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Obesity has been associated with increased production of reactive oxygen species (ROS), which may be involved in the development of cardiovascular disease and type 2 diabetes (T2D). Endurance exercise lowers ROS production and increases antioxidant capacity in muscle cells, but it is currently unknown whether high intensity interval training (HIT) elicits the same effects. Twelve sedentary obese subjects at risk of developing T2D took part in a six-week intervention, performing three HIT sessions per week (five 1-min sets of high-intensity cycling (125% of VO 2 peak), with 90 s recovery in between sets). Muscle biopsies were obtained for assessment of ROS production (H 2 O 2 emission), mitochondrial respiratory capacity, and antioxidant protein levels before and after the intervention. H 2 O 2 emission decreased 60.4% after the intervention (Succinate 3 mmol･l−1), concurrent with a 35.1% increase in protein levels of the antioxidant manganese superoxide dismutase (MnSOD) and a trend towards increased levels of the antioxidant catalase (p = 0.06, 72.9%). These findings were accompanied by a 19% increased mitochondrial respiratory capacity (CI + II), a 6.9% increased VO 2 peak and a 1.7% lower body fat percentage. These effects were achieved after just 15 min of high-intensity work and 40 min of total time spent per week. Overall, this suggests that a relatively small amount of HIT is sufficient to induce beneficial effects on ROS production and antioxidant status in muscle cells, which may lower oxidative stress and potentially protect against the development of cardiovascular disease. [Display omitted] • HIT reduces H 2 O 2 emission in muscle cells of obese adults in risk of developing T2D. • HIT leads to increased protein levels of antioxidant enzymes in skeletal muscle cells. • HIT improves mitochondrial respiratory capacity and general health parameters. • The effects occur after just 40 min of weekly time commitment for 6 weeks. [ABSTRACT FROM AUTHOR]