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Maija Huttunen-Lenz,1 Sylvia Hansen,1 Pia Christensen,2 Thomas Meinert Larsen,2 Finn Sandø-Pedersen,2 Mathijs Drummen,3 Tanja C Adam,3 Ian A Macdonald,4,5 Moira A Taylor,5 J Alfredo Martinez,6–8 Santiago Navas-Carretero,6–8 Svetoslav Handjiev,9 Sally D Poppitt,10 Marta P Silvestre,10 Mikael Fogelholm,11 Kirsi H Pietiläinen,12,13 Jennie Brand-Miller,14 Agnes AM Berendsen,15 Anne Raben,2 Wolfgang Schlicht1 1Department of Exercise and Health Sciences, University of Stuttgart, Stuttgart, Germany; 2Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark; 3Department of Nutrition and Movement Sciences, Maastricht University, Maastricht, the Netherlands; 4MRC/ARUK Centre for Musculoskeletal Ageing Research, National Institute for Health Research (NIHR) Nottingham Biomedical Research Centre, School of Life Sciences, University of Nottingham, Nottingham, UK; 5School of Life Sciences, University of Nottingham Medical School, Nottingham, UK; 6Center for Nutrition Research at the University of Navarra, Pamplona, Spain; 7Madrid Institute of Advanced Studies (IMDEA Food), Madrid, Spain; 8Biomedical Research Centre Network in Physiopathology of Obesity and Nutrition (CIBERobn), Carlos III Institute, Madrid, Spain; 9Department of Pharmacology and Toxicology, Medical University – Sofia, Sofia, Bulgaria; 10Human Nutrition Unit, School of Biological Sciences, University of Auckland, Auckland, New Zealand; 11Department of Food and Nutrition, University of Helsinki, Helsinki, Finland; 12Obesity Research Unit, Research Program Unit, Diabetes and Obesity, University of Helsinki, Helsinki, Finland; 13Abdominal Center, Endocrinology, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland; 14Charles Perkins Centre and School of Life and Environmental Biosciences, University of Sydney, Camperdown, NSW, Australia; 15Division of Human Nutrition & Health, Wageningen University & Research, Wageningen, the Netherlands Purpose: Onset of type 2 diabetes (T2D) is often gradual and preceded by impaired glucose homeostasis. Lifestyle interventions including weight loss and physical activity may reduce the risk of developing T2D, but adherence to a lifestyle change is challenging. As part of an international T2D prevention trial (PREVIEW), a behavior change intervention supported participants in achieving a healthier diet and physically active lifestyle. Here, our aim was to explore the influence of this behavioral program (PREMIT) on social-cognitive variables during an 8-week weight loss phase. Methods: PREVIEW consisted of an initial weight loss, Phase I, followed by a weight-­maintenance, Phase II, for those achieving the 8-week weight loss target of ≥ 8% from initial bodyweight. Overweight and obese (BMI ≥25 kg/m2) individuals aged 25 to 70 years with confirmed pre-diabetes were enrolled. Uni- and multivariate statistical methods were deployed to explore differences in intentions, self-efficacy, and outcome expectancies between those who achieved the target weight loss (“achievers”) and those who did not (“non-achievers”). Results: At the beginning of Phase I, no significant differences in intentions, self-efficacy and outcome expectancies between “achievers” (1,857) and “non-achievers” (163) were found. “Non-achievers” tended to be younger, live with child/ren, and attended the PREMIT sessions less frequently. At the end of Phase I, “achievers” reported higher intentions (healthy eating χ2(1)=2.57; P

The glycemic index (GI) of dietary carbohydrates influences glycogen storage in skeletal muscle and circulating nonesterified fatty acid (NEFA) concentrations. We hypothesized that diets differing only in GI would alter intramuscular lipid oxidation and glycogen usage in skeletal muscle and liver during subsequent exercise. Endurance-trained individuals (n = 9) cycled for 90 min at 70% [Vo.sub.2 peak] and then consumed either high- or low-GI meals over the following 12 h. The following day after an overnight fast, the 90-min cycle was repeated. [sup.1]H and [sup.13]C magnetic resonance spectroscopy was used before and after exercise to assess intramuscular lipid and glycogen content of the vastus muscle group and liver. Blood and expired air samples were collected at 15-min intervals throughout exercise. NEFA availability was reduced during exercise in the high- compared with the low-GI trial (area under curve 44.5 [+ or -] 6.0 vs. 38.4 [+ or -] 7.30 mM/h, P < 0.05). Exercise elicited an ~55% greater reduction in intramyocellular triglyceride (IMCL) in the high- vs. low-GI trial (1.6 [+ or -] 0.2 vs. 1.0 [+ or -] 0.3 mmol/kg wet wt, P < 0.05). There was no difference in the exercise-induced reduction of the glycogen pool in skeletal muscle (76 [+ or -] 8 vs. 68 [+ or -] mM) or in liver (65 [+ or -] 8 vs. 71 [+ or -] 4 mM) between the low- and high-GI trials, respectively. High-GI recovery diets reduce NEFA availability and increase reliance on IMCL during moderate-intensity exercise. Skeletal muscle and liver glycogen storage or usage are not affected by the GI of an acute recovery diet. glycemic index; intramuscular lipid; glycogen; magnetic resonance spectroscopy; exercise; skeletal muscle; liver