Peripheral lactate and oxygen metabolism in man: The influence of oral glucose loading

We investigated the influence of oral glucose loading (100 g) on glucose, lactate, and oxygen metabolism by deep (mainly muscle) and superfician (mainly skin and adipose tissue) forearm tissues. In normal men aged 19 to 32 years (mean ± SE, 24 ± 1), basal arterialized venous-deep venous (A-DV) and arterialized venous-superficial venous (A-SV) plasma glucose concentration differences were 4.1 ± 1.0 (P < 0.001) and 4.7 ± 1.0 (P < 0.005) mg/dL, respectively, but increased markedly following glucose loading. During the first, second, and third hours after glucose ingestion, A-DV differences were 54 ± 6, 43 ± 3, and 20 ± 4 mg/dL, respectively, while the corresponding A-SV differences were 39 ± 4, 17 ± 2, and 8 ± 2 mg/dL, respectively. Forearm glucose uptake by deep (FGU-D) and superficial (FGU-S) tissues basally was 0.057 ± 0.010 and 0.012 ± 0.002 mg100 mL forearm/min respectively. From 15 to 180 minutes after glucose loading, mean FGU-D and FGU-S rose to 0.524 ± 0.083 and 0.056 ± 0.006 mg100 mL forearm/min, respectively. Basal A, SV, and DV lactate concentrations were 0.55 ± 0.04, 0.78 ± 0.03, and 0.57 ± 0.04 mmol/L, respectively (A-SV, P < 0.001; SV-DV, P < 0.001; A-DV, NS). Lactate production by superficial tissues (0.079 ± 0.015 μmol100 mL forearm min) accounted for 62% of concurrent FGU-S. After glucose loading the 2.2-fold rise in arterial lactate levels to a peak at 75 minutes was associated with a fall in net lactate output by superficial tissues (transiently to zero at 45 and 60 minutes) while in muscle lactate uptake was observed between 15 and 105 minutes. Basal A, SV, and DV oxygen levels were 8.21 ± 0.2, 5.62 ± 0.03, and 3.97 ± 0.03 mmol/L respectively (P < 0.001 for A-SV, A-DV, and SV-DV) and forearm oxygen uptake by deep and superficial forearm tissues was 6.61 ± 0.63 and 0.94 ± 0.12 μmol100 mL forearm/min, respectively. Of the latter, basal FGU-D and FGU-S could account for only 17% and 25% of corresponding oxygen utilization, respectively. Neither oxygen levels nor oxygen uptake by deep or superficial forearm tissues were altered by glucose loading. We reached the following conclusions: (1) striking differences exist between glucose, lactate and oxygen concentrations in A, SV, and DV blood before and after glucose loading, (2) in the basal state superficial tissues (presumably skin) are the major site of net forearm lactate release while muscle is the dominant site of oxygen consumption, (3) since after glucose loading, peripheral lactate output is decreased, the concurrent rise in arterial lactate levels may reflect increase splanchnic lactate production, and (4) because glucose ingestion is not accompanied by increased peripheral oxygen uptake, the known concurrent rise in whole body oxygen consumption may reflect enhanced splanchnic oxygen utilization.