Type 2 diabetes mellitus (T2DM) leads to exaggerated cardiovascular responses to exercise, in part due to an exaggerated exercise pressor reflex. Accumulating data suggest excessive oxidative stress contributes to an exaggerated exercise pressor reflex in cardiovascular-related diseases. Excessive oxidative stress is also a primary underlying mechanism for the development and progression of T2DM. However, whether oxidative stress plays a role in mediating the exaggerated exercise pressor reflex in T2DM is not known. Therefore, this review explores the potential role of oxidative stress leading to increased activation of the afferent arm of the exercise pressor reflex. Several lines of evidence support direct and indirect effects of oxidative stress on the exercise pressor reflex. For example, intramuscular ROS may directly and indirectly (by attenuating contracting muscle blood flow) increase group III and IV afferent activity. Oxidative stress is a primary underlying mechanism for the development of neuropathic pain, which in turn is associated with increased group III and IV afferent activity. These are the same type of afferents that evoke muscle pain and the exercise pressor reflex. Furthermore, oxidative stress-induced release of inflammatory mediators may modulate afferent activity. Collectively, these alterations may result in a positive feedback loop that further amplifies the exercise pressor reflex. An exaggerated reflex increases the risk of adverse cardiovascular events. Thus, identifying the contribution of oxidative stress could provide a potential therapeutic target to reduce this risk in T2DM.

中文翻译：

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2 型糖尿病中过度运动升压反射：氧化应激的潜在作用

2 型糖尿病 (T2DM) 会导致心血管对运动的过度反应，部分原因是运动升压反射过度。越来越多的数据表明，过度的氧化应激会导致心血管相关疾病的运动升压反射过度。过度氧化应激也是 T2DM 发生和进展的主要潜在机制。然而，氧化应激是否在调节 T2DM 过度运动升压反射中发挥作用尚不清楚。因此，本综述探讨了氧化应激导致运动加压反射传入臂激活增加的潜在作用。多项证据支持氧化应激对运动升压反射的直接和间接影响。例如，肌内 ROS 可以直接和间接（通过减弱收缩肌肉血流）增加 III 组和 IV 组传入活动。氧化应激是神经性疼痛发生的主要潜在机制，而神经性疼痛又与 III 组和 IV 组传入活动的增加有关。这些与引起肌肉疼痛和运动加压反射的传入神经类型相同。此外，氧化应激诱导的炎症介质释放可能调节传入活动。总的来说，这些改变可能会导致正反馈循环，进一步放大运动加压反射。过度的反射会增加不良心血管事件的风险。因此，确定氧化应激的作用可以为降低 T2DM 风险提供潜在的治疗靶点。