Since endothelium-derived relaxing factor (EDRF) was identified as nitric oxide (NO), numerous studies have been performed for determining the cellular origin and the physiological role of NO. Up to now, it has been reported that various kinds of cells, including endothelium, neuron, mucosal epithelium, smooth muscle, skeletal muscle and macrophage can generate NO, and this endogenous NO has wide physiological roles, such as control of vascular tone, neurotransmission, host defense, etc. On the other hand, high altitude training has been used for the improvement of aerobic work capacity in various kinds of athletic sports, such as marathoning, swimming, skating and bicycling. It has been found that a hypoxia induces pulmonary vasoconstriction, and that endothelium derived NO reduces pulmonary vasoconstriction.
　In the present study, therefore, the effect of high-altitude training both on the NO production in the exhaled air during ramp exercise in humans, and on the pulmonary circulation and an isolated vascular reaction to vasoconstrictor agents in rats were investigated.
　High altitude training for 5 weeks improved arterial oxygenation during inhalation of hypoxic gas at rest, but induced no significant change in VO₂, VE and exhaled NO output (VNO) during ramp exercise in humans. In the animal study, a normoxic running training or a hypoxic running training could reduce pulmonary blood pressure to exercise or hypoxia. The constrictor tone of the isolated pulmonary artery to vasoconstrictor agents was reduced in hypoxic running trained rats.
　It suggests that running training or hypoxic running training could improve pulmonary vasoconstriction to exercise or hypoxia. However, exhaled NO output may not reflect the pulmonary vasodilator activity of NO.

DESCENTE SPORTS SCIENCE Vol.19/THE DESCENTE AND ISHIMOTO MEMORIAL FOUNDATION FOR THE PROMOTION SPORTS SCIENCE