The serum and glucocorticoid inducible kinase SGK1 is heavily expressed in skeletal muscle. According to in vitro studies utilizing heterologous coexpression of genes encoding kinases with those encoding transport proteins, SGK1 stimulates a wide variety of transport systems expressed in skeletal muscle, such as the creatine transporter CreaT, the glucose transporters GLUT1 and GLUT4 and the Na+ /K+ ATPase. Following i.p. glucose injection the glucose uptake into skeletal muscle is decreased in gene targeted mice lacking functional SGK1 (sgk1-/- ) as compared to their wild type littermates (sgk1+/+ ). Thus SGK1 may be important in the regulation of substrate uptake and function of skeletal muscle. Moreover, SGK1 may affect cardiovascular function, e.g. by its ability to enhance salt uptake, renal Na+ retention and thus extracellular fluid volume. To explore whether SGK1 influences physical performance, sgk1-/- mice (n=6) and sgk1+/+ mice (n=6) were allowed to run for 36 days in running wheels. As a result, no significant differences were observed in average speed between sgk1-/- mice (1.30±0.09 km/h) and sgk1+/+ mice (1.35±0.10 km/h). Moreover, maximal speed was similar in sgk1-/- mice (3.79±0.19 km/h) and sgk1+/+ mice (4.13±0.07 km/h). However, the running distance was significantly shorter in sgk1-/- mice (4.08±0.31 km/24h) and sgk1+/+ mice (6.74±0.74 km/24h). Thus, lack of SGK1 indeed leads to subtle impairment of physical performance.