Lactate administration does not affect denervation‐induced loss of mitochondrial content and muscle mass in mice

Lactate is considered to be a signaling molecule that induces mitochondrial adaptation and muscle hypertrophy. The purpose of this study was to examine whether lactate administration attenuates denervation‐induced loss of mitochondrial content and muscle mass. Eight‐week‐old male Institute of Cancer Research mice underwent unilateral sciatic nerve transection surgery. The contralateral hindlimb served as a sham‐operated control. From the day of surgery, mice were injected intraperitoneally with PBS or sodium lactate (equivalent to 1 g·kg−1 body weight) once daily for 9 days. After 10 days of denervation, gastrocnemius muscle weight decreased to a similar extent in both the PBS‐ and lactate‐injected groups. Denervation significantly decreased mitochondrial enzyme activity, protein content, and MCT4 protein content in the gastrocnemius muscle. However, lactate administration did not have any significant effects. The current observations suggest that daily lactate administration for 9 days does not affect denervation‐induced loss of mitochondrial content and muscle mass. Lactate is considered to be a signaling molecule that induces mitochondrial adaptation and muscle hypertrophy. This study examined effects of lactate administration on denervation‐induced loss of mitochondrial content and skeletal muscle mass. The results showed that neither mitochondrial content nor skeletal muscle mass during 10 days of denervation was changed by lactate administration.