Acute mountain sickness (AMS), which affects 25 percent of travelers to altitudes between 1,900 and 3,000 m (6,232 and 9,840 ft), is characterized by frontal headaches, lassitude, insomnia and peripheral edema. Symptoms usually resolve within a few days but, if left untreated, can progress to life-threatening malignant and possibly fatal high-altitude pulmonary and cerebral edema. The exact mechanism of AMS is unknown, but important physiologic factors include a low hypoxic ventilatory drive, water retention and increased vascular permeability. Arterial oxygenation decreases as a function of hypobaria at higher altitudes, resulting in tissue hypoxia, the likely trigger for these changes. Bailey reviewed the physiologic implications of AMS.

Upper respiratory and gastrointestinal symptoms are common among travelers who ascend to high altitudes. Decreases in plasma glutamine that occur at these altitudes may increase a person's susceptibility to opportunistic infections. Studies have emphasized the role of opportunistic infections in releasing vasoactive inflammatory mediators, which in turn exacerbate arterial hypoxia. Cachexia, another common consequence of altitude, may be a protective activity caused by breakdown of skeletal muscle to replace a depleted supply of amino acids.

Prophylaxis for AMS includes acetazolamide, which inhibits carbonic anhydrous and acts as a respiratory stimulant. Alternatives include nutritional supplementation with amino acids and antioxidants, although this preventive technique is less supported by rigorous testing.