Low-volume high-intensity interval training reduces hyperglycemia and increases muscle mitochondrial capacity in patients with type 2 diabetes.

Low-volume high-intensity interval training (HIT) is emerging as a time-efficient exercise strategy for improving health and fitness. This form of exercise has not been tested in type 2 diabetes and thus we examined the effects of low-volume HIT on glucose regulation and skeletal muscle metabolic capacity in patients with type 2 diabetes. Eight patients with type 2 diabetes (63 ± 8 yr, body mass index 32 ± 6 kg/m(2), Hb(A1C) 6.9 ± 0.7%) volunteered to participate in this study. Participants performed six sessions of HIT (10 × 60-s cycling bouts eliciting ∼90% maximal heart rate, interspersed with 60 s rest) over 2 wk. Before training and from ∼48 to 72 h after the last training bout, glucose regulation was assessed using 24-h continuous glucose monitoring under standardized dietary conditions. Markers of skeletal muscle metabolic capacity were measured in biopsy samples (vastus lateralis) before and after (72 h) training. Average 24-h blood glucose concentration was reduced after training (7.6 ± 1.0 vs. 6.6 ± 0.7 mmol/l) as was the sum of the 3-h postprandial areas under the glucose curve for breakfast, lunch, and dinner (both P < 0.05). Training increased muscle mitochondrial capacity as evidenced by higher citrate synthase maximal activity (∼20%) and protein content of Complex II 70 kDa subunit (∼37%), Complex III Core 2 protein (∼51%), and Complex IV subunit IV (∼68%, all P < 0.05). Mitofusin 2 (∼71%) and GLUT4 (∼369%) protein content were also higher after training (both P < 0.05). Our findings indicate that low-volume HIT can rapidly improve glucose control and induce adaptations in skeletal muscle that are linked to improved metabolic health in patients with type 2 diabetes.

[1]  A. Zorzano,et al.  Subjects With Early-Onset Type 2 Diabetes Show Defective Activation of the Skeletal Muscle PGC-1α/Mitofusin-2 Regulatory Pathway in Response to Physical Activity , 2009, Diabetes Care.

[2]  J. Hawley,et al.  Mitochondrial function: use it or lose it , 2007, Diabetologia.

[3]  A. Bauman,et al.  Correlates of adults' participation in physical activity: review and update. , 2002, Medicine and science in sports and exercise.

[4]  J. Babraj,et al.  Extremely short duration high intensity interval training substantially improves insulin action in young healthy males , 2009, BMC endocrine disorders.

[5]  H. Kuipers,et al.  Influence of acute exercise on hyperglycemia in insulin-treated type 2 diabetes. , 2006, Medicine and science in sports and exercise.

[6]  Y. Shapiro,et al.  Physical exercise enhances hepatic insulin signaling and inhibits phosphoenolpyruvate carboxykinase activity in diabetes-prone Psammomys obesus. , 2004, Metabolism: clinical and experimental.

[7]  C. Earnest The role of exercise interval training in treating cardiovascular disease risk factors , 2009 .

[8]  C. Lebrun,et al.  Exercise and Type 2 Diabetes: American College of Sports Medicine and the American Diabetes Association: Joint Position Statement , 2011 .

[9]  Christopher Bell,et al.  Short‐term sprint interval training increases insulin sensitivity in healthy adults but does not affect the thermogenic response to β‐adrenergic stimulation , 2010, The Journal of physiology.

[10]  F. Toledo,et al.  Deficiency of electron transport chain in human skeletal muscle mitochondria in type 2 diabetes mellitus and obesity. , 2010, American journal of physiology. Endocrinology and metabolism.

[11]  E. Cauza,et al.  Strength and endurance training lead to different post exercise glucose profiles in diabetic participants using a continuous subcutaneous glucose monitoring system , 2005, European journal of clinical investigation.

[12]  W. Backes,et al.  Impaired in vivo mitochondrial function but similar intramyocellular lipid content in patients with type 2 diabetes mellitus and BMI-matched control subjects , 2006, Diabetologia.

[13]  M. Tarnopolsky,et al.  Low-volume interval training improves muscle oxidative capacity in sedentary adults. , 2011, Medicine and science in sports and exercise.

[14]  J. Holloszy,et al.  Exercise induces rapid increases in GLUT4 expression, glucose transport capacity, and insulin-stimulated glycogen storage in muscle. , 1994, The Journal of biological chemistry.

[15]  D. Klonoff Continuous glucose monitoring: roadmap for 21st century diabetes therapy. , 2005, Diabetes care.

[16]  A. Zorzano Regulation of mitofusin-2 expression in skeletal muscle. , 2009, Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme.

[17]  M. Tarnopolsky,et al.  A practical model of low‐volume high‐intensity interval training induces mitochondrial biogenesis in human skeletal muscle: potential mechanisms , 2010, The Journal of physiology.

[18]  B. Göke,et al.  Impact of fasting and postprandial glycemia on overall glycemic control in type 2 diabetes Importance of postprandial glycemia to achieve target HbA1c levels. , 2007, Diabetes research and clinical practice.

[19]  D. G. Newman,et al.  Muscle oxidative capacity is a better predictor of insulin sensitivity than lipid status. , 2003, The Journal of clinical endocrinology and metabolism.

[20]  R. Sigal,et al.  Effects of exercise on glycemic control and body mass in type 2 diabetes mellitus: a meta‐analysis of controlled clinical trials , 2002, JAMA.

[21]  J. Holloszy Skeletal muscle "mitochondrial deficiency" does not mediate insulin resistance. , 2009, The American journal of clinical nutrition.

[22]  G. King,et al.  Molecular understanding of hyperglycemia's adverse effects for diabetic complications. , 2002, JAMA.

[23]  Will G. Hopkins,et al.  Effects of Different Modes of Exercise Training on Glucose Control and Risk Factors for Complications in Type 2 Diabetic Patients: a Meta-Analysis , 2007, Diabetes Care.

[24]  R. Manders,et al.  Low-intensity exercise reduces the prevalence of hyperglycemia in type 2 diabetes. , 2010, Medicine and science in sports and exercise.

[25]  A. Bonen,et al.  Regulation of skeletal muscle mitochondrial fatty acid metabolism in lean and obese individuals. , 2009, The American journal of clinical nutrition.

[26]  A. Ceriello The possible role of postprandial hyperglycaemia in the pathogenesis of diabetic complications , 2003, Diabetologia.

[27]  M. Daly,et al.  PGC-1α-responsive genes involved in oxidative phosphorylation are coordinately downregulated in human diabetes , 2003, Nature Genetics.

[28]  Sandeep Raha,et al.  Short‐term sprint interval versus traditional endurance training: similar initial adaptations in human skeletal muscle and exercise performance , 2006, The Journal of physiology.