In a recent study (Perez et al. 2013), we showed that treating mammalian skeletal muscle fibres with low doses of glucocorticoids (GCs; =stress hormones) increases the maximum isometric force developed by slow-twitch fibres without significantly affecting that of the fast-twitch fibres. The increase in force occurred within 10 minutes and was insensitive to the transcriptional inhibitor, actinomycin D. In contrast, it was blocked by the glucocorticoid receptor (GCR; GR) inhibitor, RU486 and a monoclonal anti-GCR (Perez et al. 2013). From these results, we suggest that the increase in force was non-genomic and that it was mediated by a membrane (m) GCR. However, in that study the cellular signalling events activated by the GCs (and hence likely to mediate the increase in force) were never investigated.In this study, we extended these findings by investigating the effects of treating small skeletal muscle fibre bundles with physiological concentrations of beclomethasone diproprionate (BDP; a synthetic GC commonly used in the management of asthma) on the phosphorylation (=activation) of various mitogen-activated protein kinases (MAPKs). The fibre bundles used were isolated from the extensor digitorum longus (EDL; a fast-twitch muscle) and soleus (a slow-twitch muscles) muscles of adult CD1 mice killed as recommended in UK legislation (for summary of the legislation see Drummond, 2009). The fibre bundles were then treated with 250nM BDP for 5 or 10 minutes with or without pre-incubation with inhibitors of the GCR or focal adhesion kinase (FAK). They were then processed for immunoblotting and the activation of c-Jun N-terminal kinase (JNK; stress-activated protein kinase), p38 kinases and extracellular-signal regulated kinase (ERK) 1 and 2 were investigated. The results show that treating the muscle fibre bundles with 250nM BDP increases the activation of all the kinases except ERK 1 and 2. Thus, BDP increased the phosphorylation of JNK 1&2 and p38 kinases at both 5 and 10 minutes but not at 1hr. Moreover, the activation of these kinases was inhibited by pre-treating the muscle fibre bundles with the GCR inhibitor, RU486 and the focal adhesion kinase (FAK) inhibitor 14. From these results we suggest that the non-genomic effects of GCs in mammalian skeletal muscle fibres are mediated by the GCR and involve the activation of MAPKs by FAK.