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Prenatally Induced Changes in Muscle Structure and Metabolic Function Facilitate Exercise-Induced Obesity Prevention

Department of Physiology (K.H.), University of Veterinary Medicine, 30173 Hannover, Germany; Liggins Institute (J.L.M.) and Department of Surgery (A.M.N., N.M.T.), Faculty of Medical and Health Sciences, and Department of Psychology (M.D.), Faculty of Science, University of Auckland, Auckland 1142, New Zealand; and Institute of Food, Nutrition, and Human Health (B.H.B.), Massey University, Albany Campus, Auckland 0632, New Zealand

Address all correspondence and requests for reprints to: Professor Korinna Huber, Department of Physiology, University of Veterinary Medicine, Bischofsholer Damm 15/102, 30173 Hannover, Germany. E-mail: korinna.huber{at}tiho-hannover.de.

Effective regulation of energy metabolism is vital for the maintenance of optimal health, and an inability to make these dynamic adjustments is a recognized cause of obesity and metabolic disorders. Epidemiological and experimental studies have highlighted the role of prenatal factors in the disease process, and it is now generally accepted that maternal nutrition during pregnancy significantly influences intrauterine development, shaping postnatal health. Consequences of impaired nutrition during fetal development include intrauterine growth restriction (IUGR) and subsequent obesity development in adult life. We have previously shown that prenatal undernutrition has a lasting effect on behavior, with IUGR offspring expressing a higher preference for voluntary exercise, and moderate daily exercise preventing obesity development. The present study investigated skeletal muscle structure in IUGR offspring and how moderate daily exercise drives changes in metabolic pathways that promote obesity prevention. Pregnant Wistar rats were either fed chow ad libitum or undernourished, generating control or IUGR offspring respectively. Although red muscle structure indicated higher oxidative capacity in IUGR offspring, obesity prevention was not due to increased fatty acid oxidation, indicated by decreased peroxisomal proliferator-activated receptor- coactivator 1 and carnitine-palmitoyltransferase 1 expression. In contrast, increased protein kinase C expression and glycogen content in white muscle of exercised IUGR offspring suggests an enhanced capacity for anaerobic utilization of glucose. Furthermore, exercise-induced lactate accumulation was effectively prevented by stimulation of a lactate shuttle, driven by the increases in monocarboxylate transporters-4 and -1 in white muscle. This enhanced metabolic flexibility in IUGR offspring may facilitate muscle contractile performance and therefore support moderate daily exercise for effective obesity prevention.