Literature DB >> 23970530

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

Daniel M Croymans1, Ergit Paparisto, Mary M Lee, Nina Brandt, Brian K Le, Derek Lohan, Cathy C Lee, Christian K Roberts.   

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.

Entities:  

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

Mesh:

Substances:

Year:  2013        PMID: 23970530      PMCID: PMC3841835          DOI: 10.1152/japplphysiol.00485.2013

Source DB:  PubMed          Journal:  J Appl Physiol (1985)        ISSN: 0161-7567


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