Cross Acclimation between Heat and Hypoxia: Heat Acclimation Improves Cellular Tolerance and Exercise Performance in Acute Normobaric Hypoxia

Abstract

Background: The potential for cross acclimation between environmental stressors is not well understood. Thus, the aim of this investigation was to determine the effect of fixed-workload heat or hypoxic acclimation on cellular, physiological, and performance responses during post acclimation hypoxic exercise in humans.

Method: Twenty-one males (age 22 ± 5 years; stature 1.76 ± 0.07 m; mass 71.8 ± 7.9 kg; [Formula: see text]O2 peak 51 ± 7 mL(.)kg(-1.)min(-1)) completed a cycling hypoxic stress test (HST) and self-paced 16.1 km time trial (TT) before (HST1, TT1), and after (HST2, TT2) a series of 10 daily 60 min training sessions (50% N [Formula: see text]O2 peak) in control (CON, n = 7; 18°C, 35% RH), hypoxic (HYP, n = 7; fraction of inspired oxygen = 0.14, 18°C, 35% RH), or hot (HOT, n = 7; 40°C, 25% RH) conditions.

Results: TT performance in hypoxia was improved following both acclimation treatments, HYP (-3:16 ± 3:10 min:s; p = 0.0006) and HOT (-2:02 ± 1:02 min:s; p = 0.005), but unchanged after CON (+0:31 ± 1:42 min:s). Resting monocyte heat shock protein 72 (mHSP72) increased prior to HST2 in HOT (62 ± 46%) and HYP (58 ± 52%), but was unchanged after CON (9 ± 46%), leading to an attenuated mHSP72 response to hypoxic exercise in HOT and HYP HST2 compared to HST1 (p < 0.01). Changes in extracellular hypoxia-inducible factor 1-α followed a similar pattern to those of mHSP72. Physiological strain index (PSI) was attenuated in HOT (HST1 = 4.12 ± 0.58, HST2 = 3.60 ± 0.42; p = 0.007) as a result of a reduced HR (HST1 = 140 ± 14 b.min(-1); HST2 131 ± 9 b.min(-1) p = 0.0006) and Trectal (HST1 = 37.55 ± 0.18°C; HST2 37.45 ± 0.14°C; p = 0.018) during exercise. Whereas PSI did not change in HYP (HST1 = 4.82 ± 0.64, HST2 4.83 ± 0.63).

Conclusion: Heat acclimation improved cellular and systemic physiological tolerance to steady state exercise in moderate hypoxia. Additionally we show, for the first time, that heat acclimation improved cycling time trial performance to a magnitude similar to that achieved by hypoxic acclimation.

Keywords: cross-acclimation; cycling; heat; heat shock proteins; hypoxia.

Figure 1

Schematic of the experimental design, anthropometric and physiological characteristics of participants, indicating the typical days on which specific tests were undertaken.

Figure 2

Monocyte HSP72 responses before and after the acclimation period. (A) mHSP72 is increased post exercise on day 1 of HYP and HOT, but not CON. (B) Resting mHSP72 was unchanged in CON and increased in HYP and HOT on day 10 of acclimation compared to day 1 of acclimation. Subsequently, the post exercise mHSP72 response in HYP and HOT was attenuated compared to post exercise on day 1. (C) The magnitude of change in resting mHSP72 on day 10 of acclimation was no different between HYP and HOT (C). Open bars and shaded bars represent pre and post exercise, respectively. Lines (A, B) and dots (C) represent individual participant responses (n = 21) and bars show the mean group response. The dashed line (C) represents baseline mHSP72. ^*Different from day 1 pre-exercise (p < 0.01). ^#Different from control (p < 0.01). ^†Different from control (p < 0.05).

Figure 3

Extracellular HIF-1α responses before and after the acclimation period. (A) eHIF-1α is increased following an acute period of hypoxic exercise and is more variable following HOT. No post exercise changes in eHIF-1α were seen in CON (B) Resting eHIF-1α was elevated after 10 days of HYP and HOT acclimation, blunting the post exercise response on day 10 of acclimation. No changes in eHIF-1α were observed in CON. (C) The magnitude of change in resting eHIF-1α on day 10 of acclimation was no different between HYP and HOT. Open bars and shaded bars represent pre and post exercise, respectively. Lines (A,B) and dots (C) represent individual participant responses (n = 21) and bars the mean group response. The dashed line (C) represents baseline HIF-1α. ⁺Different from day 1 rest (p < 0.05). ^#Different from control (p < 0.01). ^Different from day 1 pre exercise (p < 0.10). ^*Different from control (p < 0.05).

Figure 4

Monocyte HSP72 before and after HST1 and HST2. (A) mHSP72 is increased after a HST in 20 of 21 participants. (B) Resting mHSP72 was increased prior to onset of HST2 in HYP and HOT. The post exercise increase in mHSP72 was subsequently only observed in CON. (C) The magnitude of change in resting mHSP72 prior to HST2 was not different between HYP and HOT and were each elevated in comparison to CON. Lines (A,B) and dots (C) represent individual participant responses and bars the mean group response (n = 21). The dashed line (C) represents baseline mHSP72. ^†Different from pre-exercise (p < 0.01). ^¥Different from HST1 pre-exercise (p < 0.05). ^*Different from HST1 pre-exercise (p < 0.01).

Figure 5

Extracellular HIF-1α responses before and after HST1 and HST2. (A) eHIF-1α increased in response to exercise in HST1 in all experimental groups. (B) Prior to HST2 resting levels of eHIF-1α were elevated in HYP when compared to pre HST1, and showed a varied individual response in HOT.eHIF-1α increased in response to exercise in HST2 in CON, but was unchanged in both HYP and HOT, although individual variation in the data is present. (C) The magnitude of change in resting eHIF-1α was not different between HYP and HOT prior to HST2, and each were elevated in comparison to CON. Lines (A,B) and dots (C) represent individual participant responses and bars the mean group response. The dashed line (C) represents baseline HIF-1α. Different from rest (p < 0.01) within trial. ^*Different from HST1 pre-exercise (p < 0.01). ^¥Different from HST1 pre-exercise (p < 0.05). – TDifferent from HST2 pre-exercise (p < 0.10). ^†Different from control (p < 0.05).

Figure 6

Mean power output during each kilometer of the 16.1 km time trial for CON (A), HYP (B) and HOT (C). ^*Difference from TT1 (p < 0.05).