Is Elevated PCWP during Exercise Sufficient to Reduce Exercise Capacity in Diabetics?

Dear Editor-in-Chief: In a recent issue of this journal, Regensteiner et al. (8) reported insightful observations regarding the presence of cardiac abnormalities during exercise in a small group of women with uncomplicated type 2 diabetes. The authors observed a disproportionate increment in pulmonary capillary wedge pressure (PCWP) during graded exercise compared with controls. Also, the high PCWP at peak exercise was inversely correlated with altered myocardial perfusion. These are interesting data obtained during exercise as diastolic function is most often investigated at rest. They also reported a similar absolute peak oxygen uptake between groups but a decrease in relative peak oxygen uptake in diabetics. Although the difference in body weight was not statistically significant between groups, the higher body weight in women with type 2 diabetes (∼7.5 kg) is most likely explaining the statistical difference in relative peak oxygen uptake. The absence of difference in exercise capacity between uncomplicated type 2 diabetics and control subjects is not surprising to us. We have evaluated the cardiopulmonary function at rest and during exercise in 10 men with type 2 diabetes and 9 control subjects matched for age (∼55 yr), gender, and body mass index (∼30 kg·m−2) (1). We found no differences in maximal oxygen uptake and cardiopulmonary parameters at maximal exercise between groups. The HbA1c, lipid profile, left atrial and ventricular masses and volumes, resting left ventricular (LV) systolic function, resting transmitral Doppler-derived LV diastolic function, pulmonary function, chemoreflex sensitivity, and HR variability were all similar between diabetics and controls. Patients with diabetes had a higher fasting blood glucose (6.5 ± 1.7 vs 5.2 ± 0.5 mmol·L−1; P < 0.045), lower tissue Doppler early velocities (7.8 ± 2.2 vs 10.7 ± 2.6 cm·s−1; P < 0.02) and a higher peak early transmitral filling velocity during early diastole/tissue Doppler early velocities ratio (9.0 ± 2.8 vs 6.7 ± 1.6; P < 0.04), suggesting that type 2 diabetes was associated with a lower myocardial relaxation and higher LV filling pressures. If the presence of type 2 diabetes eventually leads to a decrease in exercise capacity (3), the study by Regensteiner et al. (8), combined with our pilot data, suggest that well-controlled, uncomplicated type 2 diabetes per se is not necessarily associated with a lowered exercise capacity, notwithstanding the presence of early cardiac abnormalities during exercise. LV diastolic dysfunction (LVDD) is known to negatively affect exercise performance (4), whereas aerobic exercise training improves exercise capacity and has the potential to normalize LVDD in patients with uncomplicated type 2 diabetes (2). We could speculate that exercise performance is not affected in type 2 diabetics before the appearance of LVDD, the latter altering the generation of an adequate cardiac output, and not by an elevated PCWP per se without LVDD (5). Although a disproportionate PCWP during exercise was present in diabetics compared with controls (8), the similar cardiac output at peak exercise between the groups supports this hypothesis. In our pilot study, five subjects in both our diabetes and controls had LVDD, which could explain the reason why there was no difference in exercise capacity between our groups. Another interpretation may be that exercise performance is already affected before the diagnosis of type 2 diabetes, as in subjects with the metabolic syndrome and healthy first-degree relatives of patients with type 2 diabetes, in whom subclinical metabolic and/or cardiovascular abnormalities are present (6,7).