Skeletal Muscle Deoxygenation After the Onset of Moderate Exercise Suggests Slowed Microvascular Blood Flow Kinetics in Type 2 Diabetes

OBJECTIVE:--People with type 2 diabetes have impaired exercise responses even in the absence of cardiovascular complications. One key factor associated with the exercise intolerance is abnormally slowed oxygen uptake (VO₂) kinetics during submaximal exercise. The mechanisms of this delayed adaptatio...

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Published inDiabetes care Vol. 30; no. 11; pp. 2880 - 2885
Main Authors Bauer, Timothy A, Reusch, Jane E.B, Levi, Moshe, Regensteiner, Judith G
Format Journal Article
LanguageEnglish
Published Alexandria, VA American Diabetes Association 01.11.2007
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Summary:OBJECTIVE:--People with type 2 diabetes have impaired exercise responses even in the absence of cardiovascular complications. One key factor associated with the exercise intolerance is abnormally slowed oxygen uptake (VO₂) kinetics during submaximal exercise. The mechanisms of this delayed adaptation during exercise are unclear but probably relate to impairments in skeletal muscle blood flow. This study was conducted to compare skeletal muscle deoxygenation (deoxygenated hemoglobin/myoglobin [HHb]) responses and estimated microvascular blood flow (Qm) kinetics in type 2 diabetic and healthy subjects after the onset of moderate exercise. RESEARCH DESIGN AND METHODS--Pulmonary VO₂ kinetics and [HHb] (using near-infrared spectroscopy) were measured in 11 type 2 diabetic and 11 healthy subjects during exercise transitions from unloaded to moderate cycling exercise. Qm responses were calculated using VO₂ kinetics and [HHb] responses via rearrangement of the Fick principle. RESULTS:--VO₂ kinetics were slowed in type 2 diabetic compared with control subjects (43.8 ± 9.6 vs. 34.2 ± 8.2 s, P < 0.05), and the initial [HHb] response after the onset of exercise exceeded the steady-state level of oxygen extraction in type 2 diabetic compared with control subjects. The mean response time of the estimated Qm increase was prolonged in type 2 diabetic compared with healthy subjects (47.7 ± 14.3 vs. 35.8 ± 10.7 s, P < 0.05). CONCLUSIONS:--Type 2 diabetic skeletal muscle demonstrates a transient imbalance of muscle O₂ delivery relative to O₂ uptake after onset of exercise, suggesting a slowed Qm increase in type 2 diabetic muscle. Impaired vasodilatation due to vascular dysfunction in type 2 diabetes during exercise may contribute to this observation. Further study of the mechanisms leading to impaired muscle oxygen delivery may help explain the abnormal exercise responses in type 2 diabetes.
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ISSN:0149-5992
1935-5548
DOI:10.2337/dc07-0843