Hypoxia
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Anecdotal reports from Parkinson's disease patients suggest that time spent at high altitudes, where oxygen is naturally lower, may bring unexpected relief from symptoms. Intrigued by this possibility, researchers designed an experiment to investigate the biological mechanisms that might explain it.
The researchers began by injecting mice with preformed clumps of α-synuclein, a protein that misfolds, accumulates, and damages brain cells in Parkinson's disease. The animals were then housed in either normal air (21% oxygen) or reduced oxygen (11%).
Continuous low-oxygen exposure produced notable benefits:
Continuous low-oxygen exposure preserved neurons and prevented movement problems, even though harmful protein clumps still accumulated in the brain.
Starting low-oxygen treatment six weeks after symptom onset reversed existing movement and anxiety problems and halted further nerve cell loss. However, neuronal cells already lost were not restored, and protein clumps remained in the brain.
In Parkinson's, misfolded proteins damage mitochondria, causing inefficient oxygen use and harmful oxygen buildup (hyperoxia), which leads to oxidative stress. Breathing low-oxygen air may reduce this excess. Additionally, low oxygen can activate protective genes via hypoxia-inducible factor (HIF), triggering stress resistance and survival pathways, and boost lactate metabolism, helping cells manage energy and reduce stress.
Taken together, the results highlight low-oxygen exposure as a potentially powerful strategy to slow or reverse disease processes in Parkinson's. However, these findings come only from animal models. Whether carefully controlled oxygen reduction is safe or effective in humans remains unknown and requires further study. Learn more about Parkinson's disease in episode #60 featuring Dr. Giselle Petzinger.
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Heat shock proteins enhance elite cyclists' performance in low-oxygen conditions. www.sciencedaily.com
During exposure to temperature extremes or hypoxia (low oxygen levels), cells increase their expression of heat shock proteins to stabilize unfolded proteins and repair damaged ones. This phenomenon, referred to as the heat shock response, occurs at the expense of other cellular proteins to protect the cell. Evidence from a 2016 study suggests that the heat shock response enhances athletic performance in low-oxygen environments characteristic of high altitudes.
The study involved 21 elite cyclists who engaged in ten 60-minute training sessions in either low-oxygen or hot conditions. Before and after the intervention, they performed a time trial, where researchers tested their tolerance to low-oxygen levels.
The researchers found that training during heat exposure improved athletic performance nearly as well as low oxygen exposure. Expression of heat shock protein 72 and hypoxia-inducible factor 1-α, a protein that mediates the body’s response to low oxygen levels, increased in both scenarios.
Heat-shock proteins comprise a large, highly conserved family of proteins that are present in all cells. They play prominent roles in many cellular processes, including immune function, cell signaling, and cell-cycle regulation. Cells maintain a constant level of HSPs to facilitate aspects of the protein synthesis machinery, including assembly, folding, export, turn-over, and regulation. However, stress can upregulate HSP production.
These findings suggest that training in a hot environment enhances performance in low-oxygen settings. Learn more about heat exposure via sauna use in our comprehensive overview article.