Abstract

Lactate is considered as not only an oxidizable fuel, but also a signal molecule inducing mitochondrial biogenesis. In this study, we hypothesized that lactate administration prior to training augments mitochondrial adaptations. ICR male mice were randomly assigned to Con (n=9), Tr (n=7) or La+Tr (n=8) group. Mice in Tr and La+Tr were performed treadmill running (20 m/min, 60 min) immediately after administration of PBS (same volume as lactate) or sodium lactate (1 mg/g BW) via i.p. injection for 21 consecutive days. Mice in Con were administrated same volume of PBS on the same days. All the mice were performed lactate tolerance test (LTT: i.p. injection of 1 mg/g BW of sodium lactate) 24h after final training. Blood samples were collected pre, 5, 15, 30, 60 and 180 minutes after the lactate administration. Soleus and plantaris muscle were taken for the biochemical analysis 24h after LTT. As a result, some mitochondrial enzyme activities in soleus and plantaris muscle were significantly higher in La+Tr than Tr (CS: P<0.05, β‐HAD: P=0.05, COX: P<0.01 in soleus, CS: n.s., β‐HAD: n.s., COX: P<0.05 in plantaris). However, mitochondrial OXPHOS protein content was not different between Tr and La+Tr. MCT1 protein content was significantly higher in La+Tr than Con (+18%; P<0.01) in plantaris muscle, but not MCT4. As a result of LTT, blood lactate concentrations after lactate administration were significantly lower in Tr (60 min: P<0.05 vs. Con) and La+Tr (30 min: p<0.01, 60 min: P<0.01 vs. Con) than Con. These data indicate that lactate upregulates mitochondria functionally, and that lactate administration increased MCT1 protein content leading to lower blood lactate concentration after lactate administration.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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