The aim of the study was to investigate if myostatin dysfunction would promote the gain in muscle mass and peak isometric force (P₀) of soleus muscle (SOL) in response to functional overloading (FO) after ablation of the gastrocnemius muscle. Fifteen male Berlin high (BEH) mice homozygous for the compact mutation causing dysfunction of myostatin and 17 mice with the corresponding wild‐type allele (BEH+/+) were subjected to FO of SOL for 28 days at the age of 14 weeks. Compared with BEH+/+ mice, SOL of BEH was heavier (mean ± SD, 13.5 ± 1.5 vs 21.4 ± 1.8 mg, respectively, P < 0.001). After FO, SOL mass increased relatively more in BEH+/+ than BEH strain (34.9 ± 11.5 vs 17.7 ± 11.9%, respectively, P < 0.01). P₀ fell (P < 0.01) only in BEH strain, which also showed an increase (P < 0.01) in optimal muscle length. Specific P₀ became even more depressed in BEH compared with BEH+/+ strain (8.4 ± 1.4 vs 10.8 ± 1.3 N/g, respectively, P < 0.001). Phosphorylation p70 S6 kinase did not differ between the strains. In summary, myostatin dysfunction impairs adaptation of SOL muscle to high functional demands.