The breathing of newborns is destablized by warm temperatures. We hypothesized that in unanesthetized, intact newborn rats, body temperature (T_B) influences the peripheral chemoreflex response (PCR response) and total response (i.e. peripheral + central chemoreflex) to hypercapnia. To test this, we delivered square-wave challenges of 8% CO₂ in air to P4-P5 rats held at T_B of 30°C (Cold, n=11), 33°C (Cool, n=10) and 35°C (TNZ, n=11), while measuring ventilation (V_E) directly with a pneumotach and mask. Cool animals were challenged with 8% CO₂ balanced in either air or hyperoxia (n=10) to identify the PCR response. Breath-to-breath analysis was performed on 30 room air breaths and every breath of the 1 min CO₂ challenge. As expected, warmer T_B was associated with an unstable breathing pattern in room air: TNZ animals had a co-efficient of variation in V_E (V_E CV%) that was double that of animals held at cooler T_B (P<0.001). Hyperoxia markedly suppressed the hypercapnic ventilatory response over the first 10 breaths (or ~4 sec), suggesting that this domain is dominated by the PCR response. The PCR response (P=0.03) and total response (P=0.04) were significantly greater in TNZ animals compared to hypothermic animals. The total response had a significant, negative relationship with VCO₂ (R²=0.53; P<0.001). Breathing stability was positively related to the total response (R²=0.36; P<0.001) and to a lesser extent the PCR response (R²=0.19; P=0.01), and was negatively related to VCO₂ (R²=0.34; P<0.001). ANCOVA confirmed a significant effect of TB alone on breathing stability (P<0.01), with no independent effects of VCO₂ (P=0.41), the PCR response (P=0.82), or the total V_E response (P=0.08). Our data suggest that in early postnatal life, the chemoreflex responses to CO₂ are highly influenced by T_B, and while related to breathing stability, are not predictors of stability after accounting for the independent effect of T_B.