Effects of tetraethylammonium-sensitive K+ channel blockade on cholinergic and thermal sweating in endurance-trained and untrained men
Effects of tetraethylammonium-sensitive K+ channel blockade on cholinergic and thermal sweating in endurance-trained and untrained men
复制标题
四乙铵敏感性 K 通道阻断对经过耐力训练和未经训练的男性胆碱能和热出汗的影响
DOI：
10.1113/ep090251
复制
发表时间：
2022
影响因子：
2.7
通讯作者：
and Kondo N
中科院分区：
文献类型：
--
作者：
Amano T;Fujii N;Kenny GP;Okamoto Y;Inoue Y;and Kondo N
新发现本研究的中心问题是什么？抑制K+通道是否调节运动训练诱导的胆碱能和热出汗增加？主要发现及其重要性是什么？四乙基铵（一种K+通道阻滞剂）的离子电渗给药可减弱低剂量（0.001%）胆碱能药物毛果芸香碱诱导的出汗，但不能减弱热诱导的出汗。然而，在年轻的耐力训练和未经训练的男性之间没有观察到胆碱能出汗的差异。因此，虽然K+通道在调节外分泌出汗中发挥作用，但它们不会导致耐力训练的成年人中常见的出汗增加。我们的研究结果提供了重要的新的见解的机制的调节出汗耐力conditioning.AbstractWe评估的假设，K+通道的激活介导的运动训练诱导的增强胆碱能和热出汗。在不同的日子里，11名耐力训练和10名未经训练的男子参加了两个实验方案。在每个方案之前，我们通过经皮离子电渗疗法在双臂的前臂皮肤部位施用2%四乙基铵（TEA，K+通道阻断剂）和盐水（对照）。在方案1中，在60分钟内在TEA处理和对照部位给予低（0.001%）和高（1%）剂量的毛果芸香碱。在方案2中，参与者通过将下肢浸入热水（43°C）中进行被动加热，直到核心（直肠）温度（Tc）高于静息水平0.8°C。TEA的管理衰减胆碱能出汗（P= 0.001），在最初的20分钟后，低剂量的匹鲁卡品治疗，而组间的反应是相似的（P= 0.163）。训练组的胆碱能出汗和热出汗均高于未训练组（P均≤0.033）。在被动加热的最初20分钟期间，在0.8°C的T升高下，热出汗达到响应的约90%，这对应于方案1中TEA减弱胆碱能出汗的时期。然而，两组中对照和TEA部位之间的出汗没有差异（P= 0.704）。我们发现，K+通道的激活似乎并不介导由低剂量的毛果芸香碱在受过训练的男性引起的出汗反应升高。我们还证明了K+通道在热应激期间对任何一组的出汗都没有贡献。
New FindingsWhat is the central question of this study?Does inhibition of K+channels modulate the exercise‐training‐induced augmentation in cholinergic and thermal sweating?What is the main finding and its importance?Iontophoretic administration of tetraethylammonium, a K+channel blocker, blunted sweating induced by a low dose (0.001%) of the cholinergic agent pilocarpine, but not heat‐induced sweating. However, no differences in the cholinergic sweating were observed between young endurance‐trained and untrained men. Thus, while K+channels play a role in the regulation of eccrine sweating, they do not contribute to the increase in sweating commonly observed in endurance‐trained adults. Our findings provide important new insights into the mechanisms underlying the regulation of sweating by endurance conditioning.AbstractWe evaluated the hypothesis that the activation of K+channels mediates the exercise‐training‐induced augmentation of cholinergic and thermal sweating. On separate days, 11 endurance‐trained and 10 untrained men participated in two experimental protocols. Prior to each protocol, we administered 2% tetraethylammonium (TEA, K+channels blocker) and saline (Control) at forearm skin sites on both arms via transdermal iontophoresis. In protocol 1, low (0.001%) and high (1%) doses of pilocarpine were administered at the TEA‐treated and Control sites over a 60‐min period. In protocol 2, participants were passively heated by immersing their lower limbs in hot water (43°C) until core (rectal) temperature (Tc) increased by 0.8°C above resting levels. Administration of TEA attenuated cholinergic sweating (P= 0.001) during the initial 20 min after the treatment of low dose of pilocarpine only whilst the response was similar between the groups (P= 0.163). Cholinergic and thermal sweating were higher in the trained relative to the untrained men (allP ≤0.033). Thermal sweating reached ∼90% of the response at aTcelevation of 0.8°C during the initial 20 min of passive heating, which corresponds to the period wherein TEA attenuated cholinergic sweating in protocol 1. However, sweating did not differ between the Control and TEA sites in either group (P= 0.704). We showed that activation of K+channels does not appear to mediate the elevated sweating response induced by a low dose of pilocarpine in trained men. We also demonstrated that K+channels do not contribute to sweating during heat stress in either group.