Repeated prolonged whole-body low-intensity exercise: effects on insulin sensitivity and limb muscle adaptations Joern W. Helge a,b, T , Kristian Overgaard d , Rasmus Damsgaard a,b , Karsten Sørensen d , Jesper L. Andersen a , Stig E.U. Dyrskog e , Kjeld Hermansen e , Bengt Saltin a , Jbrgen F.P. Wojtaszewski c a Copenhagen Muscle Research Centre, State Hospital, 2200 Copenhagen, Denmark b Department of Medical Physiology, Panum Institute, University of Copenhagen, Dk 2200 N Copenhagen, Denmark c Department of Human Physiology, Institute of Exercise & Sports Sciences, University of Copenhagen, 2200 Copenhagen, Denmark d Department of Sports Science, University of Aarhus, 8200 Aarhus, Denmark e Department of Endocrinology and Metabolism C, University of Aarhus, 8000 Aarhus, Denmark Received 8 April 2005; accepted 22 August 2005 Abstract This study investigates the effect of prolonged whole-body low-intensity exercise on insulin sensitivity and the limb muscle adaptive response. Seven male subjects (weight, 90.2 F 3.2 kg; age, 35 F 3 years) completed a 32-day unsupported crossing of the Greenland icecap on cross-country skies pulling sleighs. The subjects were studied before and 3 to 4 days after the crossing of the icecap. Subjects came in overnight fasted, and an intravenous glucose tolerance test (IVGTT) was done. A biopsy was obtained from the vastus lateralis and deltoid muscle. On a separate day, a progressive test was performed to establish maximal oxygen uptake. During the crossing, subjects skied for 342 F 41 min/d. Peak oxygen uptake (4.6 F 0.2 L/min) was decreased ( P b .05) by 7% after the crossing and body mass decreased ( P b .05) by 7.1 F 0.2 kg, of which 4.4 F 0.5 kg was fat mass and 2.7 F 0.2 kg lean body mass. Glycosylated hemoglobin (5.6% F 0.01%) was not affected by the crossing. The IVGTT data revealed that insulin sensitivity (7.3 F 0.6 mU d L 1 d min 1 ) and glucose effectiveness (0.024 F 0.002 min 1 ) were not changed after the crossing. Similarly, the IVGTT data, when expressed per kilogram of lean body mass or body mass, were not affected by the crossing. Citrate synthase activity was higher ( P b .05) in the leg (29 F 1 lmol d g 1 d min 1 ) than in the arm muscle (16 F 2 lmol d g 1 d min 1 ) and was unchanged after the crossing. Muscle GLUT4 protein concentration was higher ( P b .05) in the leg (104 F 10 arbitrary units) than in the arm (54 F 9 arbitrary units) and was not changed in the leg, but was increased ( P b .05) by 70% to 91 F 9 arbitrary units in the arm after the crossing. In conclusion, the increased glucose transporter expression in arm muscle may compensate for the loss of lean body mass and the decrease in aerobic fitness and thereby contribute to the maintenance of whole-body insulin sensitivity after prolonged low-intensity exercise training. D 2006 Elsevier Inc. All rights reserved. 1. Introduction The appearance of insulin resistance and the subsequent lifestyle diseases have reached epidemic proportions in the Western world, and lifestyle changes such as increased physical activity are promoted as a means to combat this phenomenon. Regular physical activity and thus training is generally considered to lead to marked improvement in whole-body insulin sensitivity [1,2]. In addition, there is evidence that regular strength training leads to improved insulin sensitivity, most likely because of an increase in muscle mass [3,4]. However, it is less clear to what degree aerobic training performed at lower intensities, where aerobic fitness is not improved, will also improve insulin sensitivity. When low-intensity training was performed for 2 weeks with a limited muscle mass, the one-leg kicking model, total muscle GLUT4 protein content was increased and aerobic fitness was unchanged [5]. Albeit insulin sensitivity was not measured, an increased glucose transport capacity is believed to mediate an increased insulin sensitivity [6,7]. We studied prolonged whole-body low-intensity exercise in a 0026-0495/$ – see front matter D 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.metabol.2005.08.015 T Corresponding author. Section Pathophysiology, Department of Medical Physiology, Panum Institute, Dk 2200 N Copenhagen, Denmark. Tel.: +45 35 32 75 06; fax: +45 35 32 74 20. E-mail address: jhelge@mfi.ku.dk (J.W. Helge). Metabolism Clinical and Experimental 55 (2006) 217 – 223 www.elsevier.com/locate/metabol