Four-month operational heat acclimatization positively affects the level of heat tolerance 6 months later

The study addresses whether adaptations from prior heat acclimatization persist beyond the commonly cited 5–7 week decay period and whether such prior exposure confers improved heat tolerance months later. Although short-term acclimation (about 10 days) yields reductions in core and skin temperatures, heart rate, sweat osmolality, thermal discomfort, and perceived exertion, these adaptations are considered transient and presumed to decay by approximately 2.5% per day without heat exposure. The duration required for complete decay and characteristics of re-induction remain uncertain, with large inter-study variability and few data beyond 25 days. Operationally, athletes and professionals (e.g., soldiers) may face repeated missions in hot climates separated by months, making it important to know if prior acclimatization enhances initial readiness. The authors reanalyzed data from French soldiers to test the hypothesis that those who completed a 4-month hot-climate mission 6 months earlier would show greater heat tolerance than soldiers with no prior heat acclimatization.

Prior work shows complete phenotypic heat acclimation/acclimatization can occur within ~10 days, improving physiological and perceptual markers (Sawka et al.; Tyler et al.; Périard et al.). Meta-analytic evidence (Daanen et al.) suggests decay of improvements in heart rate, core temperature, and sweat rate at ~2.5% per day outside the heat, implying a return to baseline within 5–7 weeks, with fewer days needed for re-acclimation than for initial acclimation. However, variability in protocols, uncontrolled activity/environment during decay, and few studies beyond 25 days create uncertainty. Some studies indicate partial retention at 12–26 days (Weller et al.), while others show variable decay of heart rate and core temperature and retention of perceptual adaptations at 16–26 days. Re-acclimation has typically been examined after incomplete decay. Most research concerns laboratory acclimation rather than natural acclimatization. One study (Corbett et al.) found no carryover from a 10-day acclimation to a subsequent acclimation 3–18 months later, highlighting inter-individual variability and differences in exposure duration and intensity. Animal studies from Horowitz’s group support heat acclimation memory via persistent upregulation of cytoprotective genes (e.g., Hsp70/Hsp90, Bcl-xL) and epigenetic mechanisms that facilitate rapid re-induction.

Design and participants: Retrospective analysis of two cohorts of French Army soldiers tested in the United Arab Emirates in May–June 2016 and 2017. Inclusion targeted 50 male soldiers split into two groups: HA (n=25) with a 4-month mission in hot climates completed 5–7 months prior (mean 6.0 ± 0.6 months), and CT (n=25) with no prior professional heat acclimatization. Soldiers had not been on hot-climate missions in the preceding 6 months; personal travel to hot climates within 8 months led to exclusion. An initial pool of 120 soldiers yielded 90 eligible (32 HA, 58 CT), but groups differed in age and fitness due to career stage. To balance, the oldest in HA (>32 y) and the youngest/least fit in CT (<21 y or Cooper <2500 m) were removed, resulting in matched groups (see Table 1 in paper for characteristics: age ~25 y, VO2max ~53–54 ml·kg−1·min−1). Both groups originated from the same four regiments with balanced representation.

Prior exposures: HA group missions occurred in hot regions (e.g., Central African Republic, Ivory Coast, Mali, Djibouti, New Caledonia, Lebanon), with daily ambient temperatures typically 23–31 °C (WBGT 21–26 °C) and substantial outdoor exposure, often in military attire, over 4 months. CT group remained in temperate France (mean ~12.5 °C) over the same timeframe.

Heat stress test (HST): Conducted outdoors the second day after arrival in UAE; the first day involved mainly passive heat exposure (meetings without air conditioning) and brief physical tasks (luggage handling). The HST comprised three 8-minute runs at 50% of estimated speed at VO2max (derived from the Cooper 12-min run). Environmental conditions during HST (mean ± SD): dry-bulb 42.6 ± 3.2 °C, RH 25.4 ± 11.6%, wet-bulb 27.3 ± 2.2 °C, globe 56.0 ± 3.2 °C, WBGT 34.6 ± 1.6 °C, wind 1.7 ± 0.4 km·h−1. Sessions were split into four groups per day with similar HA/CT ratios.

Measurements: Before and after HST: rectal temperature (Trec) via electric thermometer at 6 cm depth; nude dry body mass; heart rate via Polar monitor (resting HR measured for 5 min pre-HST; end-exercise HR averaged over last 30 s). Sweat loss estimated by pre-post body mass difference; localized sweat collected on chest for osmolality by freezing-point osmometer. Thermal discomfort rated on a 0–10 cm visual analog scale; rate of perceived exertion (RPE) on a 0–10 scale at end of exercise.

Statistical analysis: Normality assessed by Shapiro–Wilk. Between-group comparisons via Student’s t-test or Mann–Whitney U as appropriate. Effect sizes (Cohen’s d) interpreted as small (>0.2), moderate (>0.5), large (>0.8). Magnitude-based inferences complemented p-values using smallest worthwhile change (0.2 × pooled SD) with likelihood categories (possibly, likely, very likely, most likely). Significance set at p < 0.05. Analyses performed in SPSS v20.

• At rest: No differences between HA and CT in rectal temperature (37.4 ± 0.2 vs 37.4 ± 0.4 °C; p = 0.421; ES = −0.230) or heart rate (91 ± 10 vs 89 ± 13 bpm; p = 0.290; ES = −0.176).
• End of HST: Lower rectal temperature in HA (38.4 ± 0.4 °C) vs CT (38.7 ± 0.6 °C); p = 0.023; ES = 0.572; mean difference 0.27 °C (95% CI −0.01 to 0.54). Lower heart rate in HA (156 ± 15 bpm) vs CT (165 ± 15 bpm); p = 0.033; ES = 0.621; mean difference 9.3 bpm (95% CI 0.8 to 17.8).
• During HST responses: Smaller increase in rectal temperature in HA (1.0 ± 0.4 °C) vs CT (1.3 ± 0.5 °C); p = 0.015; ES = 0.710; mean difference 0.34 °C (95% CI 0.07 to 0.61). Smaller increase in heart rate in HA (65 ± 14 bpm) vs CT (76 ± 14 bpm); p = 0.016; ES = 0.805; mean difference 11.4 bpm (95% CI 3.3 to 19.4).
• Sweat responses: Sweat loss not significantly different (1.19 ± 0.16 L vs 1.05 ± 0.23 L; p = 0.231), though effect size suggested a moderate tendency toward greater sweat loss in HA (ES = −0.682). Sweat osmolality similar (140 ± 37 vs 144 ± 31 mOsm·kg−1; p = 0.756; ES = 0.121).
• Perceptual responses: Thermal discomfort not different at rest (3.8 ± 2.4 vs 4.1 ± 2.2; p = 0.591; ES = 0.159) and showed a non-significant trend at end of HST (5.1 ± 1.8 vs 6.1 ± 2.2; p = 0.077; ES = 0.497). RPE lower in HA (5.3 ± 1.6) vs CT (6.3 ± 1.9); p = 0.043; ES = 0.545; mean difference 0.95 (95% CI 0.04 to 1.94).
• Magnitude-based inferences: Previous acclimatization was likely to very likely beneficial for reducing end-exercise Trec and HR, reducing the increases in Trec and HR during HST, lowering RPE, and likely increasing sweat rate; effects on sweat osmolality were unclear.

Findings indicate that soldiers with a 4-month history of natural heat acclimatization retained or rapidly regained superior heat tolerance relative to never-acclimatized peers, even after approximately 6 months without hot-environment exposure. This directly addresses the research question, challenging the assumption of complete decay by 5–7 weeks. Two non-exclusive explanations are proposed: (1) The unusually long and intense acclimatization (extensive daily and sometimes nocturnal heat exposure in military attire over 4 months) may induce more durable physiological adaptations than classical short-term (4–14 days) laboratory acclimation. Literature and animal data suggest longer exposures can yield more sustained or additional adaptations (e.g., hematological changes) and may slow decay. (2) The first day of passive/low-level active heat exposure upon arrival may have triggered rapid re-acclimation, consistent with evidence that re-acclimation after partial decay occurs faster than initial acclimation, potentially facilitated by cellular and epigenetic “acclimation memory” mechanisms (e.g., persistent chromatin changes enabling swift re-induction of cytoprotective genes). The study cannot distinguish between partial retention versus rapid re-induction, and both may contribute differentially across physiological and perceptual variables. Nevertheless, the net effect is improved operational readiness in the heat for previously acclimatized individuals.

A prior 4-month operational heat acclimatization period was associated with greater heat tolerance 6 months later, evidenced by lower end-exercise core temperature and heart rate, smaller increases in these variables during exercise in the heat, and lower perceived exertion compared with never-acclimatized soldiers. While mechanisms (long-term retention vs rapid re-acclimation) remain unresolved, the findings suggest that individuals with a history of prolonged heat acclimatization may be better prepared during initial days of re-exposure to heat. Future research should directly characterize decay kinetics beyond several weeks, disentangle retention from re-induction processes (including cellular/epigenetic markers), and test whether prior long-duration acclimatization confers advantages across diverse populations and operational tasks.

• Acclimatization conditions during the 4-month missions were not controlled and likely varied between participants (locations, daily activities, clothing), though overall exposure was substantial and sufficient to induce acclimatization.
• The retrospective design precluded direct within-subject assessment of decay across the 6-month interval; thus, exact decay kinetics cannot be determined.
• Although groups were balanced for age and fitness after exclusions, initial differences due to military career stage necessitated selection adjustments; residual confounding cannot be entirely excluded.
• Both groups performed similar professional activities in temperate France during the preceding 6 months, but regular physical activity may have contributed to partial retention of adaptations in HA.
• Cellular or epigenetic markers of acclimation memory were not measured, limiting mechanistic inference.
• The first day’s passive/low-level active heat exposure before HST could have initiated rapid re-acclimation, complicating separation of retained versus re-induced adaptations.