Effect of physical training on mitochondrial respiration and reactive oxygen species release in skeletal muscle in patients with obesity and type 2 diabetes

TY - JOUR

T1 - Effect of physical training on mitochondrial respiration and reactive oxygen species release in skeletal muscle in patients with obesity and type 2 diabetes

AU - Hey-Mogensen, Martin

AU - Højlund, K

AU - Vind, B F

AU - Wang, L

AU - Dela, F

AU - Beck-Nielsen, H

AU - Fernström, M

AU - Sahlin, K

PY - 2010/9/1

Y1 - 2010/9/1

N2 - Aim/hypothesis: Studies have suggested a link between insulin resistance and mitochondrial dysfunction in skeletal muscles. Our primary aim was to investigate the effect of aerobic training on mitochondrial respiration and mitochondrial reactive oxygen species (ROS) release in skeletal muscle of obese participants with and without type 2 diabetes. Methods: Type 2 diabetic men (n∈=∈13) and control (n∈=∈14) participants matched for age, BMI and physical activity completed 10 weeks of aerobic training. Pre- and post-training muscle biopsies were obtained before a euglycaemic- hyperinsulinaemic clamp and used for measurement of respiratory function and ROS release in isolated mitochondria. Results: Training significantly increased insulin sensitivity, maximal oxygen consumption and muscle mitochondrial respiration with no difference between groups. When expressed in relation to a marker of mitochondrial density (intrinsic mitochondrial respiration), training resulted in increased mitochondrial ADP-stimulated respiration (with NADH-generating substrates) and decreased respiration without ADP. Intrinsic mitochondrial respiration was not different between groups despite lower insulin sensitivity in type 2 diabetic participants. Mitochondrial ROS release tended to be higher in participants with type 2 diabetes. Conclusions/interpretation: Aerobic training improves muscle respiration and intrinsic mitochondrial respiration in untrained obese participants with and without type 2 diabetes. These adaptations demonstrate an increased metabolic fitness, but do not seem to be directly related to training-induced changes in insulin sensitivity.

AB - Aim/hypothesis: Studies have suggested a link between insulin resistance and mitochondrial dysfunction in skeletal muscles. Our primary aim was to investigate the effect of aerobic training on mitochondrial respiration and mitochondrial reactive oxygen species (ROS) release in skeletal muscle of obese participants with and without type 2 diabetes. Methods: Type 2 diabetic men (n∈=∈13) and control (n∈=∈14) participants matched for age, BMI and physical activity completed 10 weeks of aerobic training. Pre- and post-training muscle biopsies were obtained before a euglycaemic- hyperinsulinaemic clamp and used for measurement of respiratory function and ROS release in isolated mitochondria. Results: Training significantly increased insulin sensitivity, maximal oxygen consumption and muscle mitochondrial respiration with no difference between groups. When expressed in relation to a marker of mitochondrial density (intrinsic mitochondrial respiration), training resulted in increased mitochondrial ADP-stimulated respiration (with NADH-generating substrates) and decreased respiration without ADP. Intrinsic mitochondrial respiration was not different between groups despite lower insulin sensitivity in type 2 diabetic participants. Mitochondrial ROS release tended to be higher in participants with type 2 diabetes. Conclusions/interpretation: Aerobic training improves muscle respiration and intrinsic mitochondrial respiration in untrained obese participants with and without type 2 diabetes. These adaptations demonstrate an increased metabolic fitness, but do not seem to be directly related to training-induced changes in insulin sensitivity.

KW - Aged

KW - Diabetes Mellitus, Type 2

KW - Exercise

KW - Humans

KW - Male

KW - Middle Aged

KW - Mitochondria

KW - Muscle, Skeletal

KW - Obesity

KW - Reactive Oxygen Species

U2 - 10.1007/s00125-010-1813-x

DO - 10.1007/s00125-010-1813-x

M3 - Journal article

C2 - 20526759

SN - 0012-186X

VL - 53

SP - 1976

EP - 1985

JO - Diabetologia

JF - Diabetologia

IS - 9

ER -