Gut microbiota is involved in the development of several chronic diseases, including diabetes, obesity and cancer, through its interactions with the host organs. It has been suggested that the cross-talk between gut microbiota and skeletal muscle plays a role in different pathological conditions, such as intestinal chronic inflammation and cachexia. However, it remains unclear whether gut microbiota directly influences skeletal muscle function. In this work, we studied the impact of gut microbiota modulation on mice skeletal muscle function and investigated the underlying mechanisms. We determined the consequences of gut microbiota depletion after treatment with a mixture of broad spectrum antibiotics for 21 days and after 10-days natural reseeding. We found that in gut microbiota-depleted mice, running endurance was decreased, as well as the extensor digitorum longus muscle fatigue index in an ex vivo contractile test. Importantly, the muscle endurance capacity was efficiently normalized by natural reseeding. These endurance changes were not related to variation in muscle mass, fiber typology or mitochondrial function. However, several pertinent glucose metabolism markers such as ileum gene expression of short fatty acid chain and glucose transporters, Gpr41 and sglt1 and muscle glycogen level, paralleled the muscle endurance changes observed after ATB treatment and reseeding. As glycogen is a key energetic substrate for prolonged exercise, modulating its muscle availability via gut microbiota represents one potent mechanism that can contribute to the gut microbiota/skeletal muscle axis. Taken together, our results strongly support the hypothesis that gut bacteria are required for host optimal skeletal muscle function.

Virtual reality using head-mounted displays (HMD) could provide enhanced physical load during active gaming (AG) compared to traditional displays. We aimed to compare the physical load elicited by conventional exercise and AG with an HMD. We measured energy expenditure (EE) and heart rate (HR) in nine healthy men (age: 27 ± 5 years) performing three testing components in a randomised order: walking at 6 km/h (W6), AG, and AG with an additional constraint (AG^W; wrist-worn weights). Although we found that HR was not significantly different between W6 and the two modes of AG, actual energy expenditure was consistently lower in AG and AG^W compared to W6. We observed that playing AG with wrist-worn weights could be used as a means of increasing energy expenditure only at maximum game level, but ineffective otherwise. Our findings indicate that AG in an HMD may not provide a sufficient stimulus to meet recommended physical activity levels despite increased psychophysiological load. The differential outcomes of measures of HR and EE indicates that HR should not be used as an indicator of EE in AG. Yet, adding a simple constraint (wrist-worn weights) proved to be a simple and effective measure to increase EE during AG.

Physical inactivity increases the risk to develop type 2 diabetes, a disease characterized by a state of insulin resistance. By promoting inflammatory state, ceramides are especially recognized to alter insulin sensitivity in skeletal muscle. The present study was designed to analyze, in mice, whether muscle ceramides contribute to physical-inactivity-induced insulin resistance. For this purpose, we used the wheel lock model to induce a sudden reduction of physical activity, in combination with myriocin treatment, an inhibitor of de novo ceramide synthesis. Mice were assigned to 3 experimental groups: voluntary wheel access group (Active), a wheel lock group (Inactive), and wheel lock group treated with myriocin (Inactive-Myr). We observed that 10 days of physical inactivity induces hyperinsulinemia and increases basal insulin resistance (HOMA-IR). The muscle ceramide content was not modified by physical inactivity and myriocin. Thus, muscle ceramides do not play a role in physical-inactivity-induced insulin resistance. In skeletal muscle, insulin-stimulated protein kinase B phosphorylation and inflammatory pathway were not affected by physical inactivity, whereas a reduction of glucose transporter type 4 content was observed. Based on these results, physical-inactivity-induced insulin resistance seems related to a reduction in glucose transporter type 4 content rather than defects in insulin signaling. We observed in inactive mice that myriocin treatment improves glucose tolerance, insulin-stimulated protein kinase B, adenosine-monophosphate-activated protein kinase activation, and glucose transporter type 4 content in skeletal muscle. Such effects occur regardless of changes in muscle ceramide content. These findings open promising research perspectives to identify new mechanisms of action for myriocin on insulin sensitivity and glucose metabolism.