Single‐leg exercise training augments in vivo skeletal muscle oxidative flux and vascular content and function in adults with type 2 diabetes
| Autor: | Nina Kvaratskhelia, Gregory B. Pott, Deirdre Rafferty, Irene E. Schauer, Jane E.B. Reusch, Amy G. Huebschmann, Judith G. Regensteiner, Layla A Abushamat, Melanie Cree-Green, Taro Kaelix Johnson, Rebecca L. Scalzo, Mary O. Whipple, Leslie A. Knaub |
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| Rok vydání: | 2021 |
| Předmět: |
Adult
0301 basic medicine medicine.medical_specialty endocrine system diseases Physiology Population Type 2 diabetes Oxidative phosphorylation 03 medical and health sciences Oxygen Consumption 0302 clinical medicine Diabetes mellitus Internal medicine Humans Medicine Muscle Skeletal education Exercise Leg education.field_of_study business.industry nutritional and metabolic diseases Skeletal muscle Cardiorespiratory fitness Oxygenation medicine.disease Oxidative Stress 030104 developmental biology Endocrinology medicine.anatomical_structure Diabetes Mellitus Type 2 business 030217 neurology & neurosurgery Ex vivo |
| Zdroj: | The Journal of Physiology. 600:963-978 |
| ISSN: | 1469-7793 0022-3751 |
| DOI: | 10.1113/jp280603 |
| Popis: | KEY POINTS People with type 2 diabetes (T2D) have impaired skeletal muscle oxidative flux due to limited oxygen delivery. In the current study, this impairment in oxidative flux in people with T2D was abrogated with a single-leg exercise training protocol. Additionally, single-leg exercise training increased skeletal muscle CD31 content, calf blood flow and state 4 mitochondrial respiration in all participants. ABSTRACT Cardiorespiratory fitness is impaired in type 2 diabetes (T2D), conferring significant cardiovascular risk in this population; interventions are needed. Previously, we reported that a T2D-associated decrement in skeletal muscle oxidative flux is ameliorated with acute use of supplemental oxygen, suggesting that skeletal muscle oxygenation is rate-limiting to in vivo mitochondrial oxidative flux during exercise in T2D. We hypothesized that single-leg exercise training (SLET) would improve the T2D-specific impairment in in vivo mitochondrial oxidative flux during exercise. Adults with (n = 19) and without T2D (n = 22) with similar body mass indexes and levels of physical activity participated in two weeks of SLET. Following SLET, in vivo oxidative flux measured by 31 P-MRS increased in participants with T2D, but not people without T2D, measured by the increase in initial phosphocreatine synthesis (P = 0.0455 for the group × exercise interaction) and maximum rate of oxidative ATP synthesis (P = 0.0286 for the interaction). Additionally, oxidative phosphorylation increased in all participants with SLET (P = 0.0209). After SLET, there was no effect of supplemental oxygen on any of the in vivo oxidative flux measurements in either group (P > 0.02), consistent with resolution of the T2D-associated oxygen limitation previously observed at baseline in subjects with T2D. State 4 mitochondrial respiration also improved in muscle fibres ex vivo. Skeletal muscle vasculature content and calf blood flow increased in all participants with SLET (P |
| Databáze: | OpenAIRE |
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