Summary: Researchers revealed a correlation between reduced oxygen intake, or ‘oxygen restriction,’ and extended lifespan in lab mice.
The study found that mice in an oxygen-restricted environment lived about 50% longer than those in normal oxygen levels. The oxygen-restricted mice also experienced delayed onset of aging-associated neurological deficits.
The study, however, did not establish the exact mechanism through which oxygen restriction prolongs lifespan.
- This is the first study to demonstrate that ‘oxygen restriction’ extends lifespan in a mammalian aging model.
- Mice in an oxygen-restricted environment lived about 50% longer and had delayed onset of aging-associated neurological deficits.
- The researchers found that oxygen restriction did not affect food intake, suggesting that other mechanisms extend the lifespan of the mice.
For the first time, researchers have shown that reduced oxygen intake, or “oxygen restriction,” is associated with longer lifespan in lab mice, highlighting its anti-aging potential. Robert Rogers of Massachusetts General Hospital in Boston, US, and colleagues present these findings in a study published May 23rd in the open-access journal PLOS Biology.
Research efforts to extend healthy lifespan have identified a number of chemical compounds and other interventions that show promising effects in mammalian lab animals— for instance, the drug metformin or dietary restriction.
Oxygen restriction has also been linked to longer lifespan in yeast, nematodes, and fruit flies. However, its effects in mammals have been unknown.
To explore the anti-aging potential of oxygen restriction in mammals, Rogers and colleagues conducted lab experiments with mice bred to age more quickly than other mice while showing classic signs of mammalian aging throughout their bodies.
The researchers compared the lifespans of mice living at normal atmospheric oxygen levels (about 21%) to the lifespans of mice that, at 4 weeks of age, had been moved to a living environment with a lower proportion of oxygen (11%—similar to that experienced at an altitude of 5000 meters).
They found that the mice in the oxygen-restricted environment lived about 50% longer than the mice in normal oxygen levels, with a median lifespan of 23.6 weeks compared to 15.7 weeks. The oxygen-restricted mice also had delayed onset of aging-associated neurological deficits.
Prior research has shown that dietary restriction extends the lifespan of the same kind of fast-aging mice used in this new study. Therefore, the researchers wondered if oxygen restriction extended their lifespan simply by causing the mice to eat more. However, they found that oxygen restriction did not affect food intake, suggesting other mechanisms were at play.
These findings support the anti-aging potential of oxygen restriction in mammals, perhaps including humans. However, extensive additional research will be needed to clarify its potential benefits and illuminate the molecular mechanisms by which it operates.
Rogers adds, “We find that chronic continuous hypoxia (11% oxygen, equivalent to what would be experienced at Everest Base Camp) extends lifespan by 50% and delays the onset of neurologic debility in a mouse aging model.
“While caloric restriction is the most widely effective and well-studied intervention to increase lifespan and healthspan, this is the first time that ‘oxygen restriction’ has been demonstrated as beneficial in a mammalian aging model.”
About this longevity research news
Author: Robert Rogers
Contact: Robert Rogers – PLOS
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Hypoxia extends lifespan and neurological function in a mouse model of aging” by Robert Rogers et al. PLOS Biology
Hypoxia extends lifespan and neurological function in a mouse model of aging
There is widespread interest in identifying interventions that extend healthy lifespan. Chronic continuous hypoxia delays the onset of replicative senescence in cultured cells and extends lifespan in yeast, nematodes, and fruit flies.
Here, we asked whether chronic continuous hypoxia is beneficial in mammalian aging.
We utilized the Ercc1 Δ/- mouse model of accelerated aging given that these mice are born developmentally normal but exhibit anatomic, physiological, and biochemical features of aging across multiple organs.
Importantly, they exhibit a shortened lifespan that is extended by dietary restriction, the most potent aging intervention across many organisms.
We report that chronic continuous 11% oxygen commenced at 4 weeks of age extends lifespan by 50% and delays the onset of neurological debility in Ercc1 Δ/- mice.
Chronic continuous hypoxia did not impact food intake and did not significantly affect markers of DNA damage or senescence, suggesting that hypoxia did not simply alleviate the proximal effects of the Ercc1 mutation, but rather acted downstream via unknown mechanisms.
To the best of our knowledge, this is the first study to demonstrate that “oxygen restriction” can extend lifespan in a mammalian model of aging.