The typical core temperature (T_c) profile displayed during heatstroke (HS) recovery consists of initial hypothermia followed by delayed hyperthermia. Anecdotal observations led to the conclusion that these T_c responses represent thermoregulatory dysfunction as a result of brain damage. We hypothesized that these T_c responses are mediated by a change in the temperature setpoint. T_c (± 0.1°C; radiotelemetry) of male C57BL/6J mice was monitored while they were housed in a temperature gradient with ambient temperature (T_a) range of 20–39°C to monitor behaviorally selected T_a (T_s) or an indirect calorimeter (T_a = 25°C) to monitor metabolism (V̇o₂) and calculate respiratory exchange ratio (RER). Responses to mild and severe HS (thermal area 249.6 ± 18.9 vs. 299.4 ± 19.3°C·min, respectively) were examined through 48 h of recovery. An initial hypothermia following mild HS was associated with warm T_s (∼32°C), ∼35% V̇o₂ decrease, and RER ∼0.71 that indicated reliance on fatty acid oxidation. After 24 h, mild HS mice developed hyperthermia associated with warm T_s (∼32°C), ∼20% V̇o₂ increase, and RER ∼0.85. Severe HS mice appeared poikilothermic-like in the temperature gradient with T_c similar to T_s (∼20°C), and these mice failed to recover from hypothermia and develop delayed hyperthermia. Cellular damage (hematoxylin and eosin staining) was undetectable in the hypothalamus or other brain regions in severe HS mice. Overall, decreases and increases in T_c were associated with behavioral and autonomic thermoeffectors that suggest HS elicits anapyrexia and fever, respectively. Taken together, T_c responses of mild and severe HS mice suggest a need for reinterpretation of the mechanisms of thermoregulatory control during recovery.