It may be a useful tool, but does not necessarily fix the underlying problem.
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: Intermittent hypoxia training (IHT) stimulated hepatic Ca2+ influx and mitochondrial quality control.
IHT enhanced tolerance to subsequent hypoxic exposure.
Adenine nucleotide translocase (ANT) enhanced mitochondrial Ca2+ transport and buffering capacity.
ANT enhanced mitochondrial quality control and antioxidant defenses.
memory-enhancing acute intermittent hypoxia (meAIH; ā¼10% oxygen) protocol
Results indicated that during the initial acquisition phase, the meAIH group performed significantly better on a declarative memory task than the SHAM group (p < 0.05), but not the retention phase. These novel results inform the understanding of cognitive neuroplasticity within young, healthy adults and how meAIH can be used to inform training paradigms for many populations.
In this review, we summarize current knowledge on hypoxia tolerance, oxygen transport, and oxygen consumption in humans, rats, and mice, and evaluate the extent to which findings from rodent models can be extrapolated to humans. While the anatomical, physiological, and molecular foundations of oxygen transport and utilization are broadly conserved across species, there are important quantitative differencesālargely linked to body-mass variationāas well as qualitative distinctions. Mice that evolved in high-altitude environments, display remarkable hypoxia tolerance. Their physiological repertoire includes highly efficient pulmonary gas exchange, metabolic downregulation, and substantial plasticity of the mitochondrial electron transport system under hypoxic conditions. In contrast, rats exhibit heightened vulnerability in hypoxia, manifesting as right ventricular hypertrophy, excessive erythropoiesis, and myocardial injury. These interspecies differences highlight that the robust hypoxia tolerance of miceāand the potentially comparatively greater susceptibility of rats than humansāmust be carefully considered when translating findings from rodent hypoxia research into human contexts.
IH is an effective and adaptable strategy to improve aerobic and anaerobic performance, as well as to enhance muscle strength and hypertrophy. These benefits often occur without consistent hematological changes. Future studies should focus on individualized approaches, standardization of terminology, and precise quantification of both hypoxic exposure and training load to optimize outcomes and ensure reproducibility.
Reminder, long-term intermittent hypoxia similar to the one in sleep apnea is detrimental: Prolonged intermittent hypoxia accelerates cardiovascular aging and mortality: insights from a murine model of OSA 2025
Current methods are live-high train-low (LHTL), live-low train-high (LLTH), and passive hypoxic conditioning (PHC).
Conclusion: LLTH showed a significant effect on VO2max in both athletic and non-athletic populations, while LHTL and PHC did not. Future studies should investigate factors driving the effects.
Chinese paper in a low-quality journal: Chronic intermittent hypoxia increases Parkinsonās disease susceptibility via PPARĪ±-mediated lipid droplet-mitochondrial dysfunction 2025
Results: We revealed that CIH significantly exacerbated nigrostriatal DA neurodegeneration and motor dysfunction in subtoxic PD models. Mechanistically, we identified a PPARĪ±-dependent disruption of Mfn2-Plin5 tethering, which impaired LD-mitochondrial interactions, thereby compromising LD turnover and promoting pathological LD accumulation within DA neurons. Crucially, pharmacological interventions targeting the LD-mitochondrial axis, including strategies to enhance LD catabolism, inhibit mitochondrial fission, or restore LD-mitochondrial tethering, effectively mitigated nigrostriatal DA neurodegeneration in CIH-preconditioned subtoxic PD models.
However, it is important to recognize a number of this studyās limitations. First, we found that lipid transfer between DA neurons and microglia was primarily mediated by APOE, as competitive inhibition of LDLR reduced lipid transfer by more than 50% (Figure 3). However, intercellular lipid trafficking is not restricted to the APOE pathway. Previous studies have reported that tunneling nanotubes (TNTs) and secretory vesicles, including exosomes and microvesicles, also participate in lipid transfer between cells [53,54]. In this study, we did not evaluate the contribution of these additional pathways and future investigations should systematically assess their roles by employing microtubue inhibitors (e.g., vincristine) to disrupt TNTs formation or exosome secretion inhibitors (e.g., GW4869) in combination with lipid tracing assays. Secondly, although PPARĪ± is known to regulate transcription by directly binding to the promoters of target genes, it can also act through non-geomic mechanisms, such as suppressing the activity of other transcription factors (e.g., NF-ĪŗB) [55]. In the current study, we did not determine whether the regulation of Mfn2 and Plin5 by PPARĪ± is mediated through direct promoter binding or indirect signaling pathways. Future studies should address this by performing ChIP-qPCR or ChIP-seq to directly validate PPARĪ± binding to the Mfn2 and Plin5 promoters, and by incorporating luciferase reporter assays to further clarify the transcriptional regulatory mechanisms.
Does any of this matter if you donāt have sleep apnea?
Thatās the question. It shows that too much intermittent hypoxia is bad but it doesnāt say whether a bit of it is good. (Nor does it define the threshold of ātoo muchā but given that hypoxia in OSA is daily and for hours whereas for hypoxic therapy itās for a few minutes every other day, we can assume itās low enough).
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