PulmCCM - August 26, 2016 - By JE
.."The distinction between the A-type lactate and B-type lactate in this post will rest on the notion of true oxygen deficiency. Oxygen deficiency will be defined as cessation of oxidative phosphorylation and the Krebs Cycle. When oxygen is unable or unavailable to act as the terminal electron accepter within the mitochondrion, the electron transport chain ceases to function and protons within the mitochondrial inner membrane diffuse out. Pyruvate levels rise, lactate levels rise and acidosis ensues. This is true anaerobic biochemistry! This is the A-type lactate elevation [see figure 1A].
However, “oxygen deficiency” is often invoked at the bedside when the electron-transport chain is actually fully functional – just slow. What is imperative to understand here, is that the breakdown of glucose to pyruvate is much faster than the Krebs Cycle can handle. When pyruvate levels rise in this situation – as occurs in response to the stress response [e.g. sepsis, exercise] and/or adrenergic tone – pyruvate is converted to lactate in a proton-neutralprocess [i.e. degrading glucose to pyruvate produces 2 protons and 2 pyruvate molecules and converting 2 molecules of pyruvate to lactate consumes 2 protons]. Lactate levels rise, but the Krebs Cycle slowly lumbers along – without oxygen deficiency! This is a B-type lactate..."