Lactate Entrance into the Brain is Necessary for Endurance Exercise-Induced Adaptation in Lipid Oxidation

Lactate has been recently considered as a signaling factor involved in metabolism. The aim of this study was to investigate the role of lactate entrance into the brain on endurance training-induced adaptations in lipid oxidation.  24 male rats (age: 8 weeks, weight: 197 ± 21 g) were divided into control (C), trained (T), and traind+4-CIN (T+4-CIN, which experienced the inhibition of lactate entrance into the brain during exercise). All animals performed a single session of acute endurance exercise following their 12-weeks training protocol.  Free fatty acids (FFA) and triglyceride content in plasma and adipose tissue and cAMP and Inositol triphosphate (PI3) content in epididymal fat were measured immediately after acute exercise using ELISA and were compared among the groups by one-way analysis of variance (ANOVA). Acute exercise significantly increased lactate concentration in cerebrospinal fluid (SCF) in both T and T+4-CIN compared to the C group. Lactate concentration was slightly lower in T + 4-CIN compared to the T.  Immediately after acute endurance training, a significant decrease of 61 and 31% in plasma triglyceride levels, a significant decrease of 39 and 26% in adipose tissue triglyceride levels, a significant increase of 125 and 56% in plasma FFA levels, a significant increase of 217 and 125% increase in FFA plasma levels, a significant increase of 87 and 41% in adipose tissue cAMP levels, and a significant increase of 90 and 49% in adipose tissue inositol triphosphate levels was observed in the T and T+4-CIN compared to the control group, respectively (all P < 0.01). Plasma triglyceride and adipose tissue levels in the 4-CIN + training group were significantly higher and plasma and adipose tissue FFA levels were significantly lower (all P < 0.05) than the values found in the T group.  In conclusion, the results of the present study showed that lactate can be effective on endurance training-induced adaptations in lipid oxidation due to its action in the brain.