Abstract

INTRODUCTION: Adaptations gained from heat acclimation (HA) can induce protective responses to a different stressor, such as hypoxia. Rapid ascent to altitude (hypobaric hypoxia, HH) increases the risk for acute mountain sickness (AMS). However, it is unknown whether HA can protect against the development of AMS during exposure to HH. PURPOSE: To determine if prior HA reduces the incidence of AMS during a 30 hour exposure to HH (3,500 m). METHODS: Thirteen unacclimatized healthy men (mean ± SD; age: 21 ± 3 yr; ht: 172 ± 8 cm; wt: 75.1 ± 12.2 kg; sea level VO2peak 42.9 ± 4.6 ml·kg-1·min-1) participated in three study phases consisting of: Phase 1) baseline (pre HA) 30 hour HH exposure (HH1; 3,500 m), Phase 2) 14-day washout period during which volunteers completed an 8-day exercise-HA protocol (treadmill walking: 120 minutes at 5 km·hr-1, 2% grade; 40°C and 40% RH), and Phase 3) post HA 30 hour HH exposure (HH2). During the HA protocol, heart rate (HR) and core temperature (Tc) were recorded throughout exercise. AMS was assessed using the Environmental Symptoms Questionnaire after ~12, ~21, and ~23 hours of exposure during each HH phase. HR and pulse oxygen saturation (SpO2) were measured at rest immediately after assessment of AMS. A t-test was used to assess difference in HR and Tc from Day 1 and Day 8 of HA. For the HH exposures, HR and SpO2 data were analyzed by fitting a mixed effects model as implemented by GraphPad Prism 8.1.2. RESULTS: Heat acclimation was achieved as indicated by a lower Tc (Day 1: 38.1 ± 0.3 vs Day 8: 37.8 ± 0.3 °C; p<0.01) and HR (Day 1: 134 ± 17 vs Day 8: 121 ± 13 bpm; p<0.01) at the end of exercise on Day 8 compared to Day 1. Three of 13 volunteers developed AMS during HH1 but not during HH2. A fourth volunteer only developed AMS during HH2. From HH1 to HH2, resting HR (84 ± 6 vs 83 ± 7 bpm) and SpO2 (87 ± 2 vs 88 ± 2%) were not different (both p >0.05). CONCLUSION: Our results suggest that in unacclimatized individuals, HA may be an effective, though not perfect training strategy for reducing the incidence of AMS during rapid exposure to 3,500 m. Changes in AMS incidence could not be explained by alterations in HR or SpO2. Supported by USAMRDC; author views not official US Army or DoD policy.

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