INTRODUCTION:
Heat acclimation sessions are increasingly integrated into training to improve heat tolerance or enhance oxygen delivery through increased total hemoglobin mass. Physiological responses to heat training are well-documented, while some evidence points towards concomitant anabolic and endocrine adaptations despite scarce data for underpinning mechanisms.
This study therefore investigated steroidal and endocrine responses to heat acclimation with two randomized cross-over training interventions.
METHODS:
Twenty well-trained cyclists and triathletes (11 men and 9 women) were monitored for 9 weeks including two blocks of 10 days of indoor training in temperate (TEMP, 21°, 40% humidity) or hot (HOT, 35°, 60% humidity) conditions in a climatic chamber, separated by 3 weeks wash-out.
Along with and sweat rate response, twelve blood samples were collected in total, before, during, and after each training block to monitor variations in serum steroidal (testosterone (T)) and endocrine (Insuline-Like Growth Factor I (IGF-1) and Procollagen type III N-terminal propeptide (P-III-NP)) markers. T, and IGF-1 were measured by liquid-chromatography tandem mass spectrometry (LC-MS/MS), whereas an immunoassay (ADVIA Centaur XP) allowed the analysis of P-III-NP. A repeated measures mixed-effects model with Tukey’s multiple comparisons was used for the analyses. Data are presented as means and standard deviations (±SD) with 95% confidence intervals (CI). HOT led to increases in sweat production (p<0.05) and lower sweat sodium concentrations (p<0.05) at 10 days, suggesting heat acclimation after HOT. Water balance and sweat sodium concentrations were unchanged after TEMP.
RESULTS:
In female participants, testosterone was stable both in TEMP (0.33 ± 0.03 ng/mL, CI 0.21 to 0.42) and HOT (0.31 ± 0.02 ng/mL, CI 0.22 to 0.40), with no difference between successive time points or condition.
In male participants as well, T did not vary with training in TEMP (6.21 ± 0.45 ng/mL, CI 4.87 to 7.55)
or HOT (6.15 ± 0.50 ng/mL, CI 4.83 to 7.56), with no difference between successive time points or groups.
For endocrine markers, IGF-1 was comparable and stable in TEMP (162.3 ± 4.8 µg/L, CI 140.7 to 183.9) and HOT (168.3 ± 8.2 µg/L, CI 145.1 to 191.6) in all participants. Concentrations for P-III-NP were different at baseline (p<0.01) but did not differ with the training intervention both in TEMP (7.3 ± 0.5 µg/L, CI 6.4 to 8.2) and HOT (5.7 ± 0.6 µg/L, CI 4.9 to 6.6).
CONCLUSION:
Overall, neither heat nor temperate training altered circulating steroid hormones, as T and A4 remained stable across time and conditions in both female and male participants. Similarly, key endocrine markers related to anabolic and connective tissue processes, including IGF-1, were unaffected by training environment, showing comparable and stable concentrations in HOT and TEMP.
In conclusion, 10 days of heat acclimation training did not confer additional steroidal or endocrine adaptations compared with training in temperate conditions.