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

¹Division of Cardiology, University of Colorado at Denver and Health Sciences Center, Denver, Colorado 80262;
²Division of Endocrinology, University of Colorado at Denver and Health Sciences Center, Denver, Colorado 80262;
³Division of Renal Disease, University of Colorado at Denver and Health Sciences Center, Denver, Colorado 80262;
⁴Division of General Internal Medicine, University of Colorado at Denver and Health Sciences Center, Denver, Colorado 80262;
⁵Center for Women's Health Research, Denver, Colorado;
⁶Denver VA Medical Center, Denver, Colorado

ABSTRACT

Objective:People with type 2 diabetes (T2DM) have impaired exercise responses even in the absence of cardiovascular complications. One key factor associated with the exercise intolerance is abnormally slowed oxygen uptake (O₂) kinetics during submaximal exercise. The mechanisms of this delayed adaptation during exercise are unclear but likely relate to impairments in skeletal muscle blood flow. The study was conducted to compare skeletal muscle deoxygenation ([HHb]) responses and estimated microvascular blood flow (Qm) kinetics in T2DM and healthy subjects following the onset of moderate exercise.

Research design and Methods:Pulmonary O₂ kinetics and [HHb] (using near infrared spectroscopy) were measured in 11 T2DM and 11 healthy subjects during exercise transitions from unloaded to moderate cycling exercise. Qm responses were calculated using O₂ kinetics and [HHb] responses via rearrangement of the Fick principle.

Results: O₂ kinetics were slowed in T2DM compared with controls (43.8±9.6s vs. 34.2±8.2s, P<0.05), and the initial [HHb] response following the onset of exercise exceeded the steady state level of oxygen extraction in T2DM compared with controls. Mean response time of estimated Qm increase was prolonged in T2DM compared with healthy subjects (47.7±14.3s vs. 35.8±10.7s, P<0.05).

Conclusions:T2DM skeletal muscle demonstrates a transient imbalance of muscle O₂ delivery relative to O₂ uptake following exercise onset, suggesting a slowed Qm increase in T2DM muscle. Impaired vasodilatation secondary to vascular dysfunction in T2DM during exercise may contribute to this observation. Further study of mechanisms leading to impaired muscle oxygen delivery may help explain the abnormal exercise responses in T2DM.

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