Changes in prefrontal cerebral oxygenation and microvascular blood volume in hypoxia and possible association with acute mountain sickness

Giorgio Manferdelli, Mauro Marzorati, Chris Easton, Simone Porcelli*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

1 Citation (Scopus)

Abstract

New Findings

What is the central question of this study?
The role of cerebral hemodynamic response to either normobaric or hypobaric hypoxia in people susceptible to acute mountain sickness (AMS) is still under debate. Prefrontal cortex NIRS‐derived parameters were monitored in normobaric hypoxia at rest and during moderate intensity exercise in AMS‐prone and non‐AMS individuals.

What is the main finding and its importance?
AMS‐prone individuals did not increase microvascular blood volume and showed lower prefrontal cerebral oxygenation in normobaric hypoxia both at rest and during exercise compared to non‐AMS subjects, suggesting these changes may underpin later development of AMS at altitude.

Purpose
This study aimed to evaluate changes in prefrontal cerebral oxygenation and microvascular blood volume during exercise in normobaric hypoxia and investigate possible associations with acute mountain sickness (AMS) occurrence at altitude.

Method
Twenty‐two healthy individuals (age 26 ± 4ys, V̇O2peak 42 ± 4 ml.kg−1.min−1) were tested in two different conditions: normoxia (NORM) and normobaric hypoxia (FiO2 = 0.13; HYPO). Data were collected at rest and during submaximal constant‐speed exercises. SpO2 was measured by finger pulse oximeter. Prefrontal cerebral oxygenation (ΔHbO2), deoxygenation (ΔHHb), and microvascular blood volume (ΔHbtot) were obtained by Near‐Infrared Spectroscopy (NIRS). Within two weeks from laboratory testing, subjects rapidly ascended to 3647 m and AMS was evaluated using the Lake Louise scale (LLS).

Results
8 subjects were AMS+ whereas 14 were AMS‐. During NORM, NIRS variables did not change from baseline values both at rest and during exercise, resulting similar between AMS+ and AMS‐ subjects. During HYPO, ΔHHb increased to a similar extent in both groups both at rest and during exercise. ΔHbO2 was significantly lower in AMS+ compared to AMS‐ both at rest (‐3.23 ± 5.90 vs. 1.44 ± 2.14 μM, P = 0.04, ES = 1.1, respectively) and during exercise (‐6.56 ± 5.51 vs. 0.37 ± 4.36 μM, P < 0.01, ES = 1.2, respectively). ΔHbtot did not change from baseline both at rest (‐1.67 ± 9.53 μM) and during exercise (‐0.96 ± 9.12 μM) in AMS+, resulting significantly different from AMS‐ (5.49 ± 3.99μM, P = 0.03, ES = 1.0 and 8.17 ± 7.34μM, P = 0.02, ES = 1.0, respectively).

Conclusions
AMS‐prone individuals seem to be unable to both increase microvascular blood volume and maintain oxygenation at cerebral level during exercise in acute normobaric hypoxia, suggesting these changes may underpin later development of AMS.
Original languageEnglish
Pages (from-to)76-85
Number of pages10
JournalExperimental Physiology
Volume106
Issue number1
Early online date27 Jul 2020
DOIs
Publication statusPublished - 1 Jan 2021

Keywords

  • altitude
  • hypoxic exercise
  • Lake Louise Scale
  • NIRS

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