Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba City, Japan.
Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa, Ottawa, Canada.
Exp Physiol. 2022 Aug;107(8):834-843. doi: 10.1113/EP090422. Epub 2022 Jun 5.
What is the central question of this study? Does acute intradermal administration of the antioxidant ascorbate augment local forearm cutaneous vasodilatation and sweating via nitric oxide synthase (NOS)-dependent mechanisms during exercise-heat stress in older adults with uncomplicated controlled hypertension? What is the main finding and its importance? Relative to the control site, ascorbate had no effect on forearm cutaneous vascular conductance (CVC) and sweat rate, although CVC was reduced with NOS inhibition in older adults with hypertension. Acute local administration of ascorbate to forearm skin does not modulate heat loss responses during exercise-heat stress in older adults with hypertension.
Nitric oxide synthase (NOS) contributes to the heat loss responses of cutaneous vasodilatation and sweating during exercise. However, the contribution of NOS may be attenuated in individuals with uncomplicated, controlled hypertension due to elevated oxidative stress, which can reduce NO bioavailability. We evaluated the hypothesis that the acute local intradermal administration of the antioxidant ascorbate would enhance cutaneous vasodilatation and sweating via NOS-dependent mechanisms during an exercise-heat stress in adults with hypertension. Habitually active adults who were normotensive (n = 14, 7 females, 62 ± 4 years) or had uncomplicated, controlled hypertension (n = 13, 6 females, 62 ± 5 years) performed 30 min of moderate-intensity (50% of their pre-determined peak oxygen uptake) semi-recumbent cycling in the heat (35°C, 20% relative humidity). Cutaneous vascular conductance (CVC) and sweat rate were assessed at four forearm skin sites continuously perfused with (1) lactated Ringer solution (Control), (2) 10 mM antioxidant ascorbate, (3) 10 mM N -nitro-l-arginine methyl ester (l-NAME), a non-selective NOS inhibitor, or (4) a combination of ascorbate and l-NAME. Relative to Control, no effect of ascorbate was observed on CVC or sweating in either group (P = 0.619). However, l-NAME reduced CVC relative to Control in both groups (P ≤ 0.038). No effect of any treatment on sweating was observed (P ≥ 0.306). Thus, acute local administration of ascorbate to forearm skin does not enhance the activation of heat loss responses of cutaneous vasodilatation and sweating in older adults, and those with hypertension during an exercise-heat stress.
本研究的核心问题是什么?在患有未合并控制良好的高血压的老年人进行运动-热应激期间,急性皮内给予抗氧化剂抗坏血酸是否通过一氧化氮合酶(NOS)依赖机制增强局部前臂皮肤血管舒张和出汗?主要发现及其重要性是什么?与对照部位相比,抗坏血酸对前臂皮肤血管传导率(CVC)和出汗率没有影响,尽管在高血压老年人中 NOS 抑制时 CVC 降低。急性局部给予抗坏血酸到前臂皮肤不会调节高血压老年人在运动-热应激期间的热损失反应。
NOS 有助于运动期间皮肤血管舒张和出汗的热损失反应。然而,由于氧化应激增加,NOS 的贡献可能会减弱,这会降低 NO 的生物利用度,患有未合并控制良好的高血压的个体。我们评估了这样一个假设,即在高血压成年人进行运动-热应激期间,急性局部皮内给予抗氧化剂抗坏血酸将通过 NOS 依赖机制增强皮肤血管舒张和出汗。习惯性活跃的成年人,血压正常(n=14,女性 7 名,62±4 岁)或患有未合并控制良好的高血压(n=13,女性 6 名,62±5 岁)在热(35°C,20%相对湿度)中进行 30 分钟的中等强度(50%他们预先确定的峰值摄氧量)半卧位自行车运动。连续用(1)乳酸林格溶液(对照)、(2)10mM 抗氧化剂抗坏血酸、(3)10mM N-硝基-L-精氨酸甲酯(l-NAME)、非选择性 NOS 抑制剂或(4)抗坏血酸和 l-NAME 的组合灌注四个前臂皮肤部位评估皮肤血管传导率(CVC)和出汗率。与对照相比,抗坏血酸对 CVC 或两组的出汗均无影响(P=0.619)。然而,l-NAME 降低了两组的 CVC 相对于对照(P≤0.038)。没有观察到任何处理对出汗的影响(P≥0.306)。因此,急性局部给予抗坏血酸到前臂皮肤不会增强老年人心血管舒张和出汗的热损失反应的激活,也不会增强患有高血压的成年人在运动-热应激期间的热损失反应。