LACTATE EFFLUX FROM EXERCISING HUMAN SKELETAL-MUSCLE - ROLE OF INTRACELLULAR PO-2

It remains controversial whether lactate formation during progressive dynamic exercise from submaximal to maximal effort is due to muscle hy poxia. To study this question, we used direct measures of arterial and femoral venous lactate concentration, a thermodilution blood flow tec hnique, phosphorus magnetic resonance spectroscopy (MRS), and myoglobi n (Mb) saturation measured by H-1 nuclear MRS in six trained subjects performing single-leg quadriceps exercise. We calculated net lactate e fflux from the muscle and intracellular Po-2 with subjects breathing r oom air and 12% O-2. Data were obtained at 50, 75, 90, and 100% of qua driceps maximal O-2 consumption at each fraction of inspired O-2. Mb s aturation 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 Po, at which 50% of Mb-binding sites ar e bound with O-2 of 3.2 Torr, Mb-associated Po-2 averaged 3.1 +/- 0.3 and 2.3 +/- 0.2 Torr in normoxia and hypoxia, respectively. Net blood lactate efflux was unrelated to intracellular Po, across the range of incremental exercise to maximum (r = 0.03 and 0.07 in normoxia and hyp oxia, respectively) but linearly related to O-2 consumption (r = 0.97 and 0.99 in normoxia and hypoxia, respectively) with a greater slope i n 12% O-2. Net lactate efflux was also linearly related to intracellul ar 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 i nspired O-2, lactate efflux is unrelated to muscle cytoplasmic Po-2, y et the efflux is higher in hypoxia. Catecholamine values from comparab le studies are included and indicate that lactate efflux in hypoxia ma y be due to systemic rather than intracellular hypoxia.