Effects of High Altitude

This chapter discusses the effects of high altitude and autonomic nervous system and altitude illness. Ascent to high altitude reduces the inspired partial pressure of oxygen, leading to hypobaric hypoxia. The main oxygen sensors involving the autonomic nervous system response are the peripheral chemoreceptors, located in the carotid body and in the arch of the aorta. The baroreflexes remain able to maintain adequate cardiovascular modulation during chemoreflex activation. Other climbers unable to reach extreme altitudes were characterized by higher ventilatory responses and higher sympathetic activation. Peripheral vasodilation, in addition to increase in heart rate and cardiac output causes a remarkably effective redistribution of flow to vascular beds with the greatest metabolic demand, similar to the response seen during physical exercise. At the moment it remains accepted that adrenaline increases predominantly in the early phases of exposure to high altitude, whereas noradrenaline predominates after several days of exposure. Although complete inability to increase ventilation in response to hypoxia is generally admitted as a contraindication to travel to high altitude, the extent of these autonomic or ventilatory responses are not directly proportional to performance at high altitude.