Let’s start with a quote that sets the scene: “…despite the clear biochemical evidence against a lactic acid cause of metabolic acidosis, there remains strong inertia in science for continuing to use the simple lactic acid explanation of acidosis” (Baker, McCormick and Roberts 2010).

As I am sure you may have heard at some point, maximal efforts during a period of 30-90 seconds tend to be associated with an accumulation of “lactic acid”. Now, I put lactic acid in inverted commas because it is widely misunderstood. Lactic acid is also known as “milk acid”, due to its presence in dairy products when lactose is fermented, however it is generally not what we are dealing with in the human body, but rather “lactate”. You see, “lactate” is not an acid, and can be a beneficial energy substrate, whereas it is actually the accumulation of hydrogens (H+) that accompany the rapid ATP production that cause the negative effects we normally attribute to "lactic acid". The concentration of hydrogen ions is what defines an acid in the first place.

More hydrogens = lower pH = increased acidity.

Because these hydrogens are positively charged, an abundant accumulation can affect the electrochemical gradient of the muscle, reducing its ability to produce force, which is a mechanism of fatigue largely associated with endurance exercise, but also higher repetition weight training with long periods of time under tension. Without the hydrogens, this wouldn’t be quite as much of an issue, so from now on, start giving out about the build-up of hydrogens (doesn’t sound as cool, though).

The reason we get this accumulation of lactate in the first place is due to the rapid ATP production. In this case, the pyruvate molecule is converted to lactate by the enzyme lactate dehydrogenase. Now the interesting thing is that lactate can actually be recycled. One such way that it can be used for energy is by conversion to pyruvate in the liver, at which point it can enter the mitochondria to be oxidised. This is clearly a beneficial adaptation given that our muscles are using up circulating blood glucose, and hence we would be best served to try fuel the liver with another substrate in the meantime. On the other hand, it can also be used to produce glucose (rather than the pyruvate being oxidised, it can be converted to oxaloacetic acid in the mitochondrion, then to malate, at which point it exits the mitochondrion again to form phosphoenolpyruvate, and off it goes along the gluconeogenic pathway to produce glucose – which looks a bit like the reverse of glycolysis). This is possible because glycolysis is actually a bi-directional pathway. However, muscle lacks the glucose-6-phosphatase enzyme that is present in the liver, so we can’t actually create glucose from lactate in muscle cells themselves. In the liver, however, this enzyme is present, and interestingly, its activity is ramped up in the presence of a high glucagon:insulin ratio, as we see during exercise or prolonged periods without food. Therefore, the lactate produced by working muscles can actually be recycled to maintain blood glucose levels. 

Now, this is where it gets interesting. Lactic acid, lactate, or even pyruvate have NOTHING to do with the accumulation of hydrogens that we previously spoke of. If you look at the reaction of pyruvate to lactate you will see it actually USES up hydrogens, and reduces hydrogen accumulation (one of the reasons it is so beneficial). Lactate production is a sink for hydrogens and actually reduces acidosis of the muscle.

The real hydrogen release occurs with ATP hydrolysis, and it is the fact that the rate of ATP hydrolysis is not matched by the rate of transport of phosphate, ADP and protons into the mitochondria, that leads to acidosis. ATP hydrolysis is, very simply, the process of using water molecules to break the high energy bonds in ATP that were discussed in the first article. Essentially, we are exercising at an intensity that demands a faster rate of ATP production than can be provided aerobically, so glycolysis speeds up, meaning we have faster rates of ATP hydrolysis. As a result, the leftover hydrogens increase cytosolic hydrogen concentration and even with the pyruvate to lactate conversion working furiously to use up those extra hydrogens, it simply can’t keep up, and acidosis occurs.

In summary, lactate is beneficial, and is not the cause of acidosis.

Excerpt from the Triage Militia article: Anaerobic Energy Provision - Glycolysis, Lactate & More.

Kind Regards,

Gary & Paddy

Triage Method