Cholinergic nerve contribution to cutaneous active vasodilation during exercise is similar to whole body passive heating.
Cholinergic nerve contribution to cutaneous active vasodilation during exercise is similar to whole body passive heating.
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运动期间胆碱能神经对皮肤主动血管舒张的贡献类似于全身被动加热。
DOI：
10.1152/japplphysiol.00299.2022
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发表时间：
2023
期刊：
影响因子：
--
通讯作者：
Minson,ChristopherT
中科院分区：
文献类型：
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作者：
Francisco,MichaelA;Gibson,BrandonM;Simmons,GrantH;Halliwill,JohnR;Minson,ChristopherT
交感胆碱能神经共传递被广泛认为是全身被动加热过程中皮肤主动血管舒张（CAVD）的机制。然而，最近的研究表明，CAVD加热可能存在机制差异，这取决于热负荷的方式。交感神经胆碱能共传递是否能解释运动中的CAVD尚不清楚。本研究旨在证实被动加热过程中胆碱能神经在CAVD中的作用，并将这些发现扩展到运动中。据推测，运动和被动加热过程中的CAVD将被胆碱能神经阻滞消除。8名年轻（18-30岁）娱乐活跃的个体在不同的日子以随机顺序进行锻炼（在60%V ~ o 2峰值下坐着骑自行车1小时）和被动加热（坐着被动加热11小时，平均皮肤温度通过水灌注服夹在39°C）。在研究前2 wk通过肉毒杆菌毒素阻断胆碱能神经。使用激光多普勒血流仪评估皮肤血流量，并表示为最大皮肤血管电导的百分比（%CVCmax）。在运动/被动加热结束时，内部温度升高了0.7°C。肉毒杆菌治疗部位的%CVCmax（运动：19 ± 6和被动加热：15 ± 14%CVCmax）显著低于（P< 0.001）未治疗部位（运动：35 ± 11和被动加热：38 ± 6%CVCmax），但运动和被动加热之间没有差异（模态，P= 0.909;模态-肉毒杆菌相互作用，P= 0.230）。我们的结论是，CAVD在运动和被动加热是由交感胆碱能神经介导的，一个关键的体温调节机制，似乎是独立的热loadmodel.NEW & NOTEWORTHYOUR研究建立了首要的胆碱能神经皮肤主动血管舒张运动过程中，并确认了这个模型在被动加热使用交叉研究设计。此外，加热的模式，无论是被动或运动诱导，没有改变的胆碱能成分的热效应器响应增加内部温度的敏感性。因此，皮肤活性血管扩张神经负责类似的皮肤血流反应，无论如何实现热负荷。
Sympathetic cholinergic nerve cotransmission is widely accepted as the mechanism of cutaneous active vasodilation (CAVD) during whole body passive heating (passive heating). However, recent research suggests that there may be mechanistic differences in CAVD to heating, depending on the modality of thermal loading. It is unknown whether sympathetic cholinergic cotransmission explains CAVD during exercise. This study sought to confirm the role of cholinergic nerves in CAVD during passive heating and expand these findings to exercise. It was hypothesized that CAVD during both exercise and passive heating would be abolished by cholinergic nerve blockade. Eight young (18–30 yr) recreationally active individuals exercised (1 h seated cycling at 60% V̇o2peak) and were passively heated (∼1 h seated passive heating with mean skin temperature clamped at 39°C by water-perfused suit), in randomized order on separate days. Cholinergic nerves were blocked via Botox ∼2 wk prior to the study. Skin blood flow was assessed using laser Doppler flowmetry and expressed as percent of maximum cutaneous vascular conductance (%CVCmax). At the end of exercise/passive heating, internal temperature had increased by ∼0.7°C. The %CVCmax at the Botox-treated sites (exercise: 19 ± 6 and passive heating: 15 ± 14%CVCmax) was significantly less (P< 0.001) than at the untreated sites (exercise: 35 ± 11 and passive heating: 38 ± 6%CVCmax), but there were no differences between exercise and passive heating (modality,P= 0.909; modality-Botox interaction,P= 0.230). We conclude that CAVD during both exercise and passive heating is mediated by sympathetic cholinergic nerves, a critical thermoregulatory mechanism that appears to be independent of the thermal loading modality.NEW & NOTEWORTHYOur study establishes the primacy of cholinergic nerves to cutaneous active vasodilation during exercise and confirms this model during passive heating using a crossover study design. In addition, the mode of heating, whether passive or exercise induced, did not change the sensitivity of the cholinergic component of the thermoeffector response to increased internal temperature. Thus, cutaneous active vasodilator nerves are responsible for similar skin blood flow responses regardless of how thermal loading is accomplished.