# Modelling lung and muscle oxygen diffusion capacities from sea-level to Mount Everest

**Authors:** Nicolas Bourdillon, Giorgio Manferdelli, Antoine Raberin, Grégoire P. Millet

PMC · DOI: 10.1038/s41598-025-32441-9 · Scientific Reports · 2026-03-02

## TL;DR

This study models how the lungs and muscles handle oxygen at different altitudes, from sea level to Mount Everest.

## Contribution

The study introduces a computational model to estimate lung and muscle oxygen diffusion capacities at various altitudes.

## Key findings

- Lung oxygen diffusion capacity increases up to 5500 m before decreasing but remains higher than sea-level values.
- Muscle oxygen diffusion capacity increases up to 3500 m before decreasing below sea-level values.
- The model suggests a diffusion capacity reserve in lungs and muscles, with muscles depleting their reserve at lower altitudes.

## Abstract

Lung and muscle oxygen diffusion capacities (DLO2 and DMO2, respectively) are difficult to measure at maximal-intensity exercise and at altitude and they are scarcely reported in the literature, yet they are key components of the O2 transport cascade. The goal of the present study was to compute DLO2 and DMO2 at simulated increasing altitudes between sea-level and Mount Everest. Literature data were compiled to compute DLO2 and DMO2 at maximal exercise using a forward iterative algorithm. These computations were repeated every 250 m of increasing altitude between seal level and the altitude of Mount Everest. Computed DLO2 increased from sea-level to 5500 m and then decreased to the altitude of Mount Everest; yet remaining higher than sea-level values. DMO2 increased from sea-level to 3500 m and then progressively decreased to values lower than sea-level. The computed variations in DLO2 and DMO2 fit with the ability of the lung and muscle to increase their diffusion capacity at altitude, which seemingly indicates an existing diffusion capacity reserve. The muscle reserve seems depleted at a lower altitude than the lung reserve. The clinical relevance of the proposed model requires further investigation.

## Full-text entities

- **Genes:** ASCC1 (activating signal cointegrator 1 complex subunit 1) [NCBI Gene 51008] {aka ASC1p50, CGI-18, SMABF2, p50}
- **Diseases:** oedema (MESH:C536897), blood acidosis (MESH:D000138), dehydration (MESH:D003681), heart failure (MESH:D006333), pulmonary edema (MESH:D011654), hypoxic (MESH:D002534)
- **Chemicals:** salmeterol (MESH:D000068299), dexamethasone (MESH:D003907), DLCO (-), sildenafil (MESH:D000068677), H+ (MESH:D006859), tadalafil (MESH:D000068581), CO2 (MESH:D002245), acetazolamide (MESH:D000086), carbon monoxide (MESH:D002248), lactate (MESH:D019344), carbon (MESH:D002244), O2 (MESH:D010100), 2-3DPG (MESH:D019794), CaO2 (MESH:C403632), nitric oxide (MESH:D009569)
- **Species:** Homo sapiens (human, species) [taxon 9606], Canis lupus familiaris (dog, subspecies) [taxon 9615]

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12953604/full.md

## References

23 references — full list in the complete paper: https://tomesphere.com/paper/PMC12953604/full.md

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Source: https://tomesphere.com/paper/PMC12953604