Hyperthermia-induced hyperventilation has been proposed to be a human thermolytic thermoregulatory response and contribute to the disproportionate increase in exercise ventilation (V_E) relative to metabolic needs during high intensity exercise. In this study it was hypothesized V_E would adapt similar to human eccrine sweating (E_sw) following a passive HA. All participants performed an incremental exercise test on a cycle ergometer from rest to exhaustion before and after a 10 day passive exposure for 2 h•day^-1 to either 50°C and 20% RH (n=8, Acclimation Group) or 24°C and 32% RH (n=4, Control Group). Attainment of HA was confirmed by a significant decrease (p = 0.025) of the esophageal temperature (T_es) threshold for the onset of E_sw and a significantly elevated E_sw (p 0.040) during the post-HA exercise tests. HA also gave a significant decrease in resting T_es (p = 0.006) and a significant increase in plasma volume (p = 0.005). Ventilatory adaptations during exercise following HA included significantly decreased T_es thresholds (p 0.005) for the onset of increases in the ventilatory equivalents for O₂ (V_E/VO₂) and CO₂ (V_E/VCO₂) and a significantly increased V_E (p 0.017) at all levels of T_es. The elevated V_E was a function of a significantly greater tidal volume (p = 0.003) at lower T_es and of a breathing frequency (p 0.005) at higher T_es. Following HA the ventilatory threshold (i.e. VT1) was uninfluenced and relationships between VO₂ and either V_E/VO₂ or V_E/VCO₂ did not explain the resulting hyperventilation. In conclusion, the results support exercise ventilation following passive heat acclimation adapts similarly to eccrine sweating and the mechanism accounting for this adaptation is independent of changes to the ventilatory threshold or relationships between VO₂ with each of V_E/VO₂ and V_E/VCO₂.