Heat Acclimation Does Not Modify Q(10) and Thermal Cardiac Reactivity

Heat acclimation (HA) is an essential modifier of physiological strain when working or exercising in the heat. It is unknown whether HA influences the increase of energy expenditure (Q(10) effect) or heart rate (thermal cardiac reactivity TCR) due to increased body temperature. Therefore, we studied these effects using a heat strain database of climatic chamber experiments performed by five semi-nude young males in either non-acclimated or acclimated state. Measured oxygen consumption rate (VO(2)), heart rate (HR), and rectal temperature (T(re)) averaged over the third hour of exposure were obtained from 273 trials in total. While workload (walking 4 km/h on level) was constant, heat stress conditions varied widely with air temperature 25–55°C, vapor pressure 0.5–5.3 kPa, and air velocity 0.3–2 m/s. HA was induced by repeated heat exposures over a minimum of 3 weeks. Non-acclimated experiments took place in wintertime with a maximum of two exposures per week. The influence of T(re) and HA on VO(2) and HR was analyzed separately with mixed model ANCOVA. Rising T(re) significantly (p < 0.01) increased both VO(2) (by about 7% per degree increase of T(re)) and HR (by 39–41 bpm per degree T(re)); neither slope nor intercept depended significantly on HA (p > 0.4). The effects of T(re) in this study agree with former outcomes for VO(2) (7%/°C increase corresponding to Q(10) = 2) and for HR (TCR of 33 bpm/°C in ISO 9886). Our results indicate that both relations are independent of HA with implications for heat stress assessment at workplaces and for modeling heat balance.