Lactate efflux from exercising human skeletal muscle: role of intracellular P O 2

Abstract

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 1 H nuclear MRS in six trained subjects performing single-leg quadriceps exercise. We calculated net lactate efflux from the muscle and intracellular[Formula: see text] with subjects breathing room air and 12% O 2 . Data were obtained at 50, 75, 90, and 100% of quadriceps maximal O 2 consumption at each fraction of inspired O 2 . 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[Formula: see text] at which 50% of Mb-binding sites are bound with O 2 of 3.2 Torr, Mb-associated [Formula: see text] averaged 3.1 ± 0.3 and 2.3 ± 0.2 Torr in normoxia and hypoxia, respectively. Net blood lactate efflux was unrelated to intracellular[Formula: see text] across the range of incremental exercise to maximum ( r = 0.03 and 0.07 in normoxia and hypoxia, respectively) but linearly related to O 2 consumption ( r = 0.97 and 0.99 in normoxia and hypoxia, respectively) with a greater slope in 12% O 2 . 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 O 2 , lactate efflux is unrelated to muscle cytoplasmic [Formula: see text], 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.