Skeletal muscle proteins important for work capacity are altered with type 2 diabetes - Effect of 10-20-30 training
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- Baasch-Skytte et al_Physiological Reports_2021_Vol 9_e14681
Final published version, 1.49 MB, PDF document
The study examined whether men with type 2 diabetes exhibit lower expression of muscle proteins important for exercise capacity, and whether exercise training promotes adaptations in these proteins. In a cross-sectional and longitudinal study, conducted at the University of Copenhagen. Twelve men with type 2 diabetes (T2D) were compared to eleven nondiabetes counterparts (ND) matched for age and body composition (body fat percentage). T2D underwent 10 weeks of high-intensity interval exercise training (10-20-30 training). T2D had lower expression of SOD1 (-62%; p < 0.001) and ETC complex V (-34%; p = 0.003), along with higher expression of ETC complex IV (+66%; p = 0.007), MFN2 (+62%; p = 0.001), and DRP1 (+30%; p = 0.028) compared to ND. T2D had higher (p < 0.001) expression of Na+ /K+ α1 (+98%), α2 (+114%), and NHE1 (+144%) than ND. In T2D, training increased exercise capacity (+9%; p < 0.001) as well as expression of SOD2 (+44%; p = 0.029), ETC complex II (+25%; p = 0.035), III (+52%; p = 0.041), IV (+23%; p = 0.005), and V (+21%; p = 0.035), CS activity (+32%; p = 0.006) as well as Na+ /K+ α1 (+24%; p = 0.034), Kir6.2 (+36%; p = 0.029), and MCT1 (+20%; p = 0.007). Men with type 2 diabetes exhibited altered expression of a multitude of skeletal muscle proteins important for exercise capacity. Ten weeks of 10-20-30 training upregulated expression of muscle proteins regulating antioxidant defense, mitochondrial function, and ion handling while enhancing exercise capacity in men with type 2 diabetes.
|Number of pages||13|
|Publication status||Published - 2021|
© 2021 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.
- Faculty of Science - Antioxidant defense, High-intensity interval training, Ion handling, Mitochondria