# Exercise-Induced Desaturation in Patent Foramen Ovale: Mechanisms, Diagnostic Approach, and Resolution After Closure—A Narrative Review with an Illustrative Case

**Authors:** Martina Podolec, Jiří Dostál, Petr Volf, Aneta Dvořáková, Martin Mates

PMC · DOI: 10.3390/jcm15041523 · 2026-02-14

## TL;DR

Exercise can cause low oxygen levels in people with a patent foramen ovale, a heart condition that can be diagnosed and treated effectively.

## Contribution

This review highlights the under-recognized role of patent foramen ovale in exercise-induced hypoxia and presents a case showing resolution after closure.

## Key findings

- Exercise-induced desaturation can occur due to right-to-left shunting in patent foramen ovale.
- Percutaneous closure resolved exercise-induced desaturation without improving exercise tolerance.
- Integrated imaging and physiological provocation are essential for diagnosis.

## Abstract

Exercise-induced desaturation is an uncommon but clinically significant manifestation of patent foramen ovale, which is present in approximately one-quarter of the general population. Although patent foramen ovale is usually asymptomatic, exertion may provoke transient right-to-left shunting when dynamic changes in venous return and intrathoracic pressure favour intermittent right-to-left transit across the interatrial septum. This narrative review synthesises current evidence on exertion-provoked shunting and its contribution to otherwise unexplained dyspnoea and hypoxaemia. To illustrate these concepts, we present an illustrative case with marked exercise-induced desaturation in the absence of pulmonary disease. The evaluation combined contrast transthoracic and transoesophageal echocardiography with cardiopulmonary exercise testing, and the shunt magnitude was quantified invasively using catheter-based thermodilution at rest and during Valsalva provocation. Six months after percutaneous closure, repeat cardiopulmonary exercise testing showed complete resolution of exercise-induced desaturation without a statistically significant change in exercise tolerance (work performed). Notably, normalisation of oxygen saturation during exercise may occur without a measurable increase in maximal exercise capacity. Overall, patent foramen ovale-mediated right-to-left shunting is an under-recognised yet potentially reversible cause of exertional hypoxaemia; diagnosis typically requires deliberate physiological provocation and integrated imaging, and closure can be considered in carefully selected individuals.

## Linked entities

- **Diseases:** patent foramen ovale (MONDO:0020439)

## Full-text entities

- **Genes:** NPPA (natriuretic peptide A) [NCBI Gene 4878] {aka ANF, ANP, ATFB6, ATRST2, CDD, CDD-ANF}
- **Diseases:** oedema (MESH:C536897), -induced arterial hypoxaemia (MESH:D012078), pulmonary vascular disease (MESH:D014652), hypoxemic lung disease (MESH:D008171), HAPO (MESH:C535833), ischaemic stroke (MESH:D002544), POS (MESH:D000092129), cough (MESH:D003371), induced desaturation (MESH:D000092582), Pulmonary Oedema (MESH:D011654), ASD (MESH:D001321), injury to (MESH:D014947), atrial septal aneurysm (MESH:D006344), orthostatic desaturation (MESH:D006261), chronic liver disease (MESH:D008107), inflammation (MESH:D007249), aortic (MESH:D001018), cardiogenic syndrome (MESH:D013575), hypertension (MESH:D006973), desaturation of arterial blood (MESH:D006402), deaths (MESH:D003643), Hypoxaemia Syndromes (MESH:D013577), apnoea (MESH:D001049), upper-airway obstruction (MESH:D000402), malformations (MESH:C564254), Ebstein Anomaly (MESH:D004437), R-L shunting (MESH:C562451), migraine (MESH:D008881), PFO (MESH:D054092), exertional desaturation (MESH:C564288), pulmonary embolism (MESH:D011655), EIAH (MESH:D000092202), hepatopulmonary syndrome (MESH:D020065), pulmonary hypertension (MESH:D006976), post-COVID (MESH:D000094024), decompression illness (MESH:D003665), diaphragmatic paralysis (MESH:D012133), oxygen desaturation (MESH:D000860), OSA (MESH:D020181), ventilatory impairment (MESH:D012131), embolic events (MESH:D004617), TIA (MESH:D002546), tricuspid regurgitation (MESH:D014262), pulmonary arteriovenous malformation (MESH:D001165), deformities of the anterior tricuspid leaflet (MESH:D018785), paralysis (MESH:D010243), CPET (MESH:D013736), COPD (MESH:D029424), parenchymal disease (MESH:D017563), kyphosis (MESH:D007738), stroke (MESH:D020521), paradoxical embolism (MESH:D019320), aortic root aneurysm (MESH:D000094628), migraine with aura (MESH:D020325), interatrial septal remodelling (MESH:D000074021), hypercapnia (MESH:D006935)
- **Chemicals:** starch (MESH:D013213), PAP (-), Oxygen (MESH:D010100), carbon dioxide (MESH:D002245)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12942256/full.md

---
Source: https://tomesphere.com/paper/PMC12942256