Editors' ChoiceMetabolism

Mitochondrial Workout

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Science Translational Medicine  25 Jul 2012:
Vol. 4, Issue 144, pp. 144ec134
DOI: 10.1126/scitranslmed.3004624

Olympic athletes care about their numbers—race times, judges’ scores, and now, mitochondrial population size in skeletal muscle. Indeed, mitochondria numbers influence how much energy one can generate from carbohydrate, fat, and protein during exercise, which in turn determines whether or not one has the chops to compete at world-class levels. But even for nonathletes, mitochondrial numbers are important because their functional capacity correlates with health status. Now, Phielix et al. report good news for movers and shakers: Chronic exercise can boost mitochondrial mass and, in turn, stem lipid-induced insulin resistance.

Mitochondrial dysfunction and reduced respiratory capacity can manifest when lipid accumulates in skeletal muscle and impairs insulin sensitivity, which contributes to the development of type 2 diabetes. However, whether or not active skeletal muscles eschew lipid-induced mitochondrial dysfunction and insulin resistance has not been firmly established in humans. The authors tackled this question in a study of 10 healthy, young, untrained males and 9 endurance-trained males. Compared with untrained subjects, endurance-trained males are known to have significantly higher mitochondrial respiration rates with increased mitochondrial masses. A hyperinsulinemic-euglycemic clamp study used to assess systemic insulin sensitivity revealed that lipid infusion—which leads to accumulation of intramyocellular triglycerides and induces acute insulin resistance—reduced insulin-stimulated glucose uptake by 63% in untrained subjects; in contrast, this effect was blunted to 29% in trained subjects. Lipid infusion–induced reductions in oxidative and nonoxidative glucose disposal (NOGD; that is, through the glycogen synthesis pathway) was observed in untrained subjects, whereas the NOGD pathway remained intact in trained subjects under the same conditions. Endurance training is known to improve whole-body and muscular insulin sensitivity in young, healthy, lean individuals as well as in obese and type 2 diabetic subjects. The new work supports these earlier findings and further proposes that training can maintain insulin sensitivity and high glucose uptake by shuttling glucose toward storage as glycogen under conditions of high lipid exposure. So even if daily endurance training doesn’t bring Olympic glory, at least it can protect against the development of metabolic diseases.

E. Phielix et al., High oxidative capacity due to chronic exercise training attenuates lipid-induced insulin resistance. Diabetes, 10 July 2012 (10.2337/db11-1832). [PubMed]

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