Generally speaking, when the human body undergoes aerobic metabolism, glucose will be converted into pyruvate, which enters the tricarboxylic acid cycle to produce energy; at the same time, pyruvate produces lactic acid. During aerobic metabolism, the production of lactic acid decreases.

Under hyperbaric or hypoxic conditions, the mitochondrial tricarboxylic acid cycle and oxidative phosphorylation pathways are saturated or metabolically disturbed, and energy and lactic acid are produced through glycolysis pathways. In the recovery process of the body, lactic acid can be converted into pyruvic acid and enter the tricarboxylic acid cycle, thereby reducing the content of lactic acid.

Normal people produce 15-20 mmHg/kg lactic acid every day, mainly from skin, red blood cells, brain and skeletal muscle. Most lactic acid is metabolized in the liver, while a few forms glucose in the kidneys.

Hyperlactic acidemia, and even lactic acidosis, are caused by an increase or decrease in lactic acid production. Lactic acidosis can be divided into tissue hypoxia (A) and non-tissue hypoxia (B). It is usually caused by the following reasons: insufficient injection volume in systemic or local tissues (such as shock, arterial embolism), decreased blood oxygen level or decreased tissue oxygen delivery (such as severe hypoxia, severe anemia, CO poisoning), increased glycolysis (Such as strenuous exercise) and so on. There is usually no obvious tissue hypoxia type b lactic acidosis, which can occur due to increased glycolysis caused by β receptor agonists, acetone dehydrogenase complex poisoning (such as lack of thiamine or other toxins or drugs), reduction Increased coenzyme I/oxidized coenzyme I content (such as alcoholism) and lactic acid clearance obstacles (such as liver failure) and so on.