Duchenne muscular dystrophy (DMD) is a genetic disease caused by a mutation in the dystrophin gene, leading to the absence of the structural protein – dystrophin. Patients have severe muscle weakness and die prematurely due to respiratory and cardiac failure. The mdx mouse, a model of DMD shows evidence of reduced normoxic ventilation and impaired respiratory muscle function at 8 weeks of age. 6 week old mdx (C57BL/10ScSn-Dmdmdx/J; n=24) and wild-type (WT; C57BL/10ScSn; n=23) mice received either saline (0.9% w/v) or a co-treatment of neutralizing IL-6 receptor antibodies (xIL-6R; 0.2 mg/kg) and corticotrophin releasing factor 2 receptor agonist (Urocortin-2; 30μg/kg). Animals received 6 subcutaneous injections over 2 weeks. Following this, sternohyoid muscle (pharyngeal dilator) contractile function was examined ex vivo. Muscle fibre nucleation and inflammatory cell infiltration were examined by Haematoxylin and Eosin staining. Fibre type analysis of cross-sectional area (CSA) and areal density was determined by myosin heavy chain (MHC) immunofluorescence. Values are reported as mean±SEM and data were statistically compared by two-way ANOVA with Bonferroni post-hoc test. Peak specific force (Fmax) was significantly reduced in mdx (4.3±0.5 N/cm2) compared with WT (7.7±0.6). Co-treatment restored Fmax for mdx (8.0±0.9) to values equivalent to WT. In addition, co-treatment restored mechanical power production over the load continuum in mdx sternohyoid muscle. The percentage of centrally-nucleated muscle fibres was significantly increased in mdx (25±1%) compared with WT (0.5±0.1%). The areal density of inflammatory cell infiltrates was significantly increased (5±1% vs. 0.9±0.1%; mdx vs. WT). Both indices were unaffected by drug co-treatment. Fibre type transitions were apparent in the mdx sternohyoid muscle. The areal density of MHCIIx fibres was significantly increased (31±2% vs. 20±2%; mdx vs. WT), whereas MHCIIb fibres was significantly decreased compared with WT (52±2 vs. 62±2%; mdx vs. WT). Fibre transitions were ameliorated by co-treatment. Improved force in mdx co-treated sternohyoid was not related to fibre hypertrophy. Co-treatment had a positive inotropic effect, restoring mechanical force and power in dystrophic sternohyoid muscle. Co-treatment reversed fibre transitions in mdx but did not affect the infiltration of inflammatory cells or the proportion of fibres with evidence of central nucleation. Preservation of MHCIIb fibres may underpin, at least in part, recovery of force production in the mdx co-treated mice. These data may have implications for the development of pharmacotherapies for DMD with relevance to respiratory muscle performance.