Heat acclimation attenuates physiological strain and the HSP72, but not HSP90α, mRNA response to acute normobaric hypoxia

Heat acclimation (HA) attenuates physiological strain in hot conditions via phenotypic and cellular adaptation. The aim of this study was to determine whether HA reduced physiological strain, and heat shock protein (HSP) 72 and HSP90 alpha mRNA responses in acute normobaric hypoxia. Sixteen male participants completed ten 90-min sessions of isothermic HA (40 degrees C/40% relative humidity) or exercise training [control (CON); 20 degrees C/40% relative humidity]. HA or CON were preceded (HYP1) and proceeded (HYP2) by a 30-min normobaric hypoxic exposure [inspired O-2 fraction = 0.12; 10-min rest, 10-min cycling at 40% peak O-2 uptake ((V) over dot(O2 peak)), 10-min cycling at 65% (V) over dot(O2 peak)]. HA induced greater rectal temperatures, sweat rate, and heart rates (HR) than CON during the training sessions. HA, but not CON, reduced resting rectal temperatures and resting HR and increased sweat rate and plasma volume. Hemoglobin mass did not change following HA nor CON. HSP72 and HSP90 alpha mRNA increased in response to each HA session, but did not change with CON. HR during HYP2 was lower and O-2 saturation higher at 65% (V) over dot(O2 peak) following HA, but not CON. O-2 uptake/HR was greater at rest and 65% (V) over dot(O2 peak) in HYP2 following HA, but was unchanged after CON. At rest, the respiratory exchange ratio was reduced during HYP2 following HA, but not CON. The increase in HSP72 mRNA during HYP1 did not occur in HYP2 following HA. In CON, HSP72 mRNA expression was unchanged during HYP1 and HYP2. In HA and CON, increases in HSP90 alpha mRNA during HYP1 were maintained in HYP2. HA reduces physiological strain, and the transcription of HSP72, but not HSP90 alpha mRNA in acute normobaric hypoxia.