The purpose of this study was to examine the effects of
respiratory alkalosis on human skeletal muscle metabolism at rest and during submaximal exercise. Subjects exercised on two occasions for 15 min at 55 % of their maximal
oxygen uptake while either hyperventilating (R-Alk) or breathing normally (Con). Muscle biopsies were taken at rest and after 1 and 15 min of exercise. At rest, no effects on muscle metabolism were observed in response to R-Alk. In the first minute of exercise, there was a delayed activation of
pyruvate dehydrogenase (PDH) in R-Alk compared with Con, resulting in a reduced rate of
pyruvate oxidation. Also, glycogenolysis was higher in R-Alk compared with Con, which was attributed to a higher availability of the monoprotonated form of
inorganic phosphate (P(i)), resulting in an elevated rate of
pyruvate production. The mismatch between
pyruvate production and its oxidation resulted in net
lactate accumulation. These effects were not seen after 15 min of exercise, with no further differences in muscle metabolism between conditions. The results from the present study suggest that
respiratory alkalosis may play an important role in
lactate accumulation during the transition from rest to exercise in acute hypoxic conditions, but that other factors mediate
lactate accumulation during steady-state exercise.