Objective: SGK1 participates in the regulation of a wide variety of physiological functions including metabolism and transport. SGK1 deficient mice show, however, a rather mild phenotype. Since the enzyme is considerably expressed in skeletal muscle, the current study was performed to investigate a putative impact of SGK1 on muscle structure and function. Methods: Isometric force of soleus muscles and segments of diaphragms (DIA) of wildtype and SGK1 deficient mice (sgk1-/-) was tested in vitro at 25 °C. Electrical stimulation protocols allowed to record single twitches, maximum tetanic forces (at 120 Hz) and muscle fatigue. The histological analysis of muscle cross sections included HE, Sirius Red and myosin-ATPase stainings. Histological analyses were performed with several hindlimb muscles and DIA from about 100 d old animals. Results: Muscle mass of soleus muscles, kinetics of twitches and tetani of soleus and DIA and the development of muscle fatigue were not altered in sgk1-/- mice compared to controls. However, specific muscle force (force/cross-sectional area) was significantly reduced in muscles of sgk1-/- mice (force reduction of 20% for SOL, and 25% for DIA, n=7 for both muscles, p < 0.01). The histological analysis of muscles from sgk1-/- mice yielded an overall intact structure. The area filled with connective tissue was 3.5 ± 0.7 % (wildtype, n = 6) and 3.2 ± 0.3% (sgk1-/-; n=6) in soleus muscles. Myosin ATPase staining revealed a change in fibre type composition in sgk1-/- mice, both in soleus and DIA. In soleus muscles the fraction of type 1 fibres was 48 ± 2% for the wildtype and 43 ± 4% for the sgk1-/- animals. In DIA type 1 fibre fraction was increased (6.5 ± 0.6%, wildtype vs. 9 ± 0.5% sgk1-/-). Conclusion: The lack of SGK1 does not lead to pronounced changes in muscle structure and function. The reduction of muscle fore of SGK1 deficient mice may be explained by reduction of maximal ATPase activity or changes in intracellular Ca²⁺ homeostasis.