The impact of submaximal exercise during heat and/or hypoxia on the cardiovascular and monocyte HSP72 responses to subsequent (post 24 h) exercise in hypoxia

Background: The aims of this study were to describe the cellular stress response to prolonged endurance exercise in acute heat, hypoxia and the combination of heat and hypoxia and to determine whether prior acute exposure to these stressors improved cellular tolerance to a subsequent exercise bout in hypoxia 24 h later.Methods: Twelve males (age 22 ± 4 years, height 1.77 ± 0.05 m, mass 79 ± 12.9 kg, VO₂ max 3.57 ± 0.7 L · min^-1) completed four trials (30-min rest, 90-min cycling at 50% normoxic VO₂ max) in normothermic normoxia (NORM; 18°C, F_IO₂ = 0.21), heat (HEAT; 40°C, 20% RH), hypoxia (HYP; F_IO₂ = 0.14) or a combination of heat and hypoxia (COM; 40°C, 20% RH, F_IO₂ = 0.14) separated by at least 7 days. Twenty-four hours after each trial, participants completed a hypoxic stress test (HST; 15-min rest, 60-min cycling at 50% normoxic VO₂ max, F_IO₂ = 0.14). Monocyte heat shock protein 72 (mHSP72) was assessed immediately before and after each exercise bout.Results: mHSP72 increased post exercise in NORM (107% ± 5.5%, p > 0.05), HYP (126% ± 16%, p < 0.01), HEAT (153% ± 14%, p < 0.01) and COM (161% ± 32%, p < 0.01). mHSP72 had returned to near-resting values 24 h after NORM (97% ± 8.6%) but was elevated after HEAT (130% ± 19%), HYP (118% ± 17%) and COM (131% ± 19%) (p < 0.05). mHSP72 increased from baseline after HST_NORM (118% ± 12%, p < 0.05), but did not increase further in HST_HEAT, HST_HYP and HST_COM.Conclusions: The prior induction of mHSP72 as a result of COM, HEAT and HYP attenuated further mHSP72 induction after HST and was indicative of conferred cellular tolerance.