One of the acute and chronic adaptations to altitude exposure is hypoxia, or the reduction in oxygen content of the air. This lowers the amount of oxygen bound to hemoglobin resulting in a decrease in arterial oxygen content of the blood. This results in hyperventilation to maintain alveolar PC02. The increased ventilatory drive potentiates the removal of C02 (respiratory alkalosis). In compensation, bicarbonate decreases through excretion of the kidney (renal diuresis), and thus dramatically reduces the buffering capacity of the blood. The increased ventilatory drives also decreases total body water through the loss of water vapor through respiration. The renal diuresis, coupled with increased evaporative cooling results in rapid dehydration during acute exposure to altitude, essentially because at lowers barometric pressures, water changes from a liquid to a gas more easily. Robergs (2003) reported that a loss of body fluids decreases blood volume, raises hematocrit and blood viscosity, which negatively impact the cardiovascular system

Resting and submaximal cardiac output also increase with acute exposure. The reduced concentration of arterial blood lowers to effective diffusion gradient of oxygen at the tissues, despite an increase in 2,3 DPG, AV02 difference decreases. In order to maintain V02, heart rate increases (Wolfel 1991). Stroke volume decreases due to an increase in peripheral resistance and increase in catecholamines, which further increase heart rate. Heart increases to maintain cardiac output response.

Blood pressure also increases in the acute stage of altitude due to an increase vascular resistance. This is due to an increase in blood viscosity which is due to an increase in hematocrit and catecholamine production. Blood viscosity increases due to an increase in red blood cell production and decrease in plasma volume (Brooks 2005).

Hematocrit and hemoglobin have been shown to increase very rapidly in the initial hours of acute altitude. The stimulation of red blood cells occurs as the P02 sensitive cells of the kidneys stimulate the release of erythropoietin. Although it is not known the exact altitude which this occurs, it is known the length of exposure is important as oxygen saturation below 85% still need a couple of hours before there is a detectable increase in EPO. Due to the decrease in plasma volume and a lag between EPO secretion and red blood cell production, the true initial increase in hematocrit and hemoglobin actually occur after approximately 3-4 days of exposure.

In addition, high altitude illness may also occur such as Acute Mountain Sickness (AMS). The common mechanism underlying AMS is that at lower barometric pressures and a reduced partial pressure results in a lower arterial P02 (Bartsch and Saltin 2008). However, the exact mechanisms (AMS and High Altitude Cerebral Edema, or HACE) are not entirely clear but are likely due to swelling of the central nervous system. The minimum occurrence threshold is approximately 8000 feet (Cheung 2010). Although individual variability exists, symptoms include headache, fatigue, shortness of breath (dyspnea),hyperventilation, insomnia, and loss of appetite.