Lactate is oxidized as an energy fuel during exercise, and it also plays a key role in the regulation of glycogen synthesis in the muscles and liver after exercise. Previous studies have suggested that lactate is converted to glycogen and stimulates glycogen synthesis. However, it remains unclear whether chronic post-exercise lactate administration can increase glycogen storage in skeletal muscle. We examined whether 3 wk of chronic post-exercise lactate administration with training can increase muscle glycogen storage and whether such changes are associated with monocarboxylate transporter 1 (MCT1) protein expression in mice. Mice were assigned to receive saline with training (SA+T group; n=6) or lactate with training (LA+T group; n=6). All mice performed 40 min of treadmill running at 25 m/min, following which they received saline or lactate (2.5 mg/g body weight), 6 d/wk for 3 wk. After 3 wk, glycogen concentration at rest was higher in the white tibialis anterior (TA; p<0.05, +34%), but not in the red TA, in the LA+T group. Protein expression of MCT1, the primary lactate transporter, was increased with chronic post-exercise lactate administration in the white TA (p<0.05, +32%), but not in the red TA. MCT1 protein expression was significantly correlated with muscle glycogen concentration in the red and white TA in both groups (p<0.05, r=0.969). These results suggest that chronic lactate administration after exercise increases MCT1 protein expression, which can be involved in the regulation of the observed increase in muscle glycogen storage after exercise training.