Dangerously high lactate levels suggested a condition that was potentially fatal and could result from insufficient oxygen delivery. For a study, researchers sought to examine whether hypoxemia and systemic inflammation raise lactate levels in healthy participants. 3.5 hours of hypoxemia (FiO2±11.5%), normoxemic endotoxemia (FiO2 21%, administration of 2 ng/kg endotoxin), or hypoxemic endotoxemia (n=10 per group) were applied to 30 healthy volunteers. Serial measurements of blood lactate, hemoglobin, SpO2, PaO2, PaCO2, pH, and hemodynamic parameters were performed. The hypoxemic treatment led to a decrease in SpO2 (81.7±2.6 and 81.4±2.4% in the hypoxemia and hypoxemic endotoxemia groups, respectively) and hyperventilation accompanied by a decrease in PaCO2 (0.8±0.5 and 1.5±0.6 kPa) and an increase in pH. The oxygen content of arterial blood (CaO2) fell between 20.5 and 2,9 and between 23.5 and 4.4%, respectively. Over time, lactate levels were marginally but significantly higher in both hypoxemic groups compared to the normoxemic endotoxemia group (P<0.0001 for both hypoxemic groups) but remained below 2.3 mmol/L in all participants. PaCO2, pH, and CaO2 were correlated with lactate levels, while PaO2 and SpO2 were not. No substantial lactate rises were observed as a consequence of hypoxia, regardless of whether inflammation was present or not. It was likely that the reductions in glycolysis that were brought on by hyperventilation were the cause of the slight increases in lactate that were detected.