We hypothesized that SIT causes oxidative stress preferentially in fast-twitch type 2-fibres and that this stress constitutes an important trigger of mitochondrial adaptations towards increased oxidative capacity and hence improved muscular endurance. In addition, we hypothesized that the SIT-induced signalling involves an initial ROS-dependent increase in SR Ca2+ leak followed by adaptive changes in the expression of SR Ca2+-handling proteins. To test these hypotheses, two groups of young males performed three weeks of SIT, one group received antioxidants in the form of high dosage of vitamin C and E and the other placebo. In addition to physiological exercise performance tests, we focus on changes in ROS-, SR Ca2+-, and mitochondria-related gene expression after the initial SIT session and fibre type-dependent protein expression after the last SIT session.