Effects of resistance training and detraining on glucose and insulin responses to an oral glucose load, muscle fiber type, and muscular performance in the offspring of those with type 2 diabetes (familial insulin resistant (FIR)) were investigated.
Six FIR participants and 10 controls (C) completed 9 wk of resistance training and 9 wk of detraining. Measures of strength and power, an oral glucose tolerance test, and a muscle biopsy to determine myosin heavy chain (MHC) fiber composition were taken at baseline (T1), after training (T2), and after detraining (T3).
Three-repetition maximum increased (P ≤ 0.001) similarly in both groups in all strength measures, e.g., leg press (FIR T1, T2: 121 ± 34 kg, 186 ± 50 kg; C T1, T2: 137 ± 42 kg, 206 ± 64 kg, respectively (means ± SD)). Wingate peak power increased (FIR T1, T2: 505 ± 137 W, 523 ± 143 W; C T1, T2: 636 ± 211 W, 672 ± 223 W, respectively; P ≤ 0.005 (means ± SD)). Training reduced insulin area under the curve more (P = 0.050) in FIR (T1, T2: 1219 ± 734 pmol·L−1, 837 ± 284 pmol·L−1, respectively (means ± SD)) than that in C (T1, T2: 647 ± 268 pmol·L−1, 635 ± 258 pmol·L−1, respectively (means ± SD)). MHC distribution did not change with training. Strength (three-repetition maximum measures) decreased with detraining (P ≤ 0.001) although Wingate power did not. Detraining increased insulin area under the curve (P = 0.018) in FIR (T2, T3: 837 ± 285 pmol·L−1, 1040 ± 194 pmol·L−1, respectively (means ± SD)) but not in C (T2, T3: 635 ± 258 pmol·L−1, 625 ± 213 pmol·L−1, respectively (means ± SD)). MHC IIX fibers increased with detraining (P = 0.026).
FIR appears to have exaggerated responses to resistance training and detraining, with a greater reduction in insulin release with glucose ingestion after training and increase when training ceases. Resistance training has a significant effect on insulin responses and may reduce future risk of type 2 diabetes mellitus among FIR.
1School of Physical Education, University of Otago, Dunedin, NEW ZEALAND; 2Department of Human Nutrition, University of Otago, Dunedin, NEW ZEALAND; 3High Performance Sport New Zealand, Dunedin, NEW ZEALAND; 4Institute of Sports Medicine Copenhagen, Bispebjerg Hospital, Copenhagen, DENMARK; and 5Department of Medicine, University of Otago, Dunedin, NEW ZEALAND
Address for correspondence: Nancy J. Rehrer, Ph.D., School of Physical Education, University of Otago, PO Box 56, Dunedin 9054, New Zealand; E-mail: email@example.com.
Submitted for publication October 2011.
Accepted for publication June 2012.