Effect of Oral Lactate Administration on Skeletal Muscle Mass in Mice Under Different Loading Conditions

Background/aim: Lactate is a physiologically active substance secreted by skeletal muscle that has been suggested to stimulate muscle mass gain. However, the molecular mechanism for lactate-associated muscle hypertrophy remains unclear. The purpose of the present study was to investigate whether oral administration of lactate increases muscle mass under different loading conditions.

Materials and methods: Male C57BL/6J mice were divided into 1) control, 2) lactate, 3) unloading, 4) unloading with lactate, 5) reloading after unloading, and 6) reloading after unloading with lactate groups. Mice in the unloading and reloading after unloading groups were subjected to hindlimb suspension (HS) for two weeks and 2-week ambulation recovery after HS, respectively. Mice of the lactate groups were orally administered sodium lactate five days per week. The changes in muscle mass (muscle weight and protein content) and intracellular signals in fast plantaris and slow soleus muscles were evaluated.

Results: Oral administration of lactate increased the muscle mass and suppressed 5'AMP-activated protein kinase (AMPK) phosphorylation in both plantaris and soleus muscles under normal weight-bearing and unloading conditions. However, during reloading after unloading, lactate administration increased muscle mass and suppressed AMPK phosphorylation in the plantaris muscle, but not in the soleus muscle.

Conclusion: Lactate administration is an effective countermeasure for unloading-associated skeletal muscle atrophy. This anabolic effect of lactate on skeletal muscle mass may differ depending on muscle types.