This investigation assessed the course of renal compensation of hypoxia-induced respiratory alkalosis by elimination of bicarbonate ions and impairments in anaerobic exercise after different durations of hypoxic exposure. Study A: 16 participants underwent a resting 12-h exposure to normobaric hypoxia (3,000 m). Blood gas analysis was assessed hourly. While blood pH was significantly increased, po 2 , PCO 2 , and SaO 2 were decreased within the first hour of hypoxia, and changes remained consistent. A substantial reduction in [HCO 3 − ] levels was observed after 12 h of hypoxic exposure (− 1.35 ± 0.29 mmol/L, p ≤ 0.05). Study B: 24 participants performed in a randomized, cross-over trial portable tethered sprint running (PTSR) tests under normoxia and after either 1 h (n = 12) or 12 h (n = 12) of normobaric hypoxia (3,000 m). No differences occurred for PTSR-related performance parameters, but the reduction in blood lactate levels was greater after 12 h compared with 1 h (− 1.9 ± 2.2 vs 0.0 ± 2.3 mmol/L, p ≤ 0.05). These results indicate uncompensated respiratory alkalosis after 12 h of hypoxia and similar impairment of high-intensity exercise after 1 and 12 h of hypoxic exposure, despite a greater reduction in blood lactate responses after 12 h compared with 1 h of hypoxic exposure. Hypoxia has a profound influence on acid-base balance whenever unacclimatized people ascend to high altitudes. Barometric pressure decreases with increasing altitude and, therefore, oxygen pressure in the ambient and inspired air (P I O 2) falls 1. A reduced P I O 2 leads to a decrease in arterial oxygen partial pressure (PO 2) and to hypoxemia, which stimulates the peripheral chemoreceptors to evoke carbon dioxide (CO 2) washout 2-4. Concurrently, hyperventilation occurs as an hypoxic ventilatory response during acclimatization to high altitude, CO 2 partial pressure (PCO 2) falls, and arterial pH increases according to the Henderson-Hasselbalch equation 2, 5, 6. This respiratory alkalosis is subsequently compensated by increased renal elimination of bicarbonate ions (HCO 3 −), which results in a decrease in blood bicarbonate concentration [HCO 3 − ] and arterial pH returns to normal 2, 3, 5. Metabolic compensation of respiratory alkalosis occurs after 6 h of altitude exposure and is completed after 24 h at low to moderate altitude 2, 7. This compensation is further suggested to remain incomplete after 24 h of exposure to high altitude, but is then completed after several days 1, 2, 4, 7. In contrast, lowlanders show persistent alkalosis even after 9 weeks at 5,260 m 8. Nonetheless, to the best of our knowledge, information on values of pH and [HCO 3 − ] during the first 24 h of altitude exposure is still insufficient. [HCO 3 − ] is an essential blood buffer for metabolic acids. During maximal workloads with blood lactate levels up to 15 mmol/L, there is a corresponding decrease in plasma [HCO 3 − ] levels 9. Therefore, the resulting decline in [HCO 3 − ] and blood buffer capacity in the course of adaption to altitude might signific...