A single bout of resistance exercise improves postprandial lipid metabolism in overweight/obese men with prediabetes

Abstract
Aims/hypothesis Prediabetes is associated with postprandial hypertriacylglycerolaemia. Resistance exercise acutely lowers postprandial plasma triacylglycerol (TG); however, the changes in lipid metabolism that mediate this reduction are poorly understood. The aim of this study was to identify the constitutive metabolic mechanisms underlying the changes in postprandial lipid metabolism after resistance exercise in obese men with prediabetes. Methods We evaluated the effect of a single bout of whole-body resistance exercise (seven exercises, three sets, 10–12 repetitions at 80% of one-repetition maximum) on postprandial lipid metabolism in ten middle-aged (50 ± 9 years), overweight/obese (BMI: 33 ± 3 kg/m2), sedentary men with prediabetes (HbA1c >38 but 5.7% but 5.6 mmol/l but 7.8 mmol/l but 13C4)3]tripalmitin, i.v. [U-13C16]palmitate and [2H5]glycerol) to evaluate chylomicron-TG and total triacylglycerol-rich lipoprotein (TRL)-TG kinetics. We used adipose tissue and skeletal muscle biopsies to evaluate the expression of genes regulating lipolysis and lipid oxidation, skeletal muscle respirometry to evaluate oxidative capacity, and indirect calorimetry to assess whole-body lipid oxidation. Results The single bout of resistance exercise reduced the lipaemic response to a mixed meal in obese men with prediabetes without changing chylomicron-TG or TRL-TG fractional clearance rates. However, resistance exercise reduced endogenous and meal-derived fatty acid incorporation into chylomicron-TG and TRL-TG. Resistance exercise also increased whole-body lipid oxidation, skeletal muscle mitochondrial respiration, oxidative gene expression in skeletal muscle, and the expression of key lipolysis genes in adipose tissue. Conclusions/interpretation A single bout of resistance exercise improves postprandial lipid metabolism in obese men with prediabetes, which may mitigate the risk for cardiovascular disease and type 2 diabetes.
Funding Information
  • National Center for Advancing Translational Sciences (UL1TR000448)
  • National Institute of Diabetes and Digestive and Kidney Diseases (P30 DK05634)
  • Foundation for Physical Therapy (Promotion of Doctoral Studies II Award)
  • Cambridge Isotopes Laboratories (Research Grant Program)
  • National Institute of Child Health and Human Development (T32 HD007434-25)