Resistance training improves indices of muscle insulin sensitivity and β-cell function in overweight/obese, sedentary young men

Abstract

We examined the effects of RT on oral glucose tolerance test (OGTT)-derived indices of muscle insulin sensitivity, hepatic insulin resistance, β-cell function, and skeletal muscle proteins related to glucose transport in overweight/obese, sedentary young men. Twenty-eight participants [median body mass index (BMI) 30.9 kg/m(2); age 22 yr] completed 12 wk of RT (3 sessions/wk) and were assessed for changes in OGTT-derived indices, resting metabolic rate, body composition, serum adipokines, and skeletal muscle protein content [hexokinase 2 (HK2), glucose transporter type 4 (GLUT4), RAC-β serine/threonine-protein kinase (AKT2), glycogen synthase kinase 3β, and insulin receptor substrate 1]. Individualized responses to RT were also evaluated. RT significantly improved insulin and glucose area under the curve (both P < 0.03). With the use of OGTT indices of insulin action, we noted improved muscle insulin sensitivity index (mISI; P = 0.03) and oral disposition index (P = 0.03). BMI, lean body mass (LBM), and relative strength also increased (all P < 0.03), as did skeletal muscle protein content of HK2, GLUT4, and AKT2 (26-33%; all P < 0.02). Hepatic insulin resistance index, adiponectin, leptin, and total amylin did not change. Further analysis demonstrated the presence of highly individualized responsiveness to RT for glucose tolerance and other outcomes. RT improved oral indices of muscle insulin sensitivity and β-cell function but not hepatic insulin resistance in overweight/obese young men. In addition to the increase in LBM, the improvements in insulin action may be due, in part, to increases in key insulin signaling proteins.

Keywords: OGTT; exercise; glucose tolerance; insulin sensitivity; strength training.

Figures

Fig. 1.

Effects of resistance training (RT) on (A) glucose and (B) insulin levels during a 2-h oral glucose tolerance test. Data indicate significant reductions in time points—60 and 120 min for glucose and 90 and 120 min for insulin (n = 26). Bar graphs illustrate total glucose area under the curve (AUC) and insulin AUC, pre- and postintervention, for their respective curves. Data are presented as median and median absolute deviation (MAD). *P < 0.01. C: changes in muscle insulin sensitivity index (ISI), hepatic insulin resistance index (IRI), and oral disposition index (DI; *P < 0.05). D: effects of RT on protein content of glucose transporter type 4 (GLUT4), hexokinase 2 (HK2), insulin receptor substrate 1 (IRS1), glycogen synthase kinase 3β (GSK3β), and RAC-β serine/threonine-protein kinase (AKT2; *P < 0.02). Bar graphs present median and MAD for pre- and postintervention tests.

Fig. 2.

Individual responsiveness to 12-wk RT intervention presented as a change from pre-test values for fat mass (A), lean body mass (LBM; B), relative strength (C), and glucose AUC (Glu AUC; D) and also as a percent change sorted by LBM (E) and relative strength (F) compared with the effect on glucose AUC (glucose AUC vs. LBM Spearman correlation ρ = −0.11, P = 0.59; glucose AUC vs. relative strength ρ = 0.18, P = 0.39). A–D: data are presented as median and interquartile range.