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Over the last decade, several studies in humans have found that high-intensity interval training (HIIT), an exercise training program involving brief bouts of intense exercise (90-100% of VO2 max) followed by periods of recovery, can elicit similar metabolic adaptations to classical endurance exercise training but with a much shorter time commitment. Importantly, recent studies have established that HIIT can lower blood glucose and markers of insulin resistance independently of alterations in adiposity/body mass in individuals with insulin resistance and type 2 diabetes.

Marcinko and colleagues show that HIIT leads to a substantial improvement in exercise capacity without altering body mass or adiposity and that this is accompanied by significant reductions in fasting and fed blood glucose levels. HIIT improves adipose tissue insulin sensitivity independently of adipocyte cell size, macrophage accumulation in adipose tissue, adipose tissue inflammation or markers of adipose tissue browning. It also improves liver insulin sensitivity independently of reductions in liver triacylglycerol/diacylglycerol/ceramide levels. Improvements in adipose and liver insulin sensitivity occur independently of acetyl-CoA carboxylase (ACC) phosphorylation, which the authors have previously shown is required for the insulin sensitizing effects of metformin. These findings indicate that HIIT can uncouple inflammation and lipid metabolism from insulin sensitivity and does not depend on AMP-activated protein kinase (AMPK) phosphorylation and inhibition of ACC.



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In this section authors briefly report on their work recently published in Molecular Metabolism.

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Amna Khamis
University of Lille, CNRS, Institute Pasteur de Lille, Lille, France
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