Goulding 2022 Abstract Bioblast

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Goulding Richie P, Strating S, van der Laan M, Noort W, Kolodyazhna A, Bloemers FW, Wüst RCI(2022) Mitochondrial function is not impaired in type 1 diabetes but does not respond to 4-weeks endurance training. Bioblast 2022: BEC Inaugural Conference.

Link: Bioblast 2022: BEC Inaugural Conference

Goulding Richie P, Strating S, van der Laan M, Noort W, Kolodyazhna A, Bloemers FW, Wuest Rob CI (2022)

Event: Bioblast 2022

Type 1 diabetes mellitus (T1DM) is a disease characterized by the destruction of the insulin-producing, pancreatic β-cells, where an inability to maintain glucose homeostasis causes multi-organ problems. It has been reported that young, otherwise healthy individuals with T1DM display significant skeletal muscle mitochondrial dysfunction when compared to physical activity-matched healthy controls. This suggests that skeletal muscle mitochondria possess poorer plasticity with respect to the beneficial effects of exercise training, however, this hypothesis has never been tested.

Here, we tested the hypothesis that 1) individuals with T1DM would evince a lower maximal oxygen uptake (VO2max) and mitochondrial oxidative capacity (OXPHOS) compared to healthy controls matched for age, sex and physical activity, and 2) the magnitude of increase in OXPHOS capacity following 4-weeks endurance training would be lesser in individuals with T1DM compared to controls.

Vastus lateralis muscle biopsies were taken and cardiopulmonary exercise testing was performed on patients with T1DM and healthy controls, both before and after 4-weeks of moderate intensity endurance training. Mitochondrial respiration was assessed in permeabilized fibers using high-resolution respirometry (Oroboros O2k, Innsbruck, Austria).

Data collection is still ongoing. Preliminary results suggest a lower VO2max in T1DM compared to controls (T1DM: 38.8 ± 11.5 mL.kg-1.min-1, n=18, controls: 44.7 ± 8.0 mL.kg-1.min-1, n=9) and OXPHOS capacity appears similar between groups (T1DM: 99.5 ± 38.2 pmol.s-1.mg-1, n=15, controls: 100.3 ± 20.0 pmol.s-1.mg-1, n=8), however, uneven group sizes preclude statistical comparison at present. In the subset of eight T1DM patients that have currently undergone the training intervention, exercise training improved whole-body exercise capacity in T1DM patients (peak power output, pre: 272 ± 77 W, post: 281 ± 81 W, P=0.04), however, OXPHOS capacity did not respond to exercise training (pre: 94.5 ± 39.2 pmol.s-1.mg-1, post: 94.2 ± 33.1 pmol.s-1.mg-1, P=0.98).

Inconsistent with our first hypothesis, our preliminary data indicate no deficit in mitochondrial function when compared to matched healthy controls. Consistent with our second hypothesis, however, mitochondrial oxidative capacity did not respond to four weeks of endurance training despite improvements in whole-body exercise capacity. Hence, these data provide the first empirical support for the notion that individuals with T1DM possess inherently poor mitochondrial plasticity. It is expected that data collection and analysis will be completed by August 2022, and the full data set will illuminate the mechanistic underpinnings of these initial observations.

Keywords: Type 1 diabetes, Exercise, Mitochondrial function, Oxidative capacity

O2k-Network Lab: NL Amsterdam Wuest RC


Goulding RP(1), Strating S(1), van der Laan M(1), Noort W(1), Kolodyazhna A(1), Bloemers FW(2), Wüst RCI(1)
  1. Laboratory for Myology, Faculty of Behavioural and Movement Sciences, Amsterdam Movement Sciences, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands
  2. Department of Trauma Surgery, Amsterdam Movement Sciences, Amsterdam UMC, Vrije Universiteit Amsterdam, De Boelelaan 1117, Amsterdam, The Netherlands


Labels: MiParea: Respiration, Exercise physiology;nutrition;life style  Pathology: Diabetes 

Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue 

Coupling state: OXPHOS 

HRR: Oxygraph-2k