Effects of acute simulated altitude on the maximal lactate steady state in humans

Abstract

We sought to determine the effects of acute simulated altitude on the maximal lactate steady state (MLSS) and physiological responses to cycling at and 10 W above the MLSS-associated power output (PO) (MLSSp and MLSSp+10, respectively). Eleven (4 female) participants (mean [SD]; 28 [4] years; V̇O2max: 54.3 [6.9] mL×kg-1×min-1) acclimatized to ~1100 m performed 30-min constant PO trials in simulated altitudes of 0 m (SL), 1111 m (MILD), and 2222 m (MOD). MLSSp, defined as the highest PO with stable (<1mM change) blood lactate concentration ([BLa]) between 10 and 30 min, was significantly lower in MOD (209 [54] W) compared to SL (230 [56] W; p<0.001) and MILD (225 [58] W; p=0.001), but MILD and SL were not different (p=0.12). V̇O2 and V̇CO2 decreased at higher simulated altitudes due to lower POs (p<0.05), but other end-exercise physiological responses (e.g., [BLa], ventilation (V̇E), heart rate (HR)) were not different between conditions at MLSSp or MLSSp+10 (p>0.05). At the same absolute intensity (MLSSp for MILD), [BLa], HR, and V̇E and all perceptual variables were exacerbated in MOD compared to SL and MILD (p<0.05). Maximum voluntary contraction, voluntary activation, and potentiated twitch forces were exacerbated at MLSSp+10 relative to MLSSp within conditions (p<0.05); however, condition did not affect performance fatiguability at the same relative or absolute intensity (p>0.05). As MLSSp decreased in hypoxia, adjustments in PO are needed to ensure the same relative intensity across altitudes, but common indices of exercise intensity may facilitate exercise prescription and monitoring in hypoxia.