Resistance training and insulin action in humans: effects of de-training

Abstract

Aerobic endurance training increases insulin action in skeletal muscle, but the effect of resistance training has not been well described. Controversy exists about whether the effect of resistance training is merely due to an increase in muscle mass. We studied the effect of cessation of resistance training in young, healthy subjects by taking muscle biopsies and measuring insulin-mediated whole body and leg glucose uptake rates after 90 days of heavy resistance training (T) and again after 90 days of de-training (dT). Data on leg glucose uptake were expressed relative to accurate measures of leg muscle mass by MRI scanning. Muscle strength (239 +/- 43 vs. 208 +/- 33 N m), quadriceps area (8463 +/- 453 vs. 7763 +/- 329 mm2) and glycogen content (458 +/- 22 vs. 400 +/- 26 mmol (kg dry weight muscle)(-1)) decreased, while myosin heavy chain isoform IIX increased 4-fold in dT vs. T, respectively (all P < 0.05). GLUT4 mRNA levels and enzyme activities and mRNA levels of glycolytic, lipolytic and glyconeogenic enzymes did not change with de-training. Likewise, capillary density did not change. Whole body glucose uptake decreased 11 % and leg glucose uptake decreased from 75 +/- 11 (T) to 50 +/- 6 (dT) nmol min(-1) (mm muscle)(-2) (P < 0.05) at maximal insulin, the latter decrease being due to decreased arterio-femoral venous glucose extraction. The decrease was mainly due to reduced non-oxidative glucose disposal. We have thus shown that 90 days after the termination of heavy resistance training, insulin-mediated glucose uptake rates per unit of skeletal muscle have decreased significantly.

Figure 1. Fibre types and gene expression

Seven young, healthy men carried out a heavy resistance training programme for 90 days (trained state) and thereafter abstained from training for a further 90 days (de-trained state). Skeletal muscle biopsies from vastus lateralis were taken in the trained and de-trained states and were analysed for myosin heavy chain (MHC) isoform composition (mean ± S.E.M.) (top graph) and mRNA levels (individual values are shown) of glucose transporter 4 (GLUT4), citrate synthase (CS), short chain β-hydroxyacyl-CoA dehydrogenase (HAD), glycogen synthase (GS) and lactate dehydrogenase in the muscle (LDH-M) and heart (LDH-H) forms. * Significant difference between trained and de-trained state (P < 0.05).

Figure 2. Enzyme activities, glycogen content and capillary density in skeletal muscle biopsies

Seven young, healthy men carried out a heavy resistance training programme for 90 days (trained state) and thereafter abstained from training for a further 90 days (de-trained state). Skeletal muscle biopsies from vastus lateralis were taken in the trained and de-trained states and were analysed for lactate dehydrogenase (LDH), short chain β-hydroxyacyl-CoA dehydrogenase (HAD), citrate synthase (CS), phosphofructokinase (PFK) enzyme activities, and glycogen content and capillary density. Individual values are shown. * Significant difference between trained and de-trained state (P < 0.05).

Figure 3. Glucose uptake in legs and whole body

Seven young, healthy men carried out a heavy resistance training programme for 90 days (trained state) and thereafter abstained from training for a further 90 days (de-trained state). Euglycaemic, hyperinsulinaemic clamps combined with the leg balance technique were performed in the trained and de-trained states. Basal and insulin-stimulated values of leg blood flow, leg glucose extraction and leg glucose uptake are shown (means ± S.E.M.). Whole body glucose uptake rates (= glucose infusion rates) are shown (lower, right) as the mean of averaged 5 min intervals. * Significant difference between the trained and de-trained states (P < 0.05).

Figure 4. Glucose metabolism

Seven young, healthy men carried out a heavy resistance training programme for 90 days (trained state) and thereafter abstained from training for a further 90 days (de-trained state). Oxidative and non-oxidative leg glucose metabolism was calculated by means of indirect calorimetry before (basal) and during steps I and II in euglycaemic, hyperinsulinaemic clamps in the trained and de-trained states. Data are means ± S.E.M. * Significant difference between the trained and de-trained states (P < 0.05).