Benfotiamine Supplementation Increases Thiamine in Muscle of Endurance-Trained Mice and Affects the Energy Metabolism.

Abstract

Benfotiamine, a synthetic analog of thiamine, offers greater bioavailability compared to other thiamine salts and increases thiamine stores upon oral intake. Thiamine is essential for energy metabolism. This study aimed to evaluate the effects of oral benfotiamine supplementation on energy metabolism, particularly the Krebs cycle function, in the muscle of endurance-trained mice, and to assess its impact on endurance performance. Twenty-five mice were randomly assigned to four groups: a standard diet with sedentary behavior (Sta-Sed), a benfotiamine-supplemented diet with sedentary behavior (Ben-Sed), a standard diet with swimming training (Sta-Tr), and a benfotiamine-supplemented diet with swimming training (Ben-Tr). The trained groups underwent five weekly swimming sessions for six weeks, followed by an exhaustive test. Thiamine and its esters were measured in erythrocytes and gastrocnemius muscle. Gene expression of pyruvate dehydrogenase (PDHa) and alpha-ketoglutarate dehydrogenase (OGDH), along with levels of pyruvic, lactic, and hydroxybutyric acids in muscle, was analyzed. The benfotiamine-supplemented groups had higher thiamine levels in erythrocytes and muscles compared to the standard-diet groups. No differences were observed in PDHa and OGDH gene expression. The Ben-Tr group exhibited increased muscle lactic acid levels and a higher lactic acid to pyruvic acid ratio compared to the sedentary groups. Hydroxybutyric acid levels were also elevated in the Ben-Tr group. No significant differences in exhaustive test duration were found between the groups. Benfotiamine supplementation increases thiamine levels in erythrocytes and muscle but does not affect the gene expression of thiamine-dependent enzymes. Although it alters energy metabolism in trained muscle, it does not enhance endurance performance in mice.