Lactate efflux from exercising human skeletal muscle: role of intracellular PO2.

It remains controversial whether lactate formation during progressive dynamic exercise from submaximal to maximal effort is due to muscle hypoxia. To study this question, we used direct measures of arterial and femoral venous lactate concentration, a thermodilution blood flow technique, phosphorus magnetic resonance spectroscopy (MRS), and myoglobin (Mb) saturation measured by 1H nuclear MRS in six trained subjects performing single-leg quadriceps exercise. We calculated net lactate efflux from the muscle and intracellular PO2 with subjects breathing room air and 12% O2. Data were obtained at 50, 75, 90, and 100% of quadriceps maximal O2 consumption at each fraction of inspired O2. Mb saturation was significantly lower in hypoxia than in normoxia [40 +/- 3 vs. 49 +/- 3% (SE)] throughout incremental exercise to maximal work rate. With the assumption of a PO2 at which 50% of Mb-binding sites are bound with O2 of 3.2 Torr, Mb-associated PO2 averaged 3.1 +/- 0.3 and 2.3 +/- 0.2 Torr in normoxia and hypoxia, respectively. Net blood lactate efflux was unrelated to intracellular PO2 across the range of incremental exercise to maximum (r = 0.03 and 0.07 in normoxia and hypoxia, respectively) but linearly related to O2 consumption (r = 0.97 and 0.99 in normoxia and hypoxia, respectively) with a greater slope in 12% O2. Net lactate efflux was also linearly related to intracellular pH (r = 0.94 and 0.98 in normoxia and hypoxia, respectively). These data suggest that with increasing work rate, at a given fraction of inspired O2, lactate efflux is unrelated to muscle cytoplasmic PO2, yet the efflux is higher in hypoxia. Catecholamine values from comparable studies are included and indicate that lactate efflux in hypoxia may be due to systemic rather than intracellular hypoxia.