Exercising in the heat induces thermoregulatory and other physiological strain that can lead to impairments in endurance exercise capacity. The purpose of this consensus statement is to provide up-to-date recommendations to optimize performance during sporting activities undertaken in hot ambient conditions. The most important intervention one can adopt to reduce physiological strain and optimize performance is to heat acclimatize. Heat acclimatization should comprise repeated exercise-heat exposures over 1-2 weeks. In addition, athletes should initiate competition and training in a euhydrated state and minimize dehydration during exercise. Following the development of commercial cooling systems (e.g., cooling vest), athletes can implement cooling strategies to facilitate heat loss or increase heat storage capacity before training or competing in the heat. Moreover, event organizers should plan for large shaded areas, along with cooling and rehydration facilities, and schedule events in accordance with minimizing the health risks of athletes, especially in mass participation events and during the first hot days of the year. Following the recent examples of the 2008 Olympics and the 2014 FIFA World Cup, sport governing bodies should consider allowing additional (or longer) recovery periods between and during events for hydration and body cooling opportunities when competitions are held in the heat.

Exercising in the heat induces thermoregulatory and other physiological strain that can lead to impairments in endurance exercise capacity. The purpose of this consensus statement is to provide up-to-date recommendations to optimise performance during sporting activities undertaken in hot ambient conditions. The most important intervention one can adopt to reduce physiological strain and optimise performance is to heat acclimatise. Heat acclimatisation should comprise repeated exercise-heat exposures over 1–2 weeks. In addition, athletes should initiate competition and training in a euhydrated state and minimise dehydration during exercise. Following the development of commercial cooling systems (eg, cooling-vest), athletes can implement cooling strategies to facilitate heat loss or increase heat storage capacity before training or competing in the heat. Moreover, event organisers should plan for large shaded areas, along with cooling and rehydration facilities, and schedule events in accordance with minimising the health risks of athletes, especially in mass participation events and during the first hot days of the year. Following the recent examples of the 2008 Olympics and the 2014 FIFA World Cup, sport governing bodies should consider allowing additional (or longer) recovery periods between and during events, for hydration and body cooling opportunities, when competitions are held in the heat.

Passive heat stress reduces arterial carbon dioxide partial pressure (P aCO 2 ) as reflected by 3 to 5 Torr reductions in end-tidal carbon dioxide tension (P ETCO 2 ). Heat stress also reduces cerebrovascular conductance (CBVC) by up to 30%. While P aCO 2 is a strong regulator of CBVC, it is unlikely that the relatively small change in P ETCO 2 during heating is solely responsible for the reductions in CBVC. This study tested the hypothesis that P aCO 2 , referenced by P ETCO 2 , is not the sole mechanism for reductions in CBVC during heat stress. Mean arterial blood pressure (MAP), P ETCO 2 , middle cerebral artery blood velocity (MCA V mean ), and calculated CBVC (MCA V mean /MAP) were assessed in seven healthy individuals, during three separate conditions performed sequentially: (1) normothemia, (2) control passive heat stress and (3) passive heat stress with P ETCO 2 clamped at the normothermic level (using a computer-controlled sequential gas delivery breathing circuit). MAP was similar in the three thermal conditions (P = 0.55). Control heat stress increased internal temperature ∼1.3• C, which resulted in decreases in P ETCO 2 , MCA V mean and calculated CBVC (P < 0.001 for all variables). During heat stress + clamp conditions internal temperature remained similar to that during the control heat stress condition (P = 0.31). Heat stress + clamp successfully restored P ETCO 2 to the normothermic level (P = 0.99) and increased MCA V mean (P = 0.002) and CBVC (P = 0.008) relative to control heat stress. Despite restoration of P ETCO 2 , MCA V mean (P = 0.005) and CBVC (P = 0.03) remained reduced relative to normothermia. These results indicate that heat stress-induced reductions in P aCO 2 , as referenced by P ETCO 2 , contribute to the decrease in MCA V mean and CBVC; however, other factors (e.g. perhaps elevated sympathetic nerve activity) are also involved in mediating this response.

Whole-body heat stress reduces orthostatic tolerance via a yet to be identified mechanism(s). The reduction in central blood volume that accompanies heat stress may contribute to this phenomenon. The purpose of this study was to test the hypothesis that acute volume expansion prior to the application of an orthostatic challenge attenuates heat stress-induced reductions in orthostatic tolerance. In seven normotensive subjects (age, 40 ± 10 years: mean ± s.d.), orthostatic tolerance was assessed using graded lower-body negative pressure (LBNP) until the onset of symptoms associated with ensuing syncope. Orthostatic tolerance (expressed in cumulative stress index units, CSI) was determined on each of 3 days, with each day having a unique experimental condition: normothermia, whole-body heating, and whole-body heating + acute volume expansion. For the whole-body heating + acute volume expansion experimental day, dextran 40 was rapidly infused prior to LBNP sufficient to return central venous pressure to pre-heat stress values. Whole-body heat stress alone reduced orthostatic tolerance by ∼80% compared to normothermia (938 ± 152 versus 182 ± 57 CSI; mean ± s.e.m., P < 0.001). Acute volume expansion during whole-body heating completely ameliorated the heat stress-induced reduction in orthostatic tolerance (1110 ± 69 CSI, P < 0.001). Although heat stress results in many cardiovascular and neural responses that directionally challenge blood pressure regulation, reduced central blood volume appears to be an underlying mechanism responsible for impaired orthostatic tolerance in the heat-stressed human.