Oxygen utilization (VO2) is thought to fall in the late stages of septic shock because of mitochondrial dysfunction, circulatory hypoxia or both. However, the applicability of this conceptual framework to early septic shock is unclear. We investigated this matter in a rat model of lipopolysaccharide (LPS)‐induced shock (endotoxic shock). A novel experimental preparation was devised to simultaneously monitor oxygen delivery (DO2) and VO2 in rats whose thermoregulation had not been disrupted by anesthetics. Using a β3‐adrenergic agonist known to activate brown adipocytes, we found no evidence of metabolic impairment between 20 and 150 min post‐LPS. In spite of that, VO2 fell early in the LPS‐challenged rats, and such a fall in VO2 seemed to be driving a decrease in body temperature. The fall in VO2 was not preceded by any fall in cardiac output or DO2. Furthermore, no imbalance between VO2 and DO2 were encountered, and an analysis of NAD+/NADH ratios provided no indication of tissue hypoxia. Only when hypometabolism and hypothermia were prevented by exposure to a warm environment did an imbalance in the DO2/VO2 ratio become evident, and such an imbalance was associated with tissue hypoxia (reduction in NAD+/NADH ratio). It is concluded that reduced VO2 in early endotoxic shock (i) results from neither metabolic failure nor circulatory hypoxia, (ii) reflects a thermoregulatory adjustment, and (iii) serves as preemptive strategy to avoid hypoxia. Clinical data and conduct should be reexamined in light of these new findings.FundingFAPESP, AHA & CNPq.