Abstract

We aimed to investigate the relationship between mtDNA polymorphism and physiological responses to hypobaric hypoxia. The study included 28 healthy male students, consisting of 18 students in haplogroup D and 10 in haplogroup M7+G. Measurement sensors were attached to the participants for approximately 30 min in an environment with a temperature of 28 °C. After resting for 15 min, the programmed operation of the hypobaric chamber decreased the atmospheric pressure by 11.9 Torr every minute to simulate an increase in altitude of 150 m until 9.7 Torr (equivalent to 2500 m) and then decreased 9.7 Torr every minute until 465 Torr (equivalent to 4000 m). At each altitude, the pressure was maintained for 15 min and various measurements were taken. Haplogroup D showed higher SpO2 (p < 0.05) and significantly higher SpO2 during the pressure recovery period when compared with haplogroup M7+G. The distal skin temperature was higher in haplogroup D when compared with M7+G. These results suggested that haplogroup D maintained SpO2 at a higher level with higher peripheral blood flow during acute hypobaric exposure.

Highlights

  • 100,000 years ago, humans left Africa, spreading across the world and adapting to various environments [1]

  • Participants consisted of 18 students in haplogroup D and 10 in haplogroup M7+G, which are from the same M-type lineage

  • Post hoc test results revealed that 60–75 min after the beginning of the experiment, SpO2 was significantly elevated in haplogroup D when compared with M7+G (p < 0.05)

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Summary

Introduction

100,000 years ago, humans left Africa, spreading across the world and adapting to various environments [1]. This history of human migration is frequently assessed by mitochondrial-DNA (mtDNA) analysis. Previous studies have suggested that is mtDNA evolutionarily neutral but it is the cause for natural selection against specific environmental pressures, such as cold and high altitude [2, 3]. MtDNA haplotype might be related to high-altitude adaptation [6]. The common mtDNA haplotypes determine differences in oxidative phosphorylation (OXPHOS) performance and ROS production in both mice and humans [7,8,9]

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