Endocrine Abstracts (2010) 22 P306

Exercise-related levels of acetylcarnitine in skeletal muscle of individuals with type 1 diabetes in Eu- and hyperglycaemia assessed by 1H-MR spectroscopy

Stefan Jenni1,2, Andreas Boss3, Roland Kreis3, Michael Ith3,4, Emanuel Christ1, Chris Boesch3 & Christoph Stettler1

1Division of Endocrinology, Diabetes and Clinical Nutrition, Inselspital Bern, University Hospital and University of Bern, Bern, Switzerland; 2International Centre for Circulatory Health, Imperial College at St Mary’s, London, UK; 3Department of Clinical Research, University of Bern, Bern, Switzerland; 4Institute for Diagnostic, Interventional and Pediatric Radiology, Inselspital Bern, University Hospital and University of Bern, Bern, Switzerland.

Background: Acetylcarnitine (AC) is involved in intramyocellular fuel metabolism during exercise. So far, little is known on exercise-associated myocellular AC levels in patients with type 1 diabetes. In particular, it is unknown whether AC levels differ according to glucose values in diabetic patients. 1H magnetic resonance spectroscopy (MRS) of the skeletal muscle allows for the non-invasive assessment of acetylcarnitine (AC) accumulation. The present study assessed exercise-related intramyocellular AC levels in stable eu- and hyperglycaemic conditions in individuals with type 1 diabetes.

Methods: Seven physically active men with type 1 diabetes (mean±S.E.M. age 33.5±2.4 years, diabetes duration 20.1±3.6 years, HbA1c 6.7±0.2%, VO2 peak 50.3±4.5 ml/min per kg) were studied twice while cycling 120 min at 55–60% of VO2 peak, with a glycaemia of either 5 or 11 mmol/l and identical insulinaemia. 1H-MRS spectra were obtained before and 80 min after completion of exercise from vastus intermedius. AC spectra were analyzed using a fit-strategy optimized for the AC-peak and AC content was expressed in absolute arbitrary units (a.u.) relative to the water signal intensity.

Results: In euglycaemia AC increased from 0.3±0.2 a.u. (mean±S.E.M.) pre-exercise to 4.1±0.5 a.u. postexercise (P=0.0001). In hyperglycaemia AC increased from 0.7±0.3 a.u. to 2.4±0.5 a.u. (P=0.01). The increments were significantly higher in euglycaemia compared with hyperglycaemia (P=0.004). Higher AC accumulation in euglycaemia was associated with higher lipid oxidation at end of exercise.

Conclusions: In individuals with type 1 diabetes performing aerobic exercise intramyocellular levels of AC differ according to glycaemic levels. The finding of higher AC levels in euglycaemia where fuel metabolism strongly relied on lipid oxidations is compatible with previous reports in healthy individuals and implies comparable mechanisms in patients with type 1 diabetes during physical exercise.

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