Endurance Training Improves Insulin Sensitivity, Metabolic Flexibility, and Mitochondrial Function in Type 2 Diabetes.
- 1Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
- 2The August Krogh Section for Human Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.
- 3Diabetes Pharmacology, Novo Nordisk A/S, Måløv, Denmark.
Abstract
To determine how endurance training influences insulin sensitivity, metabolic flexibility, and mitochondrial function in individuals with and without type 2 diabetes (T2D). Insulin sensitivity (2-step hyperinsulinaemic-isoglycaemic clamp), metabolic flexibility, and mitochondrial respiratory capacity and H₂O₂ emission were assessed in participants with T2D (n = 15) and controls (n = 14) before and after 12 weeks of supervised endurance training. Sensitivity analyses were performed using linear mixed-effects models including all available participants. At baseline, glucose clearance was lower in individuals with T2D compared with controls. Training increased glucose clearance (mL/min/kg FFM) in both groups, with larger model-derived improvements in T2D (Step 1: +1.43 [0.88-1.97]; Step 2: +3.18 [2.12-4.23]) than in controls (Step 1: +0.76 [0.21-1.31]; Step 2: +1.49 [0.53-2.45]). The group × time interaction was significant at the higher insulin step. Metabolic flexibility to fat-but not glucose-was reduced in T2D and improved modestly with training. Mitochondrial respiratory capacity did not differ between groups; however, training decreased mitochondria-specific respiration and H₂O₂ emission normalized to CS activity and respiration. Endurance training enhances insulin sensitivity and fat oxidation in individuals with T2D and induces favorable mitochondrial adaptations, despite the absence of intrinsic mitochondrial dysfunction.
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BibTeX
@article{hansen2026endurance,
title = {{Endurance Training Improves Insulin Sensitivity, Metabolic Flexibility, and Mitochondrial Function in Type 2 Diabetes.}},
author = {Maria Hansen and Sophie Møller and Ida Blom and Kristine K Lange and Andreas K Ziegler and Johanne E Farlov and Jacob Borch and Sofie A Hesselager and Jonathan K Hansen and Anna Liebmann and Mette H Dal and Thorbjörn Åkerström and Jørn W Helge and Ylva Hellsten and Flemming Dela},
journal = {Scandinavian journal of medicine \& science in sports},
year = {2026},
month = oct,
doi = {10.1111/sms.70383},
url = {https://europepmc.org/article/MED/42920400},
note = {CC BY},
}
RIS
TY - JOUR
TI - Endurance Training Improves Insulin Sensitivity, Metabolic Flexibility, and Mitochondrial Function in Type 2 Diabetes.
AU - Maria Hansen
AU - Sophie Møller
AU - Ida Blom
AU - Kristine K Lange
AU - Andreas K Ziegler
AU - Johanne E Farlov
AU - Jacob Borch
AU - Sofie A Hesselager
AU - Jonathan K Hansen
AU - Anna Liebmann
AU - Mette H Dal
AU - Thorbjörn Åkerström
AU - Jørn W Helge
AU - Ylva Hellsten
AU - Flemming Dela
PY - 2026
DA - 2026/10/30
JO - Scandinavian journal of medicine & science in sports
DO - 10.1111/sms.70383
UR - https://europepmc.org/article/MED/42920400
AB - To determine how endurance training influences insulin sensitivity, metabolic flexibility, and mitochondrial function in individuals with and without type 2 diabetes (T2D). Insulin sensitivity (2-step hyperinsulinaemic-isoglycaemic clamp), metabolic flexibility, and mitochondrial respiratory capacity and H₂O₂ emission were assessed in participants with T2D (n = 15) and controls (n = 14) before and after 12 weeks of supervised endurance training. Sensitivity analyses were performed using linear mixed-effects models including all available participants. At baseline, glucose clearance was lower in individuals with T2D compared with controls. Training increased glucose clearance (mL/min/kg FFM) in both groups, with larger model-derived improvements in T2D (Step 1: +1.43 [0.88-1.97]; Step 2: +3.18 [2.12-4.23]) than in controls (Step 1: +0.76 [0.21-1.31]; Step 2: +1.49 [0.53-2.45]). The group × time interaction was significant at the higher insulin step. Metabolic flexibility to fat-but not glucose-was reduced in T2D and improved modestly with training. Mitochondrial respiratory capacity did not differ between groups; however, training decreased mitochondria-specific respiration and H₂O₂ emission normalized to CS activity and respiration. Endurance training enhances insulin sensitivity and fat oxidation in individuals with T2D and induces favorable mitochondrial adaptations, despite the absence of intrinsic mitochondrial dysfunction.
SN - 0905-7188
SN - 1600-0838
ER -