Abstract

Although endurance training (ET) and calorie restriction (CR) induce metabolic adaptations in skeletal muscle, the interaction of them have yet to be clarified. This study investigated the effects of endurance training with calorie restriction on the metabolic enzyme activity and transporter levels in mouse skeletal muscle and liver. Ten-week-old male ICR mice were fed ad libitum or subjected to 30% CR. The animals were subdivided into sedentary and ET groups. The animals in the ET group performed treadmill running (20 m/min, 30 min) five days a week for five weeks. Respiratory gas analysis during 24 h of rest showed that CR, but not ET, reduced carbohydrate consumption. While ET enhanced hexokinase (HK) activity in the plantaris and soleus muscles, CR decreased HK, phosphofructokinase, and lactate dehydrogenase activities and monocarboxylate transporter (MCT) 4 protein content. Although ET and CR alone increased citrate synthase (CS) activity and MCT1 protein content in the plantaris muscle, no additive or synergistic effects were observed. In the soleus muscle, ET increased CS, β-hydroxyacyl-CoA dehydrogenase (β-HAD), and total carnitine palmitoyltransferase (CPT) activities; however, CR significantly decreased CS and β-HAD activities but enhanced total CPT activity. Additionally, CR enhanced the glucose transporter 4 protein content in the plantaris and soleus muscles. In the liver, CR enhanced the protein levels of glucose 6-phosphatase, fructose 1,6-bisphosphatase, and mitochondrial phosphoenolpyruvate carboxykinase. Moreover, ET partially normalized the CR-induced increase in fatty acid synthase and acetyl-CoA carboxylase. These observations suggest that CR enhances the capacity for glucose and fatty acid synthesis in the liver as well as the glucose and lactate uptake capacity in skeletal muscle while reducing carbohydrate consumption in skeletal muscle. It is suggested that CR partially interferes with skeletal muscle adaptations to ET. This study was supported by the Japan Society for the Promotion of Science (JSPS) KAKENHI (Grant numbers 20H04071, 21K21249, and 23K16718). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

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