INTRODUCTION: Cocoa flavanols have been shown to improve muscle function1 and exercise capacity2 and thus may offer a novel approach to protect against muscle atrophy. However, whether cocoa flavanols directly protect against atrophic conditions remains to be determined. (-)-Epicatechin (EPI) is the primary bioactive compound of cocoa flavanols, but it has a poor bioavailability and is ultimately metabolised into smaller bioactive compounds3. Hippuric acid (HA) is a colonic metabolite of EPI that is present in circulation from 12-48h3 following cocoa ingestion and may be responsible for the associations between chronic cocoa supplementation and muscle metabolic alterations.  OBJECTIVE: Accordingly, we investigated the effects of EPI and HA upon skeletal muscle morphology and metabolism within an in vitro model of skeletal muscle atrophy.  METHODS: Differentiated C2C12 myotubes were exposed to 24h ± dexamethasone (DEX; 100 μM) to create ± atrophic conditions. To examine whether cocoa flavanol compounds confer protection against dexamethasone-induced atrophy, cells were concomitantly co-incubated with one of the following treatments: vehicle control (VC), EPI (25 μM) or HA (25 μM). Following the 24h treatment, myotube diameter was assessed using fluorescence microscopy and analysed using a two-factor mixed model ANOVA (n = 5). To assess basal and leucine (LEU)-stimulated myotube protein synthesis (MPS) using the surface sensing of translation technique, cells underwent a further 90-min incubation period with LEU (5 mM) or a volume-matched control. MPS data are presented as fold change relative to control conditions (VC, no DEX) and were analysed using a 3-factor mixed model ANOVA (n = 6). Data are presented as mean ± SEM.  RESULTS: Under atrophy-inducing conditions (DEX), myotube diameter was significantly greater in HA (11.19 ± 0.39 μm) and EPI (11.01 ± 0.21 μm) treated cells compared to the VC (7.61 ± 0.16 μm, both P<0.001).  In basal and LEU-stimulated MPS measurements, there was a significant reduction in MPS rates following DEX-treatment in VC (fold change: 0.62 ± 0.07, P=0.024). Interestingly, concomitant treatment with EPI (fold change: 0.89 ± 0.16, P=0.148) and HA (fold change: 1.34 ± 0.40, P=0.205) abrogated the dexamethasone-induced reductions in MPS rates.   CONCLUSION: EPI and HA exerted anti-atrophic effects on skeletal muscle cells. Accordingly, our data suggests that HA could be partly responsible for the association between cocoa flavanols and skeletal muscle cellular metabolism and highlights the importance of colonic metabolites in the association between flavanol supplementation and health.