Oral Abstract Session
SCMR 22nd Annual Scientific Sessions
Alice Mezincescu, MD
British Heart Foundation Clinical Research Fellow
University of Aberdeen
Trevor Ahearn, PhD
Physicist
NHS Grampian
Amelia Rudd
Cardiac Physiologist
University of Aberdeen
Caroline Scally
Cardiac Research Fellow
University of Aberdeen
Lesley Cheynne
Laboratory Technician
University of Aberdeen
Hassan Abbas, BSc, MB
Clinical Research Fellow
University of Aberdeen
Graham Horgan, PhD
Principal Statistical Consultant
University of Aberdeen
Sam Philip, MD, MB
Honorary Clinical Senior Lecturer
University of Aberdeen
Mirela Delibegovic
Professor in Diabetic Medicine
University of Aberdeen
Gerald Lobley, PhD
Retired Senior Researcher
University of Aberdeen
Frank Thies, PhD
Reader
University of Aberdeen
Stuart Gray, PhD
Lecturer in Exercise and Metabolic Health
University of Glasgow
Anke Henning, PhD
Research Group Leader
Max Planck Institut for Biological Cybernetics
Dana Dawson, MD, PhD
Professor of Cardiovascular Medicine and Consultant Cardiologist
University of Aberdeen
Background:
High levels of tri- and di-acylglycerols are found in skeletal muscle of endurance trained athletic healthy volunteers (Athl-HV) and type 2 diabetes patients (T2D), however their metabolic phenotypes are at opposite ends of insulin sensitivity and cardiometabolic risk. Here we investigated if intramyocellular lipid saturation may constitute a previously unknown determinant of cardiometabolic risk. Secondly, we explored if deconditioning/exercise training impacts on intramyocellular lipid saturation in Athl-HV/T2D, respectively.
Methods:
Age matched male Athl-HV and T2D were enrolled. Athl-HV performed endurance training ≥5 years, actively training ≥360 minutes/week; T2D performed ≤150 min exercise/week. Bike-cardiopulmonary exercise testing (CPET), blood sampling for insulin sensitivity (HOMA2-IR*) and single voxel 1H-magnetic resonance spectroscopy (1H-MRS) of the right vastus lateralis were performed in all at baseline and after exercise intervention (4 week deconditioning in Athl-HV and investigator-supervised bike training at ≥65% of baseline peakVO2, 5 hours/week x 8 weeks in T2D). 1H-MRS was acquired on 3T Philips Achieva with a 16-channel coil, point-resolved spectroscopy, variable pulse power and optimized relaxation delay water suppression.
1H-MRS data were analysed in LCModel. Intensities of total, saturated and unsaturated intra- and extra-myocellular lipids and creatine resonance lines were normalized to internal water. Fractional lipid mass (fLM) [lipid/(lipid+water)] as well as fractions of saturated (fSL) (saturated/total) and unsaturated (fUL) (unsaturated/total) lipid components were calculated. Data were analysed by paired/unpaired t tests and shown as mean±SEM. Significance was set at p<0.05.
Results:
Deconditioning/exercise traning led to significant weight gain/loss in Athl-HV/T2D, respectively. Peak VO2 significantly decreased in Athl-HV and increased in T2D. Insulin sensitivity was higher in Athl-HV than T2D (Table 1).
Higher fLM was found in the skeletal muscle of T2D compared to Athl-HV, at baseline (p=0.002) and after exercise intervention (p=0.03), Figure 1A.
At baseline, T2D had a trend for lower fSL and higher fUL compared to Athl-HV (80±8 vs 86±1% and 19±3 vs 14±7%, p=0.07 for both). Neither fSL nor fUL changed with deconditioning in Athl-HV. However, exercise training resulted in a significant increase in fSL (80±8 to 88±3%) and reciprocal decrease in fUL (19±9 to 12±3%) in T2D (both p=0.004), Figure 1B and C.
Conclusion:
We demonstrate differences in total amount and saturation of intramyocellular lipids between Athl-HV and T2D. Further, intramyocellular lipid saturation is modulated by exercise training in T2D, to mirror the phenotype seen in Athl-HV, implying that this may be either an independent or an earlier marker of improved cardio-metabolic health than insulin sensitivity.