Abstract

To determine the effect of hypoxia on lactate threshold (LT), onset of blood lactate accumulation (OBLA), and gas exchange threshold (GET), the lactate level together with VO2, VCO2, VE, and acid-base status in arterial blood from 12 female distance runners performing a progressive incremental treadmill test under the condition of hypoxic gas inhalation (HC: FIO2 is 16.0% in N2) compared with normoxic conditions (NC: FIO2 is 20.9%; i.e., air) were examined. During exercise, HC shifted LT, GET, and OBLA to a lower VO2 by 12.5%, 12.9%, and 9.3%, respectively. The GET during hypoxic exercise was well correlated with LT (GET = 0.973LT + 0.04; expressed in VO2 l.min-1). The close reciprocal changes in arterial blood lactate and bicarbonate (HCO3-) were observed during hypoxic as well as normoxic exercise. These findings provide evidence for the cause and effect relationship between LT and GET, even in hypoxic exercise. During submaximal exercise below the LT, PaCO2 and HCO3- slightly increased both in NC and HC with pH remaining unchanged. However, during exercise above the LT, the PaCO2, HCO3-, and pH all decreased with pH decreasing more markedly during hypoxia. In conclusion, this study demonstrated a clear increase in arterial lactate during hypoxic exercise above the LT. Both the LT and GET are shifted to a lower work rate by hypoxia in the same manner with the correlation between them remaining high, supporting the cause and effect relationship of these two parameters.

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