Cerebral oxygenation is likely to be of critical importance in determining function at high altitude. The present study has used the technique of near-IR spectroscopy to monitor changes in cerebral regional oxygenation in response to inhaled carbon dioxide, hyperventilation and supplementary oxygen on ascent to 4680 m over 3 days. At sea level, inhaled CO 2 resulted in a significant rise in cerebral regional oxygenation [from mean 69.6% (S.D. 2.4% to 71.1±2.3%; means±S.D.; P < 0.001). At 4680 m, CO 2 increased regional cerebral oxygenation (63.8±2.5% to 65.9±2.2%; P < 0.001) and also increased peripheral oxygen saturation (75.1±6.1% to 83.6±4.0%; P < 0.001). Voluntary hyperventilation resulted in improved peripheral oxygen saturation at 2770 m, 3650 m and 4680 m, whereas cerebral regional oxygenation was reduced at sea level and at 2770 m, unchanged at 3650 m and increased at 4680 m. Supplementary oxygen (6 1itres/min) at 4680 m resulted in greater improvements in peripheral oxygen saturation (76.7±7.9% to 98.1±1.5%; P < 0.001) and cerebral regional oxygenation (64.6±3.3% to 70.6±2.9%; P < 0.001) than were found with CO 2 or hyperventilation. We conclude that attempts to increase CO 2 inhalation or ventilation at high altitude are likely to be beneficial for cerebral oxygenation in the short term.

1. Raised intracranial pressure has been noted in severe forms of acute mountain sickness and high-altitude cerebral oedema, but the role of intracranial pressure in the pathogenesis of mild to moderate acute mountain sickness is unknown. 2. Serial measurements of intracranial pressure were made indirectly by assessing changes in tympanic membrane displacement in 24 healthy subjects on rapid ascent to 5200 m. 3. Acute hypoxia at 3440 m was associated with a rise in intracranial pressure, but no difference was found in pressure changes at 4120 or 5200 m in subjects with or without symptoms of acute mountain sickness. 4. Raised intracranial pressure, though temporarily associated with acute hypoxia, is not a feature of acute mountain sickness with mild or moderate symptoms.

1. Ten male stable asthmatic subjects and 10 matched control subjects performed a progressive exercise test on a treadmill to 85% of their predicted maximum heart rate. 2. Blood lactate, pyruvate, hydrogen ion, glucose, alanine, glycerol and total ketone body concentrations were measured at frequent intervals during and up to 60 min after exercise. Carbon dioxide production, oxygen consumption, ventilation, respiratory exchange ratio and oxygen saturation were also measured during and up to 10 min after exercise. 3. There were no significant differences between the asthmatic and control subjects in levels of carbon dioxide production, oxygen consumption and ventilation. The respiratory exchange ratio was greater in the asthmatic subjects during recovery from exercise ( P < 0.05). No changes in oxygen saturation were observed during exercise in either group. 4. In both asthmatic and control subjects, lactate, pyruvate, hydrogen ion, alanine and glycerol concentrations showed an increase from baseline levels, reaching maximum levels up to 10 min after exercise and returning to baseline within 1 h after exercise. Total ketone body concentrations decreased during exercise. 5. There were no significant differences between the asthmatic and control subjects in the concentration of any metabolite over the study period. 6. These data indicate that fuel metabolism during and after short-term progressive exercise is similar in stable asthmatic and normal subjects.