Previous animal models of heat stress have been compromised by methodologies, such as restraint and anesthesia that confound our understanding of the core temperature (T_c) responses elicited by heat stress. Using biotelemetry, we developed a heat stress model to examine T_c responses in conscious, unrestrained C57BL/6J male mice. Prior to heat stress, mice were acclimated for >4 weeks to (T_a) of 25°C. Mice were exposed to ambient temperature T_a of 39.5±0.2°C, in the absence of food and water, until they reached maximum T_c (T_{c, Max}) of 42.4 (N=11), 42.7 (N=12), or 43.0°C (N=11), defined as mild, moderate and extreme heat stress, respectively. Heat stress induced ~13% BW loss that did not differ by final group T_c, whereas survival rate was affected by final T_c (100% at 42.4°C; 92% at 42.7°C; 46% at 43°C). Hypothermia (T_c<34.5°C) developed following heat stress with the depth and duration of hypothermia significantly enhanced in the moderate and extreme compared to the mild group. Regardless of heat stress severity, every mouse that transitioned out of hypothermia (survivors only) developed a virtually identical elevation in T_c the following day, but not night, compared to non-heated controls. To test the effect of recovery T_a, a group of mice (N=5) were acclimated for >4 weeks and recovered at T_a of 30°C following moderate heat stress. Recovery at 30°C resulted in 0% survival within ~2h following cessation of heat stress. Using biotelemetry to monitor T_c in the unrestrained mouse, we have shown that recovery from acute heat stress is associated with prolonged hypothermia followed by an elevation in daytime T_c that is dependent on T_a. These thermoregulatory responses to heat stress are key biomarkers that may provide insight into heat stroke pathophysiology.