Abstract
High intensity interval training (HIT) is a time-efficient training concept mostly studied in healthy populations. We hypothesized that HIT improves hepatic and peripheral insulin sensitivity and increases muscle mitochondrial function in patients with type 2 diabetes. To this end, we examined 11 sedentary male patients with type 2 diabetes (age: 58 ± 6 years, BMI: 31.1 ± 2.5 kg.m-2), who performed a 12-week cycling protocol (4 × 4 min intervals at 85% of maximal heart rate, three minutes recovery, three days weekly) at baseline, after one bout, after 12 weeks of HIT and after 4 weeks of detraining. Two-step hyperinsulinemic euglycemic clamps with somatostatin infusion, magnetic resonance spectroscopy for liver fat quantification and high resolution respirometry in skeletal muscle biopsies were performed. After one bout of exercise, insulin sensitivity (in mg.kg-1.min-1) remained unchanged (baseline: 2.8 ± 1.7), but increased by 46% after 12 weeks (4.1 ± 2.0, p = 0.04) and returned to baseline after detraining (p = 0.89). This training period also resulted in decreases in free fatty acids (baseline: 441 ± 161 vs. 12 weeks: 293 ± 52 µmol/l, p = 0.008) and liver fat content (16 ± 8% vs. 13 ± 7%, p = 0.02) but suppression of endogenous glucose production during the low-insulin phase of the clamp remained unchanged (p = 0.19). Muscle maximal uncoupled respiration (state u) was increased after 12 weeks and remained higher after detraining (baseline: 67 ± 11, 12 weeks: 89 ± 20 vs. detraining: 83 ± 21 pmol/mg wet tissue/s, p < 0.01). In conclusion, 12 weeks of HIT result in increased peripheral but not hepatic insulin sensitivity and improvements in mitochondrial function, which persist after 4 weeks of detraining.
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