Effect of Lactate Intake on Total Fat Mass and Resting Metabolic Rate in Mice.

Lactate, once considered a "metabolic end-product", is now recognized as an important substrate for energy metabolism as pathways for reuse as an energy source have been revealed. In a previous study, it was investigated that the intake of lactate at rest increases the activation of oxidative phosphorylation factors (pyruvate dehydrogenase, cluster of differentiation 36). In addition, it was investigated through respiratory gas, glycogen contents, and glycolysis-related factor (hexokinase 2) that intake of lactate before exercise increases carbohydrate oxidation in during exercise. However, in the previous studies were the result of acute treatment and did not investigate the effect of long-term lactate intake on energy metabolism. Therefore, the purpose of this study is to investigate the effect of 5 weeks of exercise and lactate intake on body metabolism. The male 8-week-old ICR mice were randomly divided into 4 groups. Con (sedentary; non-trained), Lac (sedentary; non-trained and lactate intake), EX (moderate intensity-trained), and EXLA (moderate intensity-trained and lactate intake). All groups were fed ad libitum and were administered 3 g/kg of saline and sodium lactate after training. Treadmill training was conducted with 5 times a week for 5 weeks, and the exercise intensity was 70 % of VO max. After 5 weeks, the resting metabolic rate (RMR) was measured for all groups through respiratory gas, and adipose tissue was collected. Long-term lactate intake did not show any significant difference in body fat mass in both the sedentary and trained groups. However, the total body fat mass was higher in Con, and Lac and EX tended to be lower than those of Con, but there was no significant difference. Interestingly, in the RMR results, total energy expenditure (EE) did not significantly difference in all groups, but fat oxidation (FO), the sedentary group was significantly higher than the trained group (p=0.001), and carbohydrate oxidation it was significantly lower (p=0.001). In addition, FO showed a higher tendency for Lac than Con within sedentary (p=0.077), although not statistically significant, and there was no significant difference within the trained group. In summary, these results showed the possibility that long-term intake of lactate can influence body fat loss by increasing fat oxidation. In addition, the body fat loss according to the intake of lactate is consistent with EX, and this seems to be due to the increase in fat oxidation at rest. Total body fat mass of Lac showed a tendency to be lower than that of Con, and was almost the same as that of EX. This seems to be due to the accumulation of increased fat oxidation in RMR results. The reduction in fat mass in the trained groups appears to be a reduction in fat mass due to exercise, when inferred from the RMR results. Therefore, to confirm the change more clearly in body fat mass following lactate intake and exercise treatment in the future, it is necessary to reconfirm through a longer-period of study.