🟢 Strong Evidence
Nasal breathing raises arterial oxygenation by approximately 10% compared to mouth breathing in healthy adults, according to research published in Acta Physiologica Scandinavica by researchers at the Karolinska Institute. The mechanism centres on nitric oxide (NO) produced continuously in the paranasal sinuses and inhaled with each nasal breath, which selectively dilates pulmonary blood vessels in well-ventilated alveolar regions, improving oxygen transfer to the bloodstream.
Key takeaways
- Nasal breathing increases arterial oxygen tension by ~10% through endogenous nitric oxide production in the paranasal sinuses
- Nitric oxide selectively dilates pulmonary vessels in well-ventilated lung regions, optimising ventilation-perfusion matching
- Mouth breathing bypasses this physiological mechanism entirely, losing the oxygen benefit of sinus-derived nitric oxide
- This represents a continuous, low-dose version of the clinical inhaled nitric oxide therapy used in pulmonary hypertension and severe ARDS
Study at a Glance
| Source | Acta Physiologica Scandinavica |
| Study type | Controlled experimental study |
| Sample size | N = 14 healthy adults (two cohorts) |
| Population | Healthy adult subjects |
| Country | Sweden (Karolinska Institute) |
Oxygen tension improvement with nasal versus mouth breathing
Transcutaneous partial pressure of oxygen (tcPO₂) across study subjects, percentage difference
Source: Lundberg et al., Acta Physiologica Scandinavica, 1996 | Georgian Medical Journal News
The nitric oxide pathway in nasal breathing
The paranasal sinuses contain specialised epithelial cells that constitutively express nitric oxide synthase (NOS), an enzyme that produces NO at high concentrations directly into the nasal airway. Unlike the inducible NOS isoform found elsewhere in the body—which is suppressed by glucocorticoids—this sinus-derived NO production is continuous and constitutive, unaffected by standard anti-inflammatory medications.
With each nasal inhalation, the sinus-produced NO is carried passively into the lower airways and lungs. This mechanism was characterised systematically in the 1990s by Prof. Jon Lundberg and colleagues at the Karolinska Institute, building on earlier observations that nasal nitric oxide levels are substantially higher than those in exhaled breath from the mouth.
Physiology of ventilation-perfusion matching
In the lungs, nitric oxide functions as a potent selective vasodilator. Its mechanism is elegantly targeted: NO preferentially widens pulmonary arterioles supplying alveoli that are well-ventilated with incoming air. This localised vasodilation improves the matching between ventilation (V) and perfusion (Q)—the fundamental principle governing oxygen transfer efficiency.
Better V/Q matching means a higher fraction of inhaled oxygen actually diffuses across the alveolar-capillary membrane into arterial blood, raising overall arterial oxygenation. Clinically, this same principle underpins the use of inhaled nitric oxide therapy in pulmonary hypertension and severe acute respiratory distress syndrome (ARDS). The key distinction is that through nasal breathing, the body produces and self-administers this therapeutic agent continuously at low physiological doses.
Experimental evidence from the Karolinska study
The most direct measurement of this effect was published by Lundberg’s group in Acta Physiologica Scandinavica in 1996. In the primary cohort, transcutaneous oxygen tension (tcPO₂)—a non-invasive proxy for arterial oxygenation—was measured during alternating periods of nasal and oral breathing in 8 healthy adult subjects. Six of the 8 subjects showed approximately 10% higher tcPO₂ during nasal breathing, demonstrating reproducibility of the effect across most individuals.
A second experimental group of 6 subjects further characterised the mechanism by measuring nasal NO levels directly. The data collectively demonstrate that the oxygen benefit of nasal breathing is neither incidental nor marginal: it represents a measurable, physiologically significant improvement in arterial oxygenation driven by endogenous nitric oxide.
Six of eight healthy subjects showed approximately 10% higher transcutaneous oxygen tension during nasal breathing compared to mouth breathing, with sinus-derived nitric oxide identified as the mechanistic driver of improved ventilation-perfusion matching in the lungs.
— Prof. Jon Lundberg, Karolinska Institute (Acta Physiologica Scandinavica, 1996)
What this means
Frequently asked questions
Why is mouth breathing less efficient than nasal breathing for oxygen uptake?
Mouth breathing completely bypasses the paranasal sinuses and their endogenous nitric oxide production. The air inhaled through the mouth lacks this sinus-derived NO, so the lungs do not receive the selective vasodilation signal that improves ventilation-perfusion matching. As a result, a smaller fraction of inhaled oxygen is transferred to arterial blood.
Is the 10% oxygen improvement clinically meaningful for healthy people?
In healthy individuals with normal lung function, a 10% improvement may be modest relative to overall oxygen-carrying capacity. However, in patients with chronic respiratory disease, high-altitude exposure, or reduced respiratory reserve, even a 10% gain in arterial oxygenation can meaningfully reduce breathlessness and improve exercise tolerance. The effect is also cumulative across many breathing cycles throughout the day.
Can this mechanism be enhanced or augmented pharmacologically?
The sinus-derived nitric oxide production is constitutive and continuous, independent of typical anti-inflammatory medications that suppress inducible NOS elsewhere. However, clinical inhaled nitric oxide therapy—used in severe pulmonary hypertension and ARDS—operates via the same V/Q matching principle. Future research may explore whether supporting nasal nitric oxide production could enhance the benefits in disease states, but current evidence supports optimising nasal breathing as a primary strategy.
The evidence from the Karolinska Institute underscores that breathing mechanics—specifically the route of air intake—has direct physiological consequences for arterial oxygenation. As respiratory medicine increasingly adopts precision approaches to optimising oxygen delivery, the role of nasal breathing as a non-pharmacological, physiologically grounded intervention merits continued investigation in both health maintenance and disease management contexts. Research into whether interventions to correct mouth breathing (such as orofacial myofunctional therapy or sleep hygiene measures) translate to sustained improvements in arterial oxygenation could inform future clinical guidelines.
Source: Nasal nitric oxide pathway characterisation study, Karolinska Institute
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Medically reviewed by Prof. Giorgi Pkhakadze, MD, MPH, PhD. Spotted an error? Contact the editorial team.
