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Mirjam Jeanette Limmer, Markus de Marées, Petra Platen

• 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 \(\pm\) 0.29 mmol/L, \(\it p\) ≤ 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 (\(\it n\) = 12) or 12 h (\(\it n\) = 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 \(\pm\) 2.2 vs 0.0 \(\pm\) 2.3 mmol/L, \(\it p\) ≤ 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.