Endocrine Abstracts (2012) 28 S5.2

Exercise effects on fat metabolism and insulin sensitivity in human muscle

Anton Wagenmakers1, Sam Shepherd1, Luc van Loon2 & Christopher Shaw1

1School of Sport and Exercise Sciences, University of Birmingham, Birmingham, United Kingdom; 2Department of Human Movement Sciences, Nutrition and Toxicology Research Institute Maatricht, Maastricht, Netherlands.

There is an accumulating amount of evidence that the metabolic adaptations to endurance exercise that result in increased intramuscular triglyceride (IMTG) stores and IMTG oxidation during exercise, also exert a protective effect on muscle insulin sensitivity. This seems to be a contradiction (known as the athlete's paradox) as large IMTG stores in sedentary and obese individuals coexist with high levels of fatty acid (FA) metabolites (specifically long-chain acylCoA, DAG and ceramide) and these abnormalities in lipid metabolism are known to lead to insulin resistance. Trained individuals have a very high capacity for lipid oxidation, with about equal amounts of plasma FA (originating from adipose tissue lipolysis) and of IMTG being oxidised. If trained athletes ingest a lipid containing meal after exercise, the FA will be efficiently channeled into TG synthesis both in muscle (IMTG) and adipose tissue and the muscle FA-metabolites will be kept low and insulin sensitivity high. As sedentary obese individuals rarely experience exercise-induced increases in adipose tissue lipolysis and lipid oxidation and appear unable to oxidise IMTG during exercise, their muscle and adipose tissue lipid stores remain full and immobile. This implies that after ingestion of a lipid containing meal the rise in plasma lipids will be large. Together with high rates of adipose tissue lipolysis in the fasted state this will lead to continuous increases in plasma FA and TG and high concentrations of the FA metabolites in muscle and insulin resistance. Exercise training interventions may help to make the IMTG stores mobile under these circumstances. Data will be presented to show that 6 weeks of endurance exercise (3×40 min per week) at 40% VO2max is enough for sedentary individuals to substantially increase IMTG oxidation during exercise. This coincides with substantial decreases in plasma TG (risk factor for CVD). For sedentary individuals with very little time high intensity intermittent exercise is an efficient alternative to increase IMTG stores and oxidation during exercise and insulin sensitivity, while patients with type 2 diabetes show large increases in IMTG without a change in insulin sensitivity after 6 months of endurance training. In all interventions we observe parallel increases in perilipin-2 and -5 and their potential role in enhancing IMTG oxidation during exercise will be discussed.

Declaration of interest: There is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.

Funding: No specific grant from any funding agency in the public, commercial or not-for-profit sector.

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