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Other/Mixed Why we produce lactate...

Other strength modalities (e.g., Clubs), mixed strength modalities (e.g., combined kettlebell and barbell), other goals (flexibility)
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mprevost

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This is glycolysis. Note that step 6 requires an NAD in order to proceed. This will be important later. Glycolysis takes place in the cytoplasm of the cell, outside of the mitochondria.
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Glycolysis ends with the production of pyruvate. Some ATP are produced as well as NADH. The pyruvate is converted to acetyl coA and shuttled into the mitochondria by the pyruvate dehydrogenase complex. All of the following steps happen inside of the mitochondria.
GVQCY.jpg

This is the TCA cycle or Krebs cycle. Note that you are also using NAD to produce NADH inside of the mitochondria. This happens inside of the mitochondria. So far we are only consuming NAD and have not produced any yet. In the next step, all of these NADH molecules that we produced will travel to the electron transport chain.
Difference-Between-Substrate-Level-Phosphorylation-and-Oxidative-Phosphorylation-2.jpg

What you should notice here is that the NADH molecules that we produced in glycolysis and the Krebs cycle are consumed in the electron transport chain and NAD is produced. This is the first time we actually produce NAD. Prior to this step we were consuming NAD and producing NADH.

Glycolysis can proceed much faster than both the krebs cycle and oxidative phosphorylation (electron transport chain). So what can happen is that there can be a build up of NADH from glycolysis, and a shortage of NAD inside of the cell (because the last step above, that consumes NADH and produces NAD cannot keep up because it is slower than glycolysis). If that happens, glycolysis has to stop and all ATP production will come to a halt. That is not good! The body has a work around.
Pyruvate_to_lactate.jpg

In the reaction above, converting pyruvate to lactate produces an NAD that can be used in step 6 of glycolysis to keep producing ATP. So when NAD runs low (and NADH builds up) during high intensity exercise, the body supplies more NAD by producing Lactate.

So that is the real reason for Lactate production. It is a REDOX potential issue.

So who cares about all of this? What would happen to cell NAD availability if you increased mitochondrial krebs cycle enzyme activity? Remember, if we run out of NAD we reduce our ability to do high intensity work. Would increasing mitochondrial krebs cycle enzymes help or hurt? Remember that the Krebs cycle consumes NAD too.

Or consider this, if in training you constantly produce a high lactate state, would the body respond by upgrading mitochondrial krebs cycle enzymes? Probably not because that would make the NAD shortage worse and when you run out of NAD you stop producing ATP. Would that type of training result in reduced mitochondria production or at the very least, inhibit mitochondrial development? Is this the link between staying alactic and promoting mitochondrial density? I don't know for sure.

There are both supporting and conflicting data out there and this has not been completely sorted out yet but it is an interesting idea.
 
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