Summary
Chris Masterjohn challenges the common misconception that lactate causes muscle acidification during exercise. He presents research showing that lactate production actually helps buffer acid in muscles, reframing our understanding of exercise physiology and fatigue.
Key Points
- Lactate production consumes hydrogen ions, alkalinizing muscle tissue
- The 'lactic acid causes soreness' narrative is scientifically inaccurate
- Lactate serves as an important fuel source during high-intensity exercise
- Understanding lactate metabolism can improve training strategies
- Muscle fatigue involves multiple mechanisms beyond pH changes
Key Moments
And it also marks the point where we have two of everything now because we've split the molecule in half
And it also marks the point where we have two of everything now because we've split the molecule in half. So everything here happened once. Everything forward is going to happen twice.
"And it also marks the point where we have two of everything now because we've split the molecule in half. So everything here happened once. Everything forward is going to happen twice. So two molecules of glyceraldehyde 3-phosphate are going to get oxidized by 2-NAD+, generating 2-NADH and 2 protons. And that's going to form 1,3-bisphosphoglycerate."
And so what you see in this table is he's showing you the different ATP complexes that can form
these competitive ion effects with how they would influence all of the different contributions to acidity in glycolytic energy metabolism during high-intensity exercise.
"it can get one proton added with one magnesium, or it can bind to potassium, or it can bind to sodium. And most of these are very small. If you look over here, where you see exponential notation, you're talking about super low quantities. Although if you're talking about exponential notation to the negative two, you're talking about, you know, it's not that small. You're moving a decimal point over two places. But in general, the large number"
it never makes lactic acid
it never makes lactic acid. Now, what is the fate of that lactate? So as extensively documented by George Brooks, especially in that article tracing the lactate shuttle to the mitochondrial...
"It's going to travel through the voltage-dependent anion channel or VDAC in the outer mitochondrial membrane into the intermembrane space of the mitochondrion. We're kind of in the intermembrane space. We're kind of in the cytosol, and that's because the VDAC is very promiscuous about what it transports, lactate, pyruvate, NADH, NAD+, hydrogen ions. Any of that stuff gets back and forth through the VDAC, whereas the inner mitochondrial membrane, which guards"
So the creatine kinase reaction is removing one proton from solution
that compiled all the different reactions of non-mitochondrial energy metabolism focusing on glucose metabolism and the phosphagen system.
"Ultimately, that could go down to uric acid. That also is removing one proton from solution. You're going to be doing a lot more of creatine kinase than AMP deaminase. ATP hydrolysis releases one proton. The phosphorylation of glucose and fructose 6-phosphate each release one proton. The glyceraldehyde dehydrogenase, 3-phosphate dehydrogenase reaction, GAPDH, it releases one proton. But remember-"
So if NAD is not abundant and the GAPDH reaction doesn't go forward, then DHAP accumulates
So if NAD is not abundant and the GAPDH reaction doesn't go forward, then DHAP accumulates. But if NADH is abundant and DHAP is abundant- then that will drive forward the reaction to form...
"to accommodate the flux going through the pathway. So clearly this is not a reflection of the use of the glycerol 3-phosphate shuttle primarily. It's a tiny bit that, and it's mostly a side reaction to generate NAD+ and to get rid of acidity. It also appears that there is inhibition of the phosphofructokinase reaction or PFK reaction, which converts fructose 6-phosphate to fructose 1,6-bisphosphate. Why do I say that? Because"
