-2010, 02:45 PM
Zé Apelido Zé Apelido is offline
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Thanks, I appreciate the explanation. I tend to like to try to apply concepts through modification in a plan like Lyle's so a better understanding helps a lot.
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