Exercise capacity is reduced in T2DM, whilst data is conflicting for T1DM subjects. Diastolic dysfunction is thought to be a key contributor to reduced exercise performance in DM. We sought to characterise exercise capacity and identify predictors of exercise performance in DM subjects.
Sixty subjects (20 T1DM, 20 T2DM, and 20 age/sex-matched controls [C]) performed VO2max testing and a semi-supine bicycle ergometer five-stage exercise echocardiography protocol. Resting cardiac function, and non-invasive estimation of central haemodynamic augmentation (including left ventricular ejection fraction [LVEF], cardiac output [CO], and pulmonary artery systolic pressure [PASP]) during exercise were measured.
Compared to T1DM participants, T2DM subjects were older (52 ± 11 vs. 35 ± 8 years, P<0.0005) and heavier (body surface area [BSA] 2.07 ± 0.17 vs. 1.90 ± 0.21, P=0.035). Glycaemic control was worse in T1DM (HbA1c 8.1 ± 1.5 vs. 7.4 ± 1.1%, P<0.0005). Self-reported exercise activity was similar between DM and C subjects. Baseline LV systolic function was normal, and frequency of diastolic dysfunction was similar between T2DM and their C subgroup (20% vs. 20%, Fisher’s χ2, P=1.0). VO2max was normal in T1DM, but reduced in T2DM compared to their C subgroup (26.5 ± 5.7 vs. 37.7 ± 8.2 ml/min/kg; ANOVA P<0.0005, posthoc P=0.01). Significant negative predictors of maximal VO2 (ml/min) on multiple regression were female sex, increasing age and T2DM, whilst increasing BSA and LV end diastolic volume (LVEDV) had positive significant associations (R2=0.806, P<0.0005). T1DM, diastolic dysfunction, and resting CO and PASP were not significant predictors in the model.
T2DM is associated with reduced exercise capacity, and is not due to diastolic dysfunction. Insulin resistance and other metabolic abnormalities rather than dysglycaemia may explain the differences observed between T2DM and T1DM.