Skeletal muscle microvascular insulin resistance in type 2 diabetes is not improved by eight weeks of regular walking.
Skeletal muscle microvascular insulin resistance in type 2 diabetes is not improved by eight weeks of regular walking.
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DOI：
10.1152/japplphysiol.00174.2020
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发表时间：
2020-07
影响因子：
3.3
通讯作者：
Lauren K. Park;E. Parks;R. Pettit-Mee;Makenzie L. Woodford;Thaysa Ghiarone;James A H Smith;A. Sales;L. Martinez‐Lemus;Camila Manrique-Acevedo;J. Padilla
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作者：
Lauren K. Park;E. Parks;R. Pettit-Mee;Makenzie L. Woodford;Thaysa Ghiarone;James A H Smith;A. Sales;L. Martinez‐Lemus;Camila Manrique-Acevedo;J. Padilla
我们的目的是检查2型糖尿病(T2D)患者是否表现出对高胰岛素-正常血糖钳夹的反应，腿部血管传导抑制和骨骼肌毛细血管灌流，并测试这两个变量是否正相关。随后，我们研究了T2D相关的骨骼肌微血管胰岛素抵抗以及整体血管功能障碍是否会通过8周的步行干预(45分钟，心率储备的60%，每周5次)得到改善。我们报告，与健康受试者相比，患有T2D的超重和肥胖者在胰岛素刺激下腿部血管传导性、骨骼肌毛细血管灌流和Akt磷酸化的增加受到抑制。值得注意的是，我们发现在患有T2D的患者中，那些对胰岛素反应的腿部血管传导性增加较少的人的肌肉毛细血管灌注量增加最低，这表明有限的肌肉毛细血管灌注量可能在一定程度上与上游阻力血管对胰岛素反应的扩张能力受损有关。此外，我们还表明，八周的步行干预没有引起体重减轻，但不足以改善先前久坐不动、超重/肥胖的T2D受试者的骨骼肌微血管胰岛素抵抗，尽管依从性和耐受性很高。然而，步行干预确实改善了(P<；0.05)动脉血流介导的扩张(+4.52%)，降低了糖化血红蛋白(-0.75%)。在T2D中，可能需要持续时间更长的体力活动干预，通过招募最大数量的肌肉纤维来吸引大型肌肉群，并导致代谢危险因素的显著减少，从而彻底改变微血管胰岛素抵抗。
We aimed to examine if individuals with type 2 diabetes (T2D) exhibit suppressed leg vascular conductance and skeletal muscle capillary perfusion in response to a hyperinsulinemic-euglycemic clamp, and to test whether these two variables are positively correlated. Subsequently, we examined if T2D-associated skeletal muscle microvascular insulin resistance, as well as overall vascular dysfunction, would be ameliorated by an eight-week walking intervention (45 minutes at 60% of heart rate reserve, 5 sessions/week). We report that, relative to healthy subjects, overweight and obese individuals with T2D exhibit depressed insulin-stimulated increases in leg vascular conductance, skeletal muscle capillary perfusion, and Akt phosphorylation. Notably, we found that within individuals with T2D, those with lesser increases in leg vascular conductance in response to insulin exhibited the lowest increases in muscle capillary perfusion, suggesting that limited muscle capillary perfusion may be, in part, linked to the impaired ability of the upstream resistance vessels to dilate in response to insulin. Furthermore, we show that the eight-week walking intervention, which did not evoke weight loss, was insufficient to ameliorate skeletal muscle microvascular insulin resistance in previously sedentary, overweight/obese subjects with T2D, despite high adherence and tolerance. However, the walking intervention did improve (P<0.05) popliteal artery flow-mediated dilation (+4.52%) and reduced HbA1c (-0.75%). It is possible that physical activity interventions that are longer in duration, engage large muscle groups with recruitment of the maximum number of muscle fibers, and lead to a robust reduction in metabolic risk factors may be required to overhaul microvascular insulin resistance in T2D.