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Sci Rep. 2017 Mar 16;7(1):204. doi: 10.1038/s41598-017-00276-8.

Effects of high-intensity interval training and moderate-intensity continuous training on glycaemic control and skeletal muscle mitochondrial function in db/db mice.

Author information

1
Université Clermont Auvergne, Laboratoire des Adaptations Métaboliques à l'Exercice en conditions Physiologiques et Pathologiques (AME2P), Clermont-Ferrand, F-63000, France. vivien.chavanelle@valbiotis.com.
2
Valbiotis S.A.S., La Rochelle, France. vivien.chavanelle@valbiotis.com.
3
Université Clermont Auvergne, Laboratoire des Adaptations Métaboliques à l'Exercice en conditions Physiologiques et Pathologiques (AME2P), Clermont-Ferrand, F-63000, France.
4
INRA, Unité de Nutrition Humaine (UNH, UMR 1019), CRNH Auvergne, France.
5
Valbiotis S.A.S., La Rochelle, France.

Abstract

Physical activity is known as an effective strategy for prevention and treatment of Type 2 Diabetes. The aim of this work was to compare the effects of a traditional Moderate Intensity Continuous Training (MICT) with a High Intensity Interval Training (HIIT) on glucose metabolism and mitochondrial function in diabetic mice. Diabetic db/db male mice (N = 25) aged 6 weeks were subdivided into MICT, HIIT or control (CON) group. Animals in the training groups ran on a treadmill 5 days/week during 10 weeks. MICT group ran for 80 min (0° slope) at 50-60% of maximal speed (Vmax) reached during an incremental test. HIIT group ran thirteen times 4 minutes (20° slope) at 85-90% of Vmax separated by 2-min-rest periods. HIIT lowered fasting glycaemia and HbA1c compared with CON group (p < 0.05). In all mitochondrial function markers assessed, no differences were noted between the three groups except for total amount of electron transport chain proteins, slightly increased in the HIIT group vs CON. Western blot analysis revealed a significant increase of muscle Glut4 content (about 2 fold) and higher insulin-stimulated Akt phosphorylation ratios in HIIT group. HIIT seems to improve glucose metabolism more efficiently than MICT in diabetic mice by mechanisms independent of mitochondrial adaptations.

PMID:
28303003
PMCID:
PMC5427962
DOI:
10.1038/s41598-017-00276-8
[Indexed for MEDLINE]
Free PMC Article

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