Grotle Ann-Katrin, Kaur Jasdeep, Stone Audrey J, Fadel Paul J
Department of Kinesiology, The University of Texas at Arlington, Arlington, TX, United States.
Department of Kinesiology and Health Education, The University of Texas at Austin, Austin, TX, United States.
Front Physiol. 2021 Apr 13;12:628840. doi: 10.3389/fphys.2021.628840. eCollection 2021.
Emerging evidence suggests that type 2 diabetes (T2D) may impair the ability to properly adjust the circulation during exercise with augmented blood pressure (BP) and an attenuated contracting skeletal muscle blood flow (BF) response being reported. This review provides a brief overview of the current understanding of these altered exercise responses in T2D and the potential underlying mechanisms, with an emphasis on the sympathetic nervous system and its regulation during exercise. The research presented support augmented sympathetic activation, heightened BP, reduced skeletal muscle BF, and impairment in the ability to attenuate sympathetically mediated vasoconstriction (i.e., functional sympatholysis) as potential drivers of neurovascular dysregulation during exercise in T2D. Furthermore, emerging evidence supporting a contribution of the exercise pressor reflex and central command is discussed along with proposed future directions for studies in this important area of research.
新出现的证据表明，2型糖尿病（T2D）可能会损害运动期间适当调节循环的能力，据报道会出现血压（BP）升高和收缩骨骼肌血流（BF）反应减弱的情况。本综述简要概述了目前对T2D中这些改变的运动反应及其潜在机制的理解，重点是交感神经系统及其在运动期间的调节。所呈现的研究支持交感神经激活增强、血压升高、骨骼肌BF减少，以及在T2D运动期间减弱交感神经介导的血管收缩（即功能性交感神经抑制）能力受损，这些是神经血管失调的潜在驱动因素。此外，还讨论了支持运动加压反射和中枢指令作用的新证据，以及该重要研究领域未来的研究方向建议。
