摘要：We tested the hypothesis that oral lactate supplementation increases mitochondrial enzyme activity given the potential role of lactate for inducing mitochondrial biogenesis. In this study, mice were assigned to a saline-ingested sedentary group (S S; n = 8), a lactate-ingested sedentary group (L S; n = 9), a saline-ingested training group (S T; n = 8), and a lactate-ingested training group (L T; n = 8). Mice in the S S and S T groups received saline, whereas mice in the L S and L T groups received sodium lactate (equivalent to 5 g/kg of body weight) via oral gavage 5 days a week for 4 weeks. At 30 min after the ingestion, mice in the S T and L T groups performed endurance training (treadmill running, 20 m/min, 30 min, 5 days/week). At 30 min after lactate ingestion, the blood lactate level reached peak value (5.8 ± 0.4 mmol/L) in the L S group. Immediately after the exercise, blood lactate level was significantly higher in the L T group (9.3 ± 0.9 mmol/L) than in the S T group (2.7 ± 0.3 mmol/L) (p < 0.01). Following a 4-week training period, a main effect of endurance training was observed in maximal citrate synthase (CS) (p < 0.01; S T: 117 ± 3% relative to S S, L T: 110 ± 3%) and cytochrome c oxidase (COX) activities (p < 0.01; S T: 126 ± 4%, L T: 121 ± 4%) in the plantaris muscle. Similarly, there was a main effect of endurance training in maximal CS (p < 0.01; S T: 105 ± 3%, L T: 115 ± 2%) and COX activities (p < 0.01; S T: 113 ± 3%, L T: 122 ± 3%) in the soleus muscle. In addition, a main effect of oral lactate ingestion was found in maximal COX activity in the soleus (p < 0.05; L S: 109 ± 3%, L T: 122 ± 3%) and heart muscles (p < 0.05; L S: 107 ± 3%, L T: 107 ± 2.0%), but not in the plantaris muscle. Our results suggest that lactate supplementation may be beneficial for increasing mitochondrial enzyme activity in oxidative phenotype muscle.
