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Introduction/objectives: To assess the effects of exercise training on insulin resistance and β-cell function in patients with systemic autoimmune myopathies (SAMs)., Method: This quasi-experimental, prospective study includes 9 patients with SAMs (six with dermatomyositis, two with antisynthetase syndrome, and one with polymyositis). Patients were submitted to a 12-week, twice a week, exercise training program comprising aerobic and resistance exercises. Baseline and after the intervention, we evaluated disease status, aerobic capacity, muscle strength, body composition, insulin resistance, and β-cell function parameters., Results: The patients have a mean age of 46.7 years and stable disease. No clinical or laboratory parameter impairment was observed after the intervention. Compared with baseline, aerobic capacity, muscle strength, and function increased after 12 weeks (P < 0.05), while no changes were observed for body composition. Data from the oral glucose tolerance test showed that exercise did not change glucose area under the curve (AUC), whereas insulin and C-peptide AUC decreased significantly (P < 0.05). Furthermore, Matsuda index and HOMA2 percentage (both surrogates of insulin resistance) also improved (P < 0.05)., Conclusion: Exercise training improved aerobic capacity, muscle strength, and muscle function in patients with SAMs. In addition, exercise training led to an attenuation of insulin resistance and improvements in β-cell function parameters. These data indicate that exercise training can mitigate metabolic impairments, attenuating the cardiovascular risk in SAMs.Key Points• Exercise training improved aerobic capacity, muscle strength, and function without disease impairment• Exercise training was capable of improve insulin resistance and β-cell function in patients with SAM• These results suggest that exercise can mitigate metabolic impairments in patients with SAM, attenuating the cardiovascular risk.

Reduced cellular response to insulin in skeletal muscle is one of the major components of the development of type 2 diabetes (T2D). Mitochondrial dysfunction involves in the accumulation of toxic reactive oxygen species (ROS) that leads to insulin resistance. The aim of this study was to verify the involvement of mitochondrial DNA damage at ROS generation in skeletal muscle during development of T2D. Wistar rats were fed a diet containing 60% fat over 8 weeks and at day 14 a single injection of STZ (25 mg/kg) was administered (T2D-induced). Control rats received standard food and an injection of citrate buffer. Blood and soleus muscle were collected. Abdominal fat was quantified as well as glucose, triglyceride, LDL, HDL, and total cholesterol in plasma and mtDNA copy number, cytochrome b (cytb) mRNA, 8-hydroxyguanosine, and 8-isoprostane (a marker of ROS) in soleus muscle. T2D-induced animal presented similar characteristics to humans that develop T2D such as changes in blood glucose, abdominal fat, LDL, HDL and cholesterol total. In soleus muscle 8-isoprostane, mtDNA copy number and 8-hydroxyguanosine were increased, while cytb mRNA was decreased in T2D. Our results suggest that in the development of T2D, when risks factors of T2D are present, intracellular oxidative stress increases in skeletal muscle and is associated with a decrease in cytb transcription. To overcome this process mtDNA increased but due to the proximity of ROS generation, mtDNA remains damaged by oxidation leading to an increase in ROS in a vicious cycle accounting to the development of insulin resistance and further T2D.