Oral Lactate Administration Additively Enhances Endurance Training-Induced Increase in Cytochrome C Oxidase Activity in Mouse Soleus Muscle

Abstract

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.

Keywords: lactate; mitochondria; monocarboxylate transporter; skeletal muscle.

Figure 1

Blood lactate concentration following lactate ingestion during sedentary period (A). Blood lactate concentration immediately after the exercise (B). Data are presented as means ± SEM (n = 8).

Figure 2

Maximal activities of CS (A, C, E) and COX (B, D, F) in the plantaris muscle (A, B), the soleus muscle (C, D), and the heart muscle (E, F) following 4-week lactate ingestion. Data are presented as means ± SEM (n = 8–9). ** p < 0.01: main effect of endurance training. ^† p < 0.05: main effect of lactate ingestion.

Figure 3

Protein contents of MCT1 (A, C) and MCT4 (B, D) in the plantaris muscle (A, B) and the soleus muscle (C, D) following 4-week lactate ingestion. Data are presented as means ± SEM (n = 8–9). * p < 0.05: main effect of endurance training.

Figure 4

Phosphorylation of intramuscular signaling kinases in the plantaris 60 min after lactate ingestion (i.e., immediately after the exercise). Data are presented as means ± SEM (n = 8). * p < 0.05, ** p < 0.01: main effect of endurance exercise.

Figure 5

Phosphorylation of intramuscular signaling kinases in the soleus muscle 60 min after lactate ingestion (i.e., immediately after exercise). Data are presented as means ± SEM (n = 8). * p < 0.05, ** p < 0.01: main effect of endurance exercise.