Central and peripheral cardiovascular impairments limit VO(2peak) in type 1 diabetes.

Abstract

Cardiovascular risk, predicted by peak O2 uptake (VO(2peak)), is increased in type 1 diabetes. We examined the contribution of central and peripheral mechanisms to VO(2peak) in physically active adults with type 1 diabetes. Seven men with type 1 diabetes and 10 healthy age-, anthropometry-, and physical activity-matched men performed incremental cycling exercise until volitional fatigue. Alveolar gas exchange (turbine and mass spectrometry), cardiac function and systemic vascular resistance (impedance cardiography), and local active leg muscle deoxygenation and blood flow (near infrared spectroscopy) were monitored. Arterial-venous O2 difference was calculated (Fick principle). Blood volume (BV) (carbon monoxide rebreathing method) and glycemic control (glycosylated hemoglobin) were determined. The group with diabetes had lower VO(2peak) than controls (47 ± 5 vs 56 ± 7 mL·min·kg fat-free mass, P < 0.05). At peak exercise, fat-free mass-adjusted stroke volume (SV) and cardiac output (CO) were lower and systemic vascular resistance was higher in the group with diabetes than those in controls (P < 0.05). Leg muscle blood flow was reduced independently of CO in the group with diabetes at peak exercise (P < 0.05), whereas arterial-venous O2 difference was similar in the groups throughout the exercise (P > 0.05). The group with diabetes had lower relative BV than controls (P < 0.01), and BV correlated positively with peak SV and peak CO (P < 0.001). In the group with diabetes, peak SV and peak CO correlated (P < 0.05) and peak leg muscle blood flow tended to correlate (P = 0.070) inversely with glycosylated hemoglobin. Both central and peripheral cardiovascular impairments limit VO(2peak) in physically active adults with type 1 diabetes. Importantly, central limitations, and probably peripheral limitations as well, are associated with glycemic control.