We examined the effect of short-term heat acclimation with permissive dehydration (STHADe) on heat acclimation (HA) and cycling performance in a temperate environment.

What is the topic of this review? This is the first review to look across the broad field of 'cold water immersion' and to determine the threats and benefits associated with it as both a hazard and a treatment. What advances does it highlight? The level of evidence supporting each of the areas reviewed is assessed. Like other environmental constituents, such as pressure, heat and oxygen, cold water can be either good or bad, threat or treatment, depending on circumstance. Given the current increase in the popularly of open cold water swimming, it is timely to review the various human responses to cold water immersion (CWI) and consider the strength of the claims made for the effects of CWI. As a consequence, in this review we look at the history of CWI and examine CWI as a precursor to drowning, cardiac arrest and hypothermia. We also assess its role in prolonged survival underwater, extending exercise time in the heat and treating hyperthermic casualties. More recent uses, such as in the prevention of inflammation and treatment of inflammation-related conditions, are also considered. It is concluded that the evidence base for the different claims made for CWI are varied, and although in most instances there seems to be a credible rationale for the benefits or otherwise of CWI, in some instances the supporting data remain at the level of anecdotal speculation. Clear directions and requirements for future research are indicated by this review.

Purpose: It has been suggested that dehydration is an independent stimulus for heat acclimation (HA), possibly through influencing fluid-regulation mechanisms and increasing plasma volume (PV) expansion. There is also some evidence that HA may be ergogenic in temperate conditions and that this may be linked to PV expansion. We investigated: (i) the influence of dehydration on the time-course of acquisition and decay of HA; (ii) whether dehydration augmented any ergogenic benefits in temperate conditions, particularly those related to PV expansion.Methods: Eight males [VO2max: 56.9(7.2) mL·kg−1·min−1] undertook two HA programmes (balanced cross-over design), once drinking to maintain euhydration (HAEu) and once with restricted fluid-intake (HADe). Days 1, 6, 11, and 18 were 60 min exercise-heat stress tests [HST (40°C; 50% RH)], days 2–5 and 7–10 were 90 min, isothermal-strain (Tre ~ 38.5°C), exercise-heat sessions. Performance parameters [VO2max, lactate threshold, efficiency, peak power output (PPO)] were determined pre and post HA by graded exercise test (22°C; 55%RH).Results: During isothermal-strain sessions hypohydration was achieved in HADe and euhydration maintained in HAEu [average body mass loss −2.71(0.82)% vs. −0.56(0.73)%, P < 0.001], but aldosterone concentration, power output, and cardiovascular strain were unaffected by dehydration. HA was evident on day 6 {reduced end-exercise Tre [−0.30(0.27)°C] and exercise heart rate [−12(15) beats.min−1], increased PV [+7.2(6.4)%] and sweat-loss [+0.25(0.22) L.h−1], P < 0.05} with some further adaptations on day 11 {further reduced end-exercise Tre [−0.25(0.19)°C] and exercise heart rate [−3(9) beats.min−1], P < 0.05}. These adaptations were not notably affected by dehydration and were generally maintained 7-days post HA. Performance parameters were unchanged, apart from increased PPO (+16(20) W, irrespective of condition).Conclusions: When thermal-strain is matched, permissive dehydration which induces a mild, transient, hypohydration does not affect the acquisition and decay of HA, or endurance performance parameters. Irrespective of hydration, trained individuals require >5 days to optimize HA.

Adaptations to heat and hypoxia are typically studied in isolation but are often encountered in combination. Whether the adaptive response to multiple stressors affords the same response as when examined in isolation is unclear. We examined ) the influence of overnight moderate normobaric hypoxia on the time course and magnitude of adaptation to daily heat exposure and) whether heat acclimation (HA) was ergogenic and whether this was influenced by an additional hypoxic stimulus. Eight males [V̇o = 58.5 (8.3) ml·kg·min] undertook two 11-day HA programs (balanced-crossover design), once with overnight normobaric hypoxia (HA): 8 (1) h per night for 10 nights [[Formula: see text] = 0.156; SO = 91 (2)%] and once without (HA). ,, and were exercise-heat stress tests [HST (40°C, 50% relative humidity, RH)]; and were isothermal strain [target rectal temperature (T) ~38.5°C], exercise-heat sessions. A graded exercise test and 30-min cycle trial were undertaken pre-, post-, and 14 days after HA in temperate normoxia (22°C, 55% RH; FO = 0.209). HA was evident on (e.g., reduced T, mean skin temperature (T̄), heart rate, and sweat [Na], < 0.05) with additional adaptations on (further reduced T̄ and heart rate). HA increased plasma volume [+5.9 (7.3)%] and erythropoietin concentration [+1.8 (2.4) mIU/ml]; total hemoglobin mass was unchanged. Peak power output [+12 (20) W], lactate threshold [+15 (18) W] and work done [+12 (20) kJ] increased following HA. The additional hypoxic stressor did not affect these adaptations. In conclusion, a separate moderate overnight normobaric hypoxic stimulus does not affect the time course or magnitude of HA. Performance may be improved in temperate normoxia following HA, but this is unaffected by an additional hypoxic stressor.

Variance in the HA response remains largely unaccounted for and future studies should identify factors contributing to this variance.