A 24-year-old woman with symptoms of major depressive disorder and anxiety had been treated for the condition since the age of 17. Symptoms were resistant to fluoxetine and then citalopram. Following the birth of her daughter, she wanted to be medication-free and symptom-free. A programme of weekly open (cold) water swimming was trialled. This led to an immediate improvement in mood following each swim and a sustained and gradual reduction in symptoms of depression, and consequently a reduction in, and then cessation of, medication. On follow-up a year later, she remains medication-free.

This study examined the acute and chronic effects of euhydrated and hypohydrated heat exposure, on biomarkers of stress and inflammation. Eight trained males [mean (SD) age: 21 (3) y; mass: 77.30 (4.88) kg; V̇O2max: 56.9 (7.2) mL kg-1 min-1] undertook two heat acclimation programmes (balanced cross-over design), once drinking to maintain euhydration and once with restricted fluid-intake (permissive dehydration). Days 1, 6, and 11 were 60 min euhydrated exercise-heat stress tests (40 °C; 50% RH, 35% peak power output), days 2-5 and 7-10 were 90 min, isothermal-strain (target rectal temperature: 38.5 °C) exercise-heat sessions. Plasma was obtained pre- and post- exercise on day 1, 2, and 11 and analysed for cortisol, interleukin-6 (IL-6), and C-reactive protein (CRP). Cortisol and CRP were also assessed on day 6. IL-6 was elevated following the initial (acute) 90 min isothermal heat strain exercise-heat exposure (day 2) with permissive dehydration ((pre exercise: 1.0 pg mL-1 [0.9], post-exercise: 1.8 pg mL-1 [1.0], P = .032) and when euhydrated (pre-exercise: 1.0 pg mL-1 [1.4], post-exercise: 1.6 pg mL-1 [2.1], P = .048). Plasma cortisol levels were also elevated but only during permissive dehydration (P = .032). Body mass loss was strongly correlated with Δcortisol (r = -0.688, P = .003). Although there was a trend for post-exercise cortisol to be decreased following both heat acclimation programmes (chronic effects), there were no within or between intervention differences in IL-6 or CRP. In conclusion, acute exercise in the heat increased IL-6 and cortisol only when fluid-intake is restricted. There were no chronic effects of either intervention on biomarkers of inflammation as evidenced by IL-6 and CRP returning to basal level at the end of heat acclimation.

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 1) the influence of overnight moderate normobaric hypoxia on the time course and magnitude of adaptation to daily heat exposure and 2) whether heat acclimation (HA) was ergogenic and whether this was influenced by an additional hypoxic stimulus. Eight males [V̇o_2max = 58.5 (8.3) ml·kg⁻¹·min⁻¹] undertook two 11-day HA programs (balanced-crossover design), once with overnight normobaric hypoxia (HA_Hyp): 8 (1) h per night for 10 nights [[ ] = 0.156; S_pO₂ = 91 (2)%] and once without (HA_Con). Days 1, 6, and 11 were exercise-heat stress tests [HST (40°C, 50% relative humidity, RH)]; days 2–5 and 7–10 were isothermal strain [target rectal temperature (T_re) ~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; F_IO₂ = 0.209). HA was evident on day 6 (e.g., reduced T_re, mean skin temperature (T̄_sk), heart rate, and sweat [Na⁺], P < 0.05) with additional adaptations on day 11 (further reduced T̄_sk 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.

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 [VO_2max: 56.9(7.2) mL·kg⁻¹·min⁻¹] undertook two HA programmes (balanced cross-over design), once drinking to maintain euhydration (HA_Eu) and once with restricted fluid-intake (HA_De). 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 (T_re ~ 38.5°C), exercise-heat sessions. Performance parameters [VO_2max, 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 HA_De and euhydration maintained in HA_Eu [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 T_re [−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 T_re [−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.