Bauer Timothy A, Reusch Jane E B, Levi Moshe, Regensteiner Judith G
Division of Cardiology, University of Colorado at Denver and Health Sciences Center, Denver, Colorado, USA.
Diabetes Care. 2007 Nov;30(11):2880-5. doi: 10.2337/dc07-0843. Epub 2007 Aug 3.
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.
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.
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).
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.
2型糖尿病患者即使在没有心血管并发症的情况下，其运动反应也会受损。与运动不耐受相关的一个关键因素是次最大运动期间氧摄取（VO₂）动力学异常减慢。运动期间这种延迟适应的机制尚不清楚，但可能与骨骼肌血流受损有关。本研究旨在比较2型糖尿病患者和健康受试者在中等强度运动开始后骨骼肌脱氧（脱氧血红蛋白/肌红蛋白[HHb]）反应和估计的微血管血流（Qm）动力学。
在11名2型糖尿病患者和11名健康受试者从无负荷运动过渡到中等强度骑自行车运动期间，测量肺VO₂动力学和[HHb]（使用近红外光谱法）。通过重新排列菲克原理，利用VO₂动力学和[HHb]反应计算Qm反应。
与对照组相比，2型糖尿病患者的VO₂动力学减慢（43.8±9.6秒对34.2±8.2秒，P<0.05），并且与对照组相比，2型糖尿病患者运动开始后的初始[HHb]反应超过了氧摄取的稳态水平。与健康受试者相比，2型糖尿病患者估计的Qm增加的平均反应时间延长（47.7±14.3秒对35.8±10.7秒，P<0.05）。
2型糖尿病患者的骨骼肌在运动开始后表现出肌肉氧输送相对于氧摄取的短暂失衡，表明2型糖尿病患者肌肉中Qm增加减慢。2型糖尿病患者运动期间由于血管功能障碍导致的血管舒张受损可能导致这一观察结果。对导致肌肉氧输送受损的机制进行进一步研究可能有助于解释2型糖尿病患者异常的运动反应。
