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 HSP90α mRNA responses in acute normobaric hypoxia. Sixteen male participants completed ten 90-min sessions of isothermic HA (40°C/40% relative humidity) or exercise training [control (CON); 20°C/40% relative humidity]. HA or CON were preceded (HYP1) and proceeded (HYP2) by a 30-min normobaric hypoxic exposure [inspired O2 fraction = 0.12; 10-min rest, 10-min cycling at 40% peak O2 uptake (V̇O2 peak), 10-min cycling at 65% V̇O2 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 HSP90α mRNA increased in response to each HA session, but did not change with CON. HR during HYP2 was lower and O2 saturation higher at 65% V̇O2 peak following HA, but not CON. O2 uptake/HR was greater at rest and 65% V̇O2 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 HSP90α mRNA during HYP1 were maintained in HYP2. HA reduces physiological strain, and the transcription of HSP72, but not HSP90α mRNA in acute normobaric hypoxia.

International competition inevitably presents logistical challenges for athletes. Events such as the Tokyo 2020 Olympic Games require further consideration given historical climate data suggest athletes will experience significant heat stress. Given the expected climate, athletes face major challenges to health and performance. With this in mind, heat alleviation strategies should be a fundamental consideration. This review provides a focused perspective of the relevant literature describing how practitioners can structure male and female athlete preparations for performance in hot, humid conditions. Whilst scientific literature commonly describes experimental work, with a primary focus on maximizing magnitudes of adaptive responses, this may sacrifice ecological validity, particularly for athletes whom must balance logistical considerations aligned with integrating environmental preparation around training, tapering and travel plans. Additionally, opportunities for sophisticated interventions may not be possible in the constrained environment of the athlete village or event arenas. This review therefore takes knowledge gained from robust experimental work, interprets it and provides direction on how practitioners/coaches can optimize their athletes' heat alleviation strategies. This review identifies two distinct heat alleviation themes that should be considered to form an individualized strategy for the athlete to enhance thermoregulatory/performance physiology. First, chronic heat alleviation techniques are outlined, these describe interventions such as heat acclimation, which are implemented pre, during and posttraining to prepare for the increased heat stress. Second, acute heat alleviation techniques that are implemented immediately prior to, and sometimes during the event are discussed.

The optimized carbon monoxide (CO) rebreathing method (oCOR-method) is routinely used to measure total haemoglobin mass (tHbmass). The tHbmass measure is subject to a test-retest typical error of ~2%, mostly from the precision of carboxyhaemoglobin (HbCO) measurement. We hypothesized that tHbmass would be robust to differences in the bolus of CO administered during the oCOR-method. Twelve participants (ten males and two females; age 27 ± 6 yr, height 177 ± 11 cm and mass 73.9 ± 12.1 kg) completed the oCOR-method on four occasions. Different bolus of CO were administered (LOW: 0.6 ml kg(-1); MED1: 1.0 ml kg(-1) and HIGH: 1.4 ml kg(-1)); to determine the reliability of MED1, a second trial was conducted (MED2). tHbmass was found to be significantly less from the HIGH CO bolus (776 ± 148 g) when compared to the LOW CO (791 ± 149 g) or MED1 CO (788 ± 149 g) trials. MED2 CO was 785 ± 150 g. The measurement of tHbmass is repeatable to within 0.8%, but a small and notable difference was seen when using a HIGH CO bolus (1.4 to 1.9% less), potentially due to differences in CO uptake kinetics. Previously, an improved precision of the oCOR-method was thought to require a higher bolus of CO (i.e. larger Δ%HbCO), as commercial hemoximeters only estimate %HbCO levels to a single decimal place (usually ± 0.1%). With the new hemoximeter used in this study, a bolus of 1.0 ml kg(-1) allows adequate precision with acceptable safety.