Sleeping in moderate hypoxia at home for prevention of acute mountain sickness (AMS): a placebo-controlled, randomized double-blind study.

Objective: Acclimatization at natural altitude effectively prevents acute mountain sickness (AMS). It is, however, unknown whether prevention of AMS is also possible by only sleeping in normobaric hypoxia.

Methods: In a placebo-controlled, double-blind study 76 healthy unacclimatized male subjects, aged 18 to 50 years, slept for 14 consecutive nights at either a fractional inspired oxygen (Fio2) of 0.

Exercise intensity typical of mountain climbing does not exacerbate acute mountain sickness in normobaric hypoxia.

Physical exertion is thought to exacerbate acute mountain sickness (AMS). In this prospective, randomized, crossover trial, we investigated whether moderate exercise worsens AMS in normobaric hypoxia (12% oxygen, equivalent to 4,500 m). Sixteen subjects were exposed to altitude twice: once with exercise [3 × 45 min within the first 4 h on a bicycle ergometer at 50% of their altitude-specific maximal workload (maximal oxygen uptake)], and once without.

Health risk for athletes at moderate altitude and normobaric hypoxia.

Altitudes at which athletes compete or train do usually not exceed 2000-2500 m. At these moderate altitudes acute mountain sickness (AMS) is mild, transient and affects at the most 25% of a tourist population at risk. Unpublished data included in this review paper demonstrate that more intense physical activity associated with high-altitude training or mountaineering does not increase prevalence or severity of AMS at these altitudes.

Transpulmonary plasma catecholamines in acute high-altitude pulmonary hypertension.

Objective: High altitude leads to an increase in sympathetic nervous system (SNS) activity and pulmonary arterial pressure (PAP). We assessed whether the SNS contributes to this increase in PAP.

Methods: Sympathetic discharge to the pulmonary vasculature was assessed by measuring plasma norepinephrine concentrations in central venous blood entering the lung and systemic arterial blood leaving the lung (arterial-central venous difference; a - cv(diff)).

High-altitude pulmonary hypertension is associated with a free radical-mediated reduction in pulmonary nitric oxide bioavailability.

High altitude (HA)-induced pulmonary hypertension may be due to a free radical-mediated reduction in pulmonary nitric oxide (NO) bioavailability. We hypothesised that the increase in pulmonary artery systolic pressure (PASP) at HA would be associated with a net transpulmonary output of free radicals and corresponding loss of bioactive NO metabolites. Twenty-six mountaineers provided central venous and radial arterial samples at low altitude (LA) and following active ascent to 4559 m (HA).