Department of Biomedical Sciences, Florida State University, Tallahassee, Florida.
Department of Nutrition, Food and Exercise Science, Florida State University, Tallahassee, Florida.
Am J Physiol Heart Circ Physiol. 2021 Jul 1;321(1):H1-H14. doi: 10.1152/ajpheart.00885.2020. Epub 2021 May 14.
We tested the hypothesis that adiponectin deficiency attenuates cardiac and coronary microvascular function and prevents exercise training-induced adaptations of the myocardium and the coronary microvasculature in adult mice. Adult wild-type (WT) or adiponectin knockout (adiponectin KO) mice underwent treadmill exercise training or remained sedentary for 8-10 wk. Systolic and diastolic functions were assessed before and after exercise training or cage confinement. Vasoreactivity of coronary resistance arteries was assessed at the end of exercise training or cage confinement. Before exercise training, ejection fraction and fractional shortening were similar in adiponectin KO and WT mice, but isovolumic contraction time was significantly lengthened in adiponectin KO mice. Exercise training increased ejection fraction (12%) and fractional shortening (20%) with no change in isovolumic contraction time in WT mice. In adiponectin KO mice, both ejection fraction (-9%) and fractional shortening (-12%) were reduced after exercise training and these decreases were coupled to a further increase in isovolumic contraction time (20%). In sedentary mice, endothelium-dependent dilation to flow was higher in arterioles from adiponectin KO mice as compared with WT mice. Exercise training enhanced dilation to flow in WT mice but decreased flow-induced dilation in adiponectin KO mice. These data suggest that compensatory mechanisms contribute to the maintenance of cardiac and coronary microvascular function in sedentary mice lacking adiponectin; however, in the absence of adiponectin, cardiac and coronary microvascular adaptations to exercise training are compromised. We report that compensatory mechanisms contribute to the maintenance of cardiac and coronary microvascular function in sedentary mice in which adiponectin has been deleted; however, when mice lacking adiponectin are subjected to the physiological stress of exercise training, beneficial coronary microvascular and cardiac adaptations are compromised or absent.
我们检验了这样一个假设，即脂联素缺乏会减弱心脏和冠状动脉微血管功能，并阻止成年小鼠的心肌和冠状动脉微血管对运动训练的适应。成年野生型（WT）或脂联素敲除（adiponectin KO）小鼠接受跑步机运动训练或保持久坐 8-10 周。在运动训练或笼养之前评估收缩期和舒张期功能。在运动训练或笼养结束时评估冠状动脉阻力动脉的血管反应性。在运动训练之前，脂联素 KO 和 WT 小鼠的射血分数和缩短分数相似，但等容收缩时间明显延长。WT 小鼠的运动训练增加了射血分数（12%）和缩短分数（20%），而等容收缩时间没有变化。在脂联素 KO 小鼠中，运动训练后射血分数（-9%）和缩短分数（-12%）均降低，并且等容收缩时间进一步增加（20%）。在久坐的小鼠中，与 WT 小鼠相比，脂联素 KO 小鼠的动脉血管内皮依赖性舒张对血流的作用更高。运动训练增强了 WT 小鼠的舒张作用，但降低了脂联素 KO 小鼠的血流诱导舒张作用。这些数据表明，在缺乏脂联素的久坐小鼠中，代偿机制有助于维持心脏和冠状动脉微血管功能；然而，在缺乏脂联素的情况下，心脏和冠状动脉微血管对运动训练的适应能力受到损害。我们报告说，在缺乏脂联素的久坐小鼠中，代偿机制有助于维持心脏和冠状动脉微血管功能；然而，当缺乏脂联素的小鼠受到运动训练的生理压力时，有益的冠状动脉微血管和心脏适应能力受损或不存在。
