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In clinical studies, the partial pressure of oxygen (PaO2) and oxygen pulse saturation are the main variables used to assess blood oxygenation and define the threshold of hypoxia/hyperoxia and hypoxemia/hyperoxemia. Determination of the optimal oxygenation target has generated a lot of interest in recent years, mainly because of the potential risk of worse outcomes associated with hyperoxia, whereas the risk associated with hypoxia has been already well known. In this short narrative review, we recall some fundamental elements of physiology regarding the meaning of PaO2, the diffusion of oxygen to cells, the definitions of hyperoxemia and hyperoxia and the mechanisms of oxygen toxicity to provide a better understanding of these concepts, to which intensive care clinicians are frequently confronted. PaO2 provides only limited information about oxygen concentration carried by blood and does not allow to determine whether cells are exposed to hyperoxia. This should be considered for the design of future studies that aim to determine optimal oxygenation target and by clinicians for their daily practice.

Skeletal muscle oxygenation reflects the balance between oxygen delivery from the microcirculation and oxygen consumption of the muscle cells. Oxygenation in the muscle tissue is an essential factor in muscle contractions for performing activities of daily living and exercise as well as muscle tissue viability. It is until the development of near-infrared spectroscopy for providing a noninvasive, continuous monitoring of muscle oxygenation. The principle of near-infrared spectroscopy is to use light property to assess oxygenation based on the appearance of oxygenated blood in red and deoxygenated blood in darker red to black. To date, there is no comprehensive review focusing on muscle oxygenation regulation and its applications in physical therapy and rehabilitation. The objectives of this comprehensive review are to: 1) highlight the recent technical advances in near-infrared spectroscopytechnology for rehabilitation researchers, 2) present the advances in pathophysiological research in muscle oxygenation, and 3) evaluate findings and evidence of recent physical therapy and rehabilitation studies on improving muscle oxygenation. The review also evaluates findings and evidence of aerobic exercise, resistance exercise, contrast bath therapy, wound healing, cupping therapy, stretching, and electrical stimulation on muscle oxygen in healthy adults and patients with cardiovascular diseases. The use of near-infrared spectroscopy allows the assessment of muscle oxidative metabolism for personalized rehabilitation and exercise training.

Transabdominal fetal pulse oximetry offers a promising approach to non-invasively monitor fetal arterial oxygen saturation (SaO₂), potentially enhancing clinical decision-making and reducing unnecessary interventions during delivery. However, accurate estimation of fetal SaO₂ (denoted as SpO₂ when measured non-invasively) is complicated by the multi-layer maternal-fetal tissue structure, distinct maternal and fetal physiological signals, and inherently low fetal oxygen saturation levels. A multi-layer self-calibrated algorithm was developed by combining the multi-layer modified Beer-Lambert law with an analytical photon partial pathlength model. This approach distinguishes maternal and fetal tissue contributions, enabling more accurate fetal SpO₂ estimation. Validation was performed using Monte Carlo photon simulations of multi-layer tissue geometries, where synthetic optical signals representing fetal cardiac pulsations were generated under two fetal depths and randomly varied maternal and fetal oxygen saturations and optical properties. Further validation was performed using in vivo sheep data, where fetal SpO₂ values derived from transabdominal continuous-wave near-infrared spectroscopy measurements were compared against reference fetal SaO₂ from CO-oximetry. In simulations, the algorithm achieved a mean absolute error (MAE) below 5% and a Pearson correlation coefficient (R) of 0.98 between estimated fetal SpO₂ and ground truth fetal SaO₂ when using optimal input parameters. In the sheep experiment, agreement with reference measurements was maintained (MAE = 10.3%, R = 0.91). However, algorithm performance was highly sensitive to accurate optical properties and tissue layer thicknesses inputs, which may be challenging to obtain in clinical settings. These results demonstrate proof-of-concept feasibility for the multi-layer self-calibrated algorithm in both simulated and in vivo conditions. While further refinement, particularly in optical property estimation and fetal depths in human pregnancies, is necessary, this work provides a foundational framework for the future clinical translation of non-invasive fetal SpO₂ monitoring.

JOURNAL/mgres/04.03/01612956-202603000-00003/figure1/v/2025-06-28T140100Z/r/image-tiff Hypoxemia during propofol sedation for gastrointestinal endoscopic procedures is a significant risk and is often exacerbated by inadequate preoxygenation. Effective preoxygenation strategies are essential for reducing the incidence of hypoxemia, especially in high-risk patients. This study aimed to evaluate the efficacy of an enhanced preoxygenation protocol for mitigating hypoxemia during propofol sedation during gastroscopy. In a prospective, randomized, controlled design, patients undergoing gastroscopy were assigned to either an intervention group (enhanced preoxygenation) or a nonintervention group (standard care). The intervention protocol involved the administration of eight tidal volume breaths over 1 minute at an oxygen flow rate of 10 L/min via a tight-fitting face mask, with clinical supervision by an endoscopy nurse. The primary outcome was the incidence of hypoxemia, defined as a peripheral oxygen saturation level of less than 90% at any point during the gastroscopy procedure. Compared with the nonintervention group, the intervention group had a significantly lower incidence of hypoxemia. This effect was particularly pronounced in high-risk patients, including elderly individuals and those with elevated body mass indices. No significant adverse events were observed during the procedure. These results suggest that enhanced preoxygenation may effectively alleviate the occurrence of hypoxemia during propofol sedation in gastrointestinal endoscopic procedures. Further research is needed to assess the broader applicability of this approach and explore additional strategies for optimizing preoxygenation in endoscopic procedures.

Spinal cord injury (SCI) is a severe trauma that leads to significant motor, sensory, and autonomic dysfunction, imposing a substantial disease burden and economic costs globally. The pathophysiology of SCI involves primary and secondary injury stages, with the latter characterized by inflammatory responses, apoptosis, and tissue necrosis. Current therapeutic interventions, including pharmacological treatments and stem cell therapies, provide limited benefits and do not fully address the therapeutic effects on SCI. Hyperbaric oxygen therapy (HBOT), which delivers 100% oxygen at pressures exceeding 1 atmosphere absolute, has shown potential in SCI animal models due to its antiapoptotic, antioxidant, anti-inflammatory, and angiogenesis-promoting effects, thereby limiting secondary injury. Clinical studies have also demonstrated some efficacy of HBOT in treating SCI; however, the optimal timing, duration, and treatment cycles of HBOT remain contentious, and long-term efficacy has yet to be assessed. This review synthesizes the basic research and clinical practice of HBOT for SCI, thereby summarizing the main mechanistic pathways and demonstrating its clinical effects. Future large-scale, multicenter clinical studies are warranted to determine the efficacy and safety of HBOT in treating SCI and explore combined therapeutic modalities for a more comprehensive treatment approach.

JOURNAL/mgres/04.03/01612956-202603000-00002/figure1/v/2025-06-28T140100Z/r/image-tiff Paroxysmal sympathetic hyperactivity syndrome (PSH) is common in patients with severe craniocerebral injuries. Carbon monoxide poisoning (ACOP) may lead to secondary PSH, and hyperbaric oxygen (HBO) is an important treatment method for ACOP that can promote the dissociation of carboxyhemoglobin and reduce the long-term sequelae of ACOP. To explore the risk factors and clinical characteristics of PSH secondary to acute ACOP and to investigate the efficacy of HBO treatment, a retrospective analysis was performed on patients with moderate to severe ACOP admitted to the Hyperbaric Oxygen Department of Beijing Chaoyang Hospital, Capital Medical University, from January 1, 2018 to December 31, 2024. Three patients developed PSH during hospitalization and were classified into the PSH group, while the remaining 50 patients were in the non-PSH group. Univariate Fisher's exact test indicated that a coma duration of more than 72 hours was related to the occurrence of PSH after ACOP, and irregular HBO treatment after onset might be associated with the occurrence of PSH after ACOP. All three PSH patients developed paroxysmal postural or dystonic disorders after onset, accompanied by sympathetic excitation manifestations such as increased heart rate, respiratory rate, elevated blood pressure, and fever. Antiepileptic drugs had poor effects, and the attacks were effectively controlled after HBO treatment combined with adjusted drug therapy. The results indicate that for patients with severe carbon monoxide poisoning, especially those with a long coma duration or irregular HBO treatment after onset, if epileptic seizures occur during the disease course and are accompanied by sympathetic excitation manifestations, the possibility of PSH should be considered. Regular HBO treatment is of great significance for controlling the onset of symptoms.

JOURNAL/mgres/04.03/01612956-202603000-00005/figure1/v/2025-06-28T140100Z/r/image-tiff Exercise-induced fatigue limits athletic performance. Molecular hydrogen is an effective treatment for relieving fatigue, but the exact mechanism is not clear. In our study, a mouse model of fatigue was established to explore the molecular mechanism by which hydrogen-rich water reduces exercise-induced fatigue. The results showed that hydrogen-rich water improved the motor function of fatigue mice, reduced the levels of fatigue-related biomarkers (blood urea nitrogen, lactate, and creatine kinase), and alleviated gastrocnemius muscle injury. Furthermore, ultrahigh-performance liquid chromatography-mass spectrometry revealed that hydrogen-rich water upregulated the expression of immune response gene 1 (IRG1), increased the abnormally reduced levels of itaconic acid due to fatigue, and subsequently activated the downstream nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway. Finally, C2C12 cells exposed to an IRG1 inhibitor (IRG1-IN) or 4-octyl itaconic acid (4-OI) were treated with hydrogen-rich water, indicating that hydrogen-rich water effectively upregulated the expression of Nrf2 and HO-1 in cells. In summary, hydrogen-rich water alleviates exercise-induced fatigue by activating the IRG1-itaconic acid/Nrf2/HO-1 pathway and inhibiting oxidative stress.