Cardiovascular Impairments Limit VO2 Peak in Type 1 Diabetes
Cardiovascular Impairments Limit VO2 Peak in Type 1 Diabetes
Purpose Cardiovascular risk, predicted by peak O2 uptake (V̇O2peak), is increased in type 1 diabetes. We examined the contribution of central and peripheral mechanisms to V̇O2peak in physically active adults with type 1 diabetes.
Methods 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.
Results The group with diabetes had lower V̇O2peak 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.
Conclusions Both central and peripheral cardiovascular impairments limit V̇O2peak in physically active adults with type 1 diabetes. Importantly, central limitations, and probably peripheral limitations as well, are associated with glycemic control.
Diabetes is associated with increased cardiovascular risk independent of CAD or hypertension. Peak O2 uptake (V̇O2peak) is a strong predictor of the risk of cardiovascular complications. Available data on the relation between type 1 diabetes and V̇O2peak are contradictory: Both reduced and similar V̇O2peak have been observed in patients with type 1 diabetes compared with that in healthy subjects. Importantly, several studies have reported that poor glycemic control reduces V̇O2peak in patients with type 1 diabetes, albeit absence of such association has also been reported.
In healthy subjects, V̇O2peak may be affected by limitations of pulmonary gas exchange, limitations of cardiac output (CO), redistribution of blood flow to active skeletal muscles, and skeletal muscle O2 extraction and use. In type 1 diabetes, both central and peripheral mechanisms are potential contributors to V̇O2peak reduction. Reduced ventilation at peak exercise, impaired lung diffusion capacity, reduced HRmax, ventricular diastolic dysfunction during exercise, and concomitant limitations of stroke volume (SV) and CO have been observed in patients with type 1 diabetes. In addition, our findings on faster active muscle deoxygenation in patients with type 1 diabetes may also reflect limited ability to increase central and peripheral O2 delivery during increasing O2 demand. Patients with type 1 diabetes, similar to patients with type 2 diabetes, have reduced blood volume (BV), which is likely one component of their ventricular diastolic dysfunction, as BV strongly correlates with diastolic filling rate. Peripheral vascular function, and herewith, peripheral O2 delivery to active muscles, may also be impaired in type 1 diabetes. Reduced leg blood flow, independent of CO, has been reported in patients with type 2 diabetes during submaximal exercise, suggesting maldistribution of active muscle blood flow. However, no studies to date have simultaneously examined the contribution of central and peripheral mechanisms to V̇O2peak in patients with type 1 diabetes.
The impedance cardiography method provides valid noninvasive evaluation of SV and CO at rest and during exercise. Near infrared spectroscopy (NIRS) is a valid noninvasive method used, for example, for monitoring active muscle deoxygenation status representing local imbalance between O2 delivery and use during exercise. The NIRS signal obtained can also be converted to reflect local blood flow in the active vastus lateralis muscle (Q̇VL). In this study, we hypothesized that men with type 1 diabetes would have lower V̇O2peak than healthy control men matched for age, anthropometry, and self-reported leisure time physical activity (LTPA). To examine the contribution of central and peripheral mechanisms to the hypothetically lower V̇O2peak, we simultaneously used the two noninvasive methods and compared cardiorespiratory and active leg muscle tissue responses to incremental exercise in the group with diabetes with those in the controls. We also determined BV of the subjects to examine its associations with cardiac responses to exercise.
Abstract and Introduction
Abstract
Purpose Cardiovascular risk, predicted by peak O2 uptake (V̇O2peak), is increased in type 1 diabetes. We examined the contribution of central and peripheral mechanisms to V̇O2peak in physically active adults with type 1 diabetes.
Methods 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.
Results The group with diabetes had lower V̇O2peak 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.
Conclusions Both central and peripheral cardiovascular impairments limit V̇O2peak in physically active adults with type 1 diabetes. Importantly, central limitations, and probably peripheral limitations as well, are associated with glycemic control.
Introduction
Diabetes is associated with increased cardiovascular risk independent of CAD or hypertension. Peak O2 uptake (V̇O2peak) is a strong predictor of the risk of cardiovascular complications. Available data on the relation between type 1 diabetes and V̇O2peak are contradictory: Both reduced and similar V̇O2peak have been observed in patients with type 1 diabetes compared with that in healthy subjects. Importantly, several studies have reported that poor glycemic control reduces V̇O2peak in patients with type 1 diabetes, albeit absence of such association has also been reported.
In healthy subjects, V̇O2peak may be affected by limitations of pulmonary gas exchange, limitations of cardiac output (CO), redistribution of blood flow to active skeletal muscles, and skeletal muscle O2 extraction and use. In type 1 diabetes, both central and peripheral mechanisms are potential contributors to V̇O2peak reduction. Reduced ventilation at peak exercise, impaired lung diffusion capacity, reduced HRmax, ventricular diastolic dysfunction during exercise, and concomitant limitations of stroke volume (SV) and CO have been observed in patients with type 1 diabetes. In addition, our findings on faster active muscle deoxygenation in patients with type 1 diabetes may also reflect limited ability to increase central and peripheral O2 delivery during increasing O2 demand. Patients with type 1 diabetes, similar to patients with type 2 diabetes, have reduced blood volume (BV), which is likely one component of their ventricular diastolic dysfunction, as BV strongly correlates with diastolic filling rate. Peripheral vascular function, and herewith, peripheral O2 delivery to active muscles, may also be impaired in type 1 diabetes. Reduced leg blood flow, independent of CO, has been reported in patients with type 2 diabetes during submaximal exercise, suggesting maldistribution of active muscle blood flow. However, no studies to date have simultaneously examined the contribution of central and peripheral mechanisms to V̇O2peak in patients with type 1 diabetes.
The impedance cardiography method provides valid noninvasive evaluation of SV and CO at rest and during exercise. Near infrared spectroscopy (NIRS) is a valid noninvasive method used, for example, for monitoring active muscle deoxygenation status representing local imbalance between O2 delivery and use during exercise. The NIRS signal obtained can also be converted to reflect local blood flow in the active vastus lateralis muscle (Q̇VL). In this study, we hypothesized that men with type 1 diabetes would have lower V̇O2peak than healthy control men matched for age, anthropometry, and self-reported leisure time physical activity (LTPA). To examine the contribution of central and peripheral mechanisms to the hypothetically lower V̇O2peak, we simultaneously used the two noninvasive methods and compared cardiorespiratory and active leg muscle tissue responses to incremental exercise in the group with diabetes with those in the controls. We also determined BV of the subjects to examine its associations with cardiac responses to exercise.
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