Introduction: Chronic hyperinsulinemia affects muscle, and may advantage speed and power athletes. Hyperinsulinaemia is associated with shifts in expression of myosin heavy chain isoforms, and muscle fibre type resulting in a faster contractile profile (I→IIa→IIb). Insulin sensitivity increases with endurance training, however, there are limited studies on insulin sensitivity with resistance training and detraining. The aims of the present study were to examine insulin sensitivity, skeletal muscle transitions and strength in offspring of Type 2 diabetics, in comparison with normal control subjects, after resistance training and detraining.
Method: Six (1 male, 5 female; 21.3 ± 1.8 yr, 164.7 ± 4.6 cm, 62.2 ± 7.1 kg, body mass index (BMI) 22.3 ± 2.5, mean ± SD) familial insulin resistant (FIR) and 10 (4 male, 6 female; 23.0 ± 2.9 yr, 170.1 ± 10.4 cm, 70.0 ± 13.2 kg, BMI 23.8 ± 2.6, mean ± SD) controls (C) completed 9 wk of resistance training (squat, leg press, leg extension, leg curl and box jump exercises) and 9 wk detraining. Measures at baseline (T1), after training (T2) and after detraining (T3) included an oral glucose tolerance test, muscle biopsy and performance tests (3RM; standing squat jump [SSJ], Wingate test, and a force-velocity curve [FVC]). Mixed model and correlation analyses were conducted.
Results: There was a significant increase in 3RM values in all exercises, vertical jump (SSJ) and peak power output (PPO) from T1 to T2 (p < 0.05). FVC moved up and right with training (p < 0.05). No significant fibre type changes occurred with training in either C or FIR. FIR reduced insulin area under the curve (AUC) to a greater extent than C with training (65.7 ± 43.4 to 43.4 ± 15.1 vs. 32.7 ± 13.3 to 32.9 ± 14.0 pmol.ml.min-1, resp., p = 0.05). There were reductions in 3RM in all exercises, with detraining (p < 0.001), and decreases in peak moment of force in FVC (p < 0.001), but no change in SSJ and PPO (p = 0.097, p = 0.439, resp.). Detraining decreased percentage type I and increased percentage type II fibres (p = 0.005, p = 0.031, resp.), although no differences in fibre type adaptations or performance were observed between groups. Detraining increased percentage MHC IIx (p = 0.026) and insulin AUC (p = 0.031), with a larger insulin AUC in FIR than in C (p = 0.018).
Conclusions: Resistance training produces similar increases in strength in both FIR and C, and decreases in strength with detraining. However, FIR exhibit a greater training effect to reduce insulin AUC and, in contrast to controls, an increase with detraining. While this population did not show clinical signs of diabetes, resistance training can increase insulin sensitivity and may reduce future risk of Type 2 diabetes amongst individuals with mild familial insulin resistance.
