OBJECTIVE: This study aimed to systematically review the effect of nitrate supplementation on blood oxygen saturation.
METHODS: We searched PubMed, Scopus, and Cochrane Library databases from their inception up to October 2022. Two reviewers independently conducted two stages of the screening process to include a randomized controlled trial with nitrate supplementation versus placebo intervention assessing oxygen saturation among lowlanders going to either real or simulated high altitude environments. We used the Cochrane Risk of Bias 2.0 tool to assess the risk of bias in the included studies. Fixed-effect model meta-analyses were conducted for laboratory-based studies. Random-effect meta-analyses were conducted for real-world studies.
RESULTS: We found 7 trials that met the eligibility criteria. A meta-analysis of studies with some bias concerns showed an increase of 1.26% in the SpO2 with 44% I2 during submaximal exercise at simulated high altitudes (GRADE: low). On the contrary, a meta-analysis of studies without heterogeneity showed that nitrate supplementation aggravated oxygen saturation decline (-2.64%, p=0.03, GRADE: high) during rest in real high-altitude environments. A meta-analysis also showed that nitrate supplementation did not affect Acute Mountain Sickness (AMS) symptoms (GRADE: high).
CONCLUSIONS: Our results suggest that nitrate supplementation did not provide benefits for AMS prevention during rest at high altitudes. The low-quality evidence showing small beneficial effects of nitrate supplementation during exercise calls for further studies.

Acute high altitude disease (AHAD) is a general term for a series of clinical reactions that occur when the body fails to adapt to the low-pressure hypoxic environment of high altitudes. Mild cases can cause symptoms such as headache, nausea and vomiting, while more severe cases can lead to life-threatening conditions such as pulmonary edema, cerebral edema and other critical conditions that can be fatal. With the increasing demand for high altitudes deployment, understanding the common preventive measures of AHAD can reduce its morbidity or mortality to a certain extent, which is of great benefit to those who reside temporarily at high altitudes. In recent years, as people\'s health awareness has improved, there has been a growing attention towards non-pharmacological methods of disease prevention. At the same time, non-pharmacological therapy has significant therapeutic effects in preventing and treating high-altitude diseases, which has attracted the attention of researchers in this field. This review summarizes the major non-pharmacological preventive components of modern medicine and outlines the current non-pharmacological approaches to AHAD from the perspective of traditional Chinese medicine, intending to serve clinical purposes and improve the onset and prognosis of AHAD.

Altitude-related illness occurs as a result of inadequate acclimatization. The mainstay of prevention is a slow, graded ascent profile which gives the body time to respond to a low-oxygen environment. The diagnosis of these conditions is often difficult in resource-limited environments, so history and a physical exam are key in identifying patients who will require descent and evacuation. Treatment modalities such as supplemental oxygen, portable hyperbaric chambers, and medications, are all temporizing measures until the patient can be safely evacuated to a lower elevation.

Background Advanced diagnostics are not easily accessible in austere topographical locations. We documented retinal changes in patients with acute mountain sickness (AMS+) and compared these with asymptomatic individuals (AMS-) with recent induction into high altitude using direct ophthalmoscopy as a screening tool. Methods We evaluated 97 individuals (43 AMS- and 54 AMS+) who were inducted to an altitude 3800 m above sea level by direct ophthalmoscopy after pupillary dilatation, on day 2 of arrival. Results Retinal vein dilatation was seen in 36 (66.7%) AMS+ v. 14 (32.6%) AMS- (p<0.01), hyperaemia of the optic disc in 30 (55.6%) AMS+ v. 14 (32.6%) AMS- (p<0.05), hyperaemia of the optic disc along with retinal vein dilatation in 27 (50%) AMS+ v. 9 (20.9%) AMS- (p<0.01), retinal vein tortuosity in 12 (22.2%) AMS+ v. 3 (7%) AMS- (p<0.02). In AMS+ with retinal vein dilatation 17 (50%) had SpO2 >91% and 19 (79.2%) had SpO2 <91% (p<0.01). An AMS score of >5 was recorded in 25 (69.4%; p<0.001) with venular dilatation and in 19 (52.8%; p<0.001) who were AMS+ with an induction number ≥3 had retinal dilatation. Conclusion Acute hypobaric hypoxia causes retinal venous dilatation, tortuosity and hyperaemia of the optic disc in those with AMS and correlates directly with SpO2 levels. The incidence of retinal vein dilatation increases with frequent re-entry into high altitude and more severe symptoms of AMS. Hence, all those being inducted to high altitude should be screened for retinal vascular changes.

Millions of people visit high-altitude regions annually and more than 80 million live permanently above 2,500 m. Acute high-altitude exposure can trigger high-altitude illnesses (HAIs), including acute mountain sickness (AMS), high-altitude cerebral oedema (HACE) and high-altitude pulmonary oedema (HAPE). Chronic mountain sickness (CMS) can affect high-altitude resident populations worldwide. The prevalence of acute HAIs varies according to acclimatization status, rate of ascent and individual susceptibility. AMS, characterized by headache, nausea, dizziness and fatigue, is usually benign and self-limiting, and has been linked to hypoxia-induced cerebral blood volume increases, inflammation and related trigeminovascular system activation. Disruption of the blood-brain barrier leads to HACE, characterized by altered mental status and ataxia, and increased pulmonary capillary pressure, and related stress failure induces HAPE, characterized by dyspnoea, cough and exercise intolerance. Both conditions are progressive and life-threatening, requiring immediate medical intervention. Treatment includes supplemental oxygen and descent with appropriate pharmacological therapy. Preventive measures include slow ascent, pre-acclimatization and, in some instances, medications. CMS is characterized by excessive erythrocytosis and related clinical symptoms. In severe CMS, temporary or permanent relocation to low altitude is recommended. Future research should focus on more objective diagnostic tools to enable prompt treatment, improved identification of individual susceptibilities and effective acclimatization and prevention options.

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Griffith Pugh, MD (1909-1994), was a pioneer in altitude physiology. During World War II, he developed training protocols in Lebanon to improve soldier performance at altitude and in the cold. In 1951 he was chosen to join the British Everest team as a scientist. In preparation, he developed strategies for success on a training expedition on Cho Oyu in 1952. Results from Cho Oyu led to the use of supplemental oxygen at higher flow rates during ascent than used previously (4 L/min vs 2 L/min) and continued use (at a reduced rate of 2 L/min) during descent, enabling increased performance and improved mental acuity. Oxygen was also used during sleep, leading to improved sleep and warmth. Adequate hydration (∼3 L/day) was also stressed, and a more appealing diet led to improved nutrition and condition of the climbers. Improved hygiene practices and acclimatization protocols were also developed. These strategies contributed to the first successful summiting of Mount Everest in 1953. Pugh was then appointed as the lead scientist for a ground-breaking eight-and-a-half-month research expedition where the team was the first to overwinter at high altitude (5800 m) in the Himalayas. This current work summarizes Pugh\'s scientific contributions as they relate to success on Mount Everest and in inspiring future altitude research by generations of successful researchers.

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Acute mountain sickness (AMS) is a common ailment in high-altitude areas caused by the body\'s inadequate adaptation to low-pressure, low-oxygen environments, leading to organ edema, oxidative stress, and impaired intestinal barrier function. The gastrointestinal tract, being the first to be affected by ischemia and hypoxia, is highly susceptible to injury. This study investigates the role of Lactobacillus delbrueckii subsp. bulgaricus in alleviating acute hypoxic-induced intestinal and tissue damage from the perspective of daily consumed lactic acid bacteria. An acute hypoxia mouse model was established to evaluate tissue injury, oxidative stress, inflammatory responses, and intestinal barrier function in various groups of mice. The results indicate that strain 4L3 significantly mitigated brain and lung edema caused by hypoxia, improved colonic tissue damage, and effectively increased the content of tight junction proteins in the ileum, reducing ileal permeability and alleviating mechanical barrier damage in the intestines due to acute hypoxia. Additionally, 4L3 helped to rebalance the intestinal microbiota. In summary, this study found that Lactobacillus delbrueckii subsp. bulgaricus strain 4L3 could alleviate acute intestinal damage caused by hypoxia, thereby reducing hypoxic stress. This suggests that probiotic lactic acid bacteria that exert beneficial effects in the intestines may alleviate acute injury under hypoxic conditions in mice, offering new insights for the prevention and treatment of AMS.

High-altitude myocardial injury (HAMI) represents a critical form of altitude illness for which effective drug therapies are generally lacking. Notoginsenoside R1, a prominent constituent derived from Panax notoginseng, has demonstrated various cardioprotective properties in models of myocardial ischemia/reperfusion injury, sepsis-induced cardiomyopathy, cardiac fibrosis, and myocardial injury. The potential utility of notoginsenoside R1 in the management of HAMI warrants prompt investigation. Following the successful construction of a HAMI model, a series of experimental analyses were conducted to assess the effects of notoginsenoside R1 at dosages of 50 mg/Kg and 100 mg/Kg. The results indicated that notoginsenoside R1 exhibited protective effects against hypoxic injury by reducing levels of CK, CK-MB, LDH, and BNP, leading to improved cardiac function and decreased incidence of arrhythmias. Furthermore, notoginsenoside R1 was found to enhance Nrf2 nuclear translocation, subsequently regulating the SLC7A11/GPX4/HO-1 pathway and iron metabolism to mitigate ferroptosis, thereby mitigating cardiac inflammation and oxidative stress induced by high-altitude conditions. In addition, the application of ML385 has confirmed the involvement of Nrf2 nuclear translocation in the therapeutic approach to HAMI. Collectively, the advantageous impacts of notoginsenoside R1 on HAMI have been linked to the suppression of ferroptosis via Nrf2 nuclear translocation signaling.