Granchilli et al. found a 24% increase in strength in mdx mice that were treated with 1mg/kg prednisone for 6 weeks and subjected to forced treadmill exercise for 30 min twice a week. These authors found that higher doses of prednisone were detrimental to strength. This result is consistent with our finding that 50-day treatment with 1mg/kg of GCs significantly improved normalized forelimb grip strength and that the rate of decline was slower than that in untreated mice, Acetrizoic acid suggesting the beneficial effects of drug treatment persist up to 100 days but become nonsignificant by 180 days. Granchelli and colleagues reported greater strength, decreased fatigue, and increased muscle fiber diameters in treated mice, suggesting a protective effect of GCs. In 2007, Golumbek et al. similarly described an improved performance per body weight and in running speed in mdx mice receiving GC treatment, but they also reported an incremental increase in the frequency of calcifications. Another study by Yang et al. examined the effect on diaphragm function of a 6-week treatment with methylprednisolone. They found a slight improvement in the contractile properties of the treated mice; however, they did not look at skeletal muscle function. The present study has shown that prolonged steroid use leads to decreased cardiac systolic function and increased cardiac fibrosis in mdx mice. These results are in agreement with those of Bauer et al., who found that 1.5 mg/kg/day prednisolone delivered via drinking water over 8 weeks in 4-month-old mdx mice resulted in increased left ventricular dilatation, decreased diastolic function, and increased cardiac fibrosis. Previous work from our laboratory has also demonstrated significantly decreased cardiac function and increased cardiac fibrosis in a subcutaneous, Xanthohumol continuous prednisone delivery protocol at a dose of 1 mg/kg/ day. Skrabek and Anderson treated 2- to 3-month-old mdx mice daily with intraperitoneal prednisone or deflazacort and found significantly decreased fibrosis only in the high-dose deflazacort-treated mdx mice. The low-dose deflazacort and prednisone did not show any significant differences from untreated mice. Thus, prednisone treatment did not increase cardiac fibrosis in this study, in part because of the short duration of the study. However, an earlier study by Marques et al. found a decrease in cardiac fibrosis in 6-month-old mdx mice treated with 1.2 mg/kg of deflazacort in the drinking water for 15 months. These results are in direct contrast to our current study and the others previously mentioned. The differences could be due to the difference in drug, sex, age, and duration of drug administration. It also appears that long-term administration of deflazacort has negative consequences on heart function in the delta-sarcoglycandeficient cardiomyopathic hamster, suggesting that careful studies are needed to confirm and validate the previously reported beneficial effects of these drugs in mdx mice.