Controlled inhalation of thin air may alleviate Parkinson's symptoms

by Maria Fernanda Ziegler, FAPESP

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Breathing thin air, such as that found at high mountain summits, is usually taxing on the body. However, a study conducted at São Paulo State University (UNESP) in Brazil showed that short, controlled exposure to low-oxygen air is safe and does not interfere with sleep. This exposure can also modulate hormones and markers associated with inflammation in people with Parkinson's disease. These preliminary results pave the way for further research into using this technique as a complementary therapy for the condition.

The approach, known scientifically as intermittent hypoxia, aims to stimulate the body's adaptive responses without overburdening it. "The initial results indicate that the technique activates protective mechanisms that can safely benefit people with Parkinson's disease without causing adverse effects. That's important because it allows us to conduct studies with a larger number of volunteers and with long-term protocols that evaluate the effects of repeated sessions," says Fabio Barbieri, coordinator of the Human Movement Research Laboratory (MOVI-LAB) and the "Ativa Parkinson" outreach project at UNESP in Bauru. Barbieri led the research.

An estimated 11 million people worldwide have Parkinson's disease. The condition is characterized by the progressive degeneration of neurons that produce dopamine, a neurotransmitter that is essential for movement control. It causes well-known motor symptoms, such as tremors, muscle rigidity and slowness of movement. However, it also triggers significant nonmotor manifestations, including metabolic changes, inflammatory processes and sleep disorders.

As Barbieri explains, medications help manage the disease, but they do not promote the metabolic and anti-inflammatory changes necessary to alleviate all symptoms. "Currently, physical exercise is the only available strategy that can improve clinical manifestations. Therefore, it's worth investigating whether controlled hypoxia would have a similar effect as a complementary treatment to physical exercise. We're by no means talking about a cure for Parkinson's disease or an approach that would replace any other treatment," the researcher emphasizes.

The study, published in August in the journal Parkinsonism & Related Disorders, involved 30 volunteers—half with Parkinson's disease and half healthy. During the 39-minute experiment, the volunteers wore masks and used equipment that alternated between four six-minute cycles of breathing air with a 10% oxygen concentration (equivalent to an altitude of 5,800 meters (19,000 feet)) and three five-minute intervals of breathing normal air (21% oxygen).

On another day, for comparison, the same volunteers underwent a control session in which they breathed only normal air the entire time.

Blood markers

The researchers observed that a single session of intermittent hypoxia was sufficient to temporarily reduce cortisol and leptin levels in volunteers with Parkinson's disease. Cortisol is a stress-related hormone, and leptin is a hormone produced by adipose tissue that regulates metabolism and satiety. However, when present in excess, leptin promotes inflammatory processes. Additionally, there was a sustained increase in adiponectin, a substance with anti-inflammatory effects that is often dysregulated in Parkinson's disease. This effect persisted for up to 24 hours after the experiment.

According to Murilo Henrique Faria, the first author of the study, the imbalance in these three substances is often linked to inflammation in the brain, hormonal imbalances and sleep problems that are common in Parkinson's disease. "Therefore, our results demonstrate that the use of intermittent hypoxia can modulate metabolism, which may trigger positive effects on sleep behavior in people with Parkinson's disease," Faria says.

The authors had initially feared that hypoxia might cause awakenings or insomnia, but the experiment did not show this to be the case. "A single session of intermittent hypoxia didn't alter general sleep parameters [such as the number of awakenings or time to fall asleep], either in people with Parkinson's disease or in healthy volunteers," Faria says.

According to Barbieri, a single session of the protocol was sufficient to modify blood biomarkers, such as reducing cortisol and increasing adiponectin, but it may not have been sufficient to reorganize the sleep-wake cycle. "Hence the need for more in-depth and longer-term studies," he says.

The study also confirmed that the procedure did not alter blood iron levels or increase levels of interleukin-6, a molecule that stimulates inflammatory processes. This finding reinforces the safety of the method. Additionally, it helped maintain the concentration of BDNF (brain-derived neurotrophic factor), a protein essential for protecting and sustaining neurons.

"Maintaining stable BDNF levels is a significant finding, as that protein typically declines during periods of physical inactivity—a decline that occurred when patients underwent the control session breathing normal air. Intermittent hypoxia prevented that decline while increasing adiponectin, paving the way for further research," says Faria.

The role of hormesis

The beneficial effect of intermittent hypoxia is explained by a concept called hormesis—the body's ability to adapt to minor stresses. "We use controlled doses of hypoxia to induce positive adaptations, something that can help people with Parkinson's disease," explains Carlos Augusto Kalva-Filho, a postdoctoral researcher at the Bauru School of Sciences (FC-UNESP) and co-author of the study.

He notes that this type of exposure to simulated high-altitude air, whether through masks and equipment or isolated chambers, is typically recommended for training athletes. "However, few research groups worldwide are investigating this strategy in people with Parkinson's disease."

The key, the researcher adds, lies in alternating between thin and normal air and strictly controlling the dose. This precisely calibrated stimulus keeps a protein called HIF-1α (hypoxia-inducible factor 1-alpha) active. HIF-1α functions as a cellular sensor that can trigger mechanisms to protect neurons and optimize energy production in cells, known as mitochondrial metabolism. "It's that precise control that generates the benefit. So, it isn't just a matter of fleeing to the mountains," he jokes.

Kalva-Filho also explains that this effect differs greatly from acute mountain sickness, which causes travelers at high altitudes to experience headaches, nausea and fatigue, and causes soccer players to lose their breath and perform poorly on the field. "When traveling to those very high-altitude locations, the body undergoes continuous and prolonged stress, which ends up overwhelming it. In the lab, however, everything is controlled."

More information

Murilo Henrique Faria et al., The acute effects of a single session of intermittent hypoxia on blood biomarker concentrations and sleep parameters in people with Parkinson's disease: A randomized, double-blind, crossover trial, Parkinsonism & Related Disorders (2026). DOI: 10.1016/j.parkreldis.2026.108922

Key medical concepts

Parkinson's DiseaseAdiponectinHydrocortisoneLeptin

Clinical categories

NeurologyHealthy aging Provided by FAPESP Who's behind this story?

Gaby Clark

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