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We examined the effects of endurance training with chronic pre-exercise concentrated Kurozu (black vinegar) supplementation on mitochondrial enzyme activity and energy metabolism in Institute of Cancer Research (ICR) mice. Mice were divided into a control group, an endurance training group, and an endurance training + concentrated Kurozu supplementation group. Mice were orally supplemented with water or concentrated Kurozu solution (500 mg/kg body weight/day) for 3 weeks. The mice in the training group were subjected to exercise on a treadmill (20–25 m/min × 30 min, five times/week) starting 30 min after the supplementation. The maximal activity of citrate synthase in the plantaris muscle in the endurance training + concentrated Kurozu supplementation group was significantly higher than that in the control group (p < 0.01). The maximal activity of β-hydroxyacyl coenzyme dehydrogenase (β-HAD) in the soleus muscle in the endurance training + concentrated Kurozu supplementation group was significantly higher than that in the other two groups (p < 0.05 for both). In the final week, significant negative correlation between blood lactate concentration after exercise and soleus β-HAD activity was observed. These findings suggest that endurance training with concentrated Kurozu supplementation increases mitochondrial enzyme activity and might enhance lipid metabolism during exercise.

We investigated the effects of chronic pre-exercise acetate administration on body weight and metabolic adaptations to endurance training in ICR mice fed with either a normal fat diet (NFD) or high fat diet (HFD), respectively. Mice were divided into a control group (Con), an acetate group (Ace), a training group (Tra), and an acetate+training group (Ace+Tra) with NFD or HFD, respectively. Mice received orally either water or acetate (72 mg/kg body weight/day) for 4 weeks. The mice in the training group were subjected to training using a treadmill (20–25 m/min×60 min, 5 times/week) immediately after administration. As a result, in the NFD mice, there was no effect of acetate in any of the measurements. In the HFD mice, the final body weight in the Ace, Tra and Ace+Tra groups was significantly lower than the Con group. Moreover, the acetate treatment tended to decrease blood glucose concentration at rest. Gastrocnemius muscle glycogen concentration in the Ace+Tra group was significantly higher than that of the Ace and Tra groups. Unexpectedly, a significant negative main effect of acetate treatment in the maximal activity of β-HAD was observed, though the endurance training increased enzyme activity of citrate synthase in the plantaris muscle. These findings show the possibility that acetate treatment with endurance training shifts the metabolic characteristics of mice toward a carbohydrate metabolism against a lipid metabolism with the HFD condition, but not with the NFD condition.