Effect of Intravenous Iron Supplementation on Acute Mountain Sickness: A Preliminary Randomized Controlled Study.

BACKGROUND: The aim of this study was to assess the role of intravenous iron supplementation in the prevention of AMS. MATERIAL AND METHODS: This was a randomized, double-blinded, placebo-controlled study. Forty-one (n=41) healthy Chinese low-altitude inhabitants living in Beijing, China (altitude of about 50 meters) were randomly assigned into intravenous iron supplementation (ISS group; n=21) and placebo (CON group; n=20) groups. Participants in the ISS group received iron sucrose supplement (200 mg) before flying to Lhasa, China (altitude of 4300 meters). Acute mountain sickness (AMS) severity was assessed with the Lake Louise scoring (LLS) system within 5 days after landing on the plateau (at high altitude). Routine check-ups, clinical biochemistry, and blood tests were performed before departure and 24 h after arrival. RESULTS: A total of 38 participants completed the study (ISS group: n=19; CON group: n=19). The rate of subjects with AMS (LLS>3) was lower in the ISS group compared with the CON group, but no significant differences were obtained (P>0.05). There were no differences in patients' baseline characteristics. The physiological indices were similar in both groups except for serum iron concentrations (19.44±10.02 vs. 85.10±26.78 µmol/L) and transferrin saturation rates (28.20±12.14 vs. 68.34±33.12%), which were significantly higher in the ISS group (P<0.05). Finally, heart rate was identified as a contributing factor of LLS. CONCLUSIONS: These preliminary findings suggest that intravenous iron supplementation has no significant protective effect on AMS in healthy Chinese low-altitude inhabitants.

Work at high altitude and oxidative stress: antioxidant nutrients.

A significant portion of the world's geography lies above 10,000 feet elevation, an arbitrary designation that separates moderate and high altitude. Although the number of indigenous people living at these elevations is relatively small, many people travel to high altitude for work or recreation, exposing themselves to chronic or intermittent hypoxia and the associated risk of acute mountain sickness (AMS) and less frequently, high altitude pulmonary edema (HAPE) and high altitude cerebral edema (HACE). The symptoms of AMS (headache, nausea, anorexia, fatigue, lassitude) occur in those who travel too high, too fast. Some investigators have linked the development of these symptoms with the condition of altered blood-brain barrier permeability, possibly related to hypoxia induced free radical formation. The burden of oxidative stress increases during the time spent at altitude and may even persist for some time upon return to sea level. The physiological and medical consequences of increased oxidative stress engendered by altitude is unclear; indeed, hypoxia is believed to be the trigger for the cascade of signaling events that ultimately leads to adaptation to altitude. These signaling events include the generation of reactive oxygen species (ROS) that may elicit important adaptive responses. If produced in excess, however, these ROS may contribute to impaired muscle function and reduced capillary perfusion at altitude or may even play a role in precipitating more serious neurological and pulmonary crisis. Oxidative stress can be observed at altitude without strenuous physical exertion; however, environmental factors other than hypoxia, such as exercise, UV light exposure and cold exposure, can also contribute to the burden. Providing antioxidant nutrients via the diet or supplements to the diet can reduce oxidative stress secondary to altitude exposure. In summary, the significant unanswered question concerning altitude exposure and antioxidant supplementation is when does oxidative stress become potentially damaging enough to merit antioxidant therapy and conversely, what degree of oxidative stress is necessary to foster the adaptive response of altitude exposure?

Improvement in hypoxemia at 4600 meters of simulated altitude with carbohydrate ingestion.

BACKGROUND: Carbohydrate ingestion increases the relative production of carbon dioxide which results in an increase in ventilation in normal individuals. An increase in ventilation at altitude can result in improvement of altitude-induced hypoxemia. HYPOTHESIS: Carbohydrate ingestion will increase the arterial blood oxygen tension and oxyhemoglobin saturation during acute high altitude simulation. METHODS: There were 15 healthy volunteers, aged 18-33 yr, who were given a 4 kcal x kg(-1) oral carbohydrate beverage administered 2.5 h into an exposure to 15,000 ft (4600 m) of simulated altitude (5.5 h after the last meal). Altitude was simulated by having subjects breath a 12% oxygen/balance nitrogen mixture while remaining at sea level. Arterial blood gas samples were drawn at baseline and at regular intervals up to 210 min after carbohydrate ingestion. Subjects were evaluated for AMS by use of the Environmental Symptoms Questionnaire (ESQ) and a weighted average of cerebral symptom score (AMS-C). RESULTS: Baseline PaO2 increased significantly (p < 0.01) from 43.0 +/- 3.0 mmHg at 4600 m before carbohydrate ingestion to 46.8 +/- 6.2 mmHg at 60 min after carbohydrate ingestion. Arterial oxygen saturation rose significantly (p < 0.01) from a baseline of 79.5% +/- 5.1 to 83.8% +/- 6.42 at 60 min. CONCLUSIONS: Carbohydrate consumption significantly increased oxygen tension and oxyhemoglobin saturation in arterial blood of normal subjects during simulated altitude. Effects reached statistical significance across all subjects at 60 min. There was no significant difference in arterial oxygen levels or arterial oxygen saturation in subjects who developed AMS vs. those who did not develop AMS.

Acute mountain sickness is not altered by a high carbohydrate diet nor associated with elevated circulating cytokines.

We investigated whether a diet of increased carbohydrate content reduces the symptoms of acute mountain sickness (AMS) and whether concentrations of circulating cytokines rise and correlate with hypoxia and AMS. There were 19 healthy volunteers who ingested in randomized order both a high carbohydrate (68% CHO) or normal carbohydrate (45% CHO) diet for 4 d. On the 4th d, subjects were exposed to 8 h of 10% normobaric oxygen. Each subject completed the Lake Louise Consensus Questionnaire (LLCQ: a questionnaire developed to quantify the common symptoms and consequences of AMS) at the beginning and end of each hypoxic session, at which times venous blood was obtained for the following cytokines: interleukins 1 beta, 6 and 8 (IL-1 beta, IL-6, IL-8) and tumor necrosis factor alpha (TNF-alpha). AMS symptoms did not differ significantly between the diets (LLCQ scores: 68% CHO = 10.1 +/- 3.8 vs. 45% CHO = 10.3 +/- 4.1). Cytokine concentrations did not change with hypoxia on either diet, nor did individual changes correlate with AMS symptoms. We conclude that a high carbohydrate diet for 4 d does not reduce the symptoms of AMS; and plasma cytokine concentrations do not change with hypoxia and the development of AMS and, thus, are not likely mediators of this syndrome.