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The mechanisms underlying the muscle metaboreflex modulation of sweating and cutaneous blood flow in passively heated humans

机译:被动加热的人出汗和皮肤血液流动的肌肉代谢反射调节的机制

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摘要

Metaboreceptors can modulate cutaneous blood flow and sweating during heat stress but the mechanisms remain unknown. Fourteen participants (31 ± 13 years) performed 1‐min bout of isometric handgrip (IHG) exercise at 60% of their maximal voluntary contraction followed by a 3‐min occlusion (OCC), each separated by 10 min, initially under low (LHS, to activate sweating without changes in core temperature) and high (HHS, whole‐body heating to a core temperature increase of 1.0°C) heat stress conditions. Cutaneous vascular conductance (CVC) and sweat rate were measured continuously at four forearm skin sites perfused with 1) lactated Ringer's solution (Control), 2) 10 mmol L‐NAME [inhibits nitric oxide synthase (NOS)], 3) 10 mmol Ketorolac [inhibits cyclooxygenase (COX)], or 4) 4 mmol theophylline (THEO; inhibits adenosine receptors). Relative to pre‐IHG levels with Control, NOS inhibition attenuated the metaboreceptor‐mediated increase in sweating under LHS and HHS (P ≤ 0.05), albeit the attenuation was greater under LHS (P ≤ 0.05). In addition, a reduction from baseline was observed with THEO under LHS during style="fixed-case">OCC (P ≤ 0.05), but not style="fixed-case">HHS (both P > 0.05). In contrast, style="fixed-case">CVC was lower than Control with L‐ style="fixed-case">NAME during style="fixed-case">OCC in style="fixed-case">HHS (P ≤ 0.05), but not style="fixed-case">LHS (P > 0.05). We show that metaboreceptor activation modulates style="fixed-case">CVC via the stimulation of style="fixed-case">NOS and adenosine receptors, whereas style="fixed-case">NOS, but not style="fixed-case">COX or adenosine receptors, contributes to sweating at all levels of heating.
机译:代谢受体可以在热应激期间调节皮肤的血液流动和出汗,但是其机制仍然未知。 14位参与者(31±13岁)在其最大自愿收缩的60%时进行了1分钟的等距把手运动(IHG),然后进行了3分钟的闭塞(OCC),每隔10分钟,最初是在低(LHS)下,以在不改变核心温度的情况下激活出汗)和较高的温度(HHS,将全身加热至核心温度升高1.0°C)热应激条件。在四个前臂皮肤部位连续测量皮肤血​​管电导(CVC)和出汗率,这些部位灌注1)乳酸林格氏液(对照),2)10 mmol L‐NAME [抑制一氧化氮合酶(NOS)],3)10 mmol酮咯酸[抑制环氧合酶(COX)],或4)4 mmol茶碱(THEO;抑制腺苷受体)。相对于控制前的IHG水平,NOS抑制作用减弱了LHS和HHS下出汗的代谢受体介导的增加(P≤0.05),尽管在LHS下衰减更大(P≤0.05)。此外,在 style =“ fixed-case”> OCC (L <0.05)期间,在LHS下观察到THEO与基线相比有所降低(P≤0.05),而在跨度>(均为P> 0.05)。相反,在 style =“ fixed-case”期间, style =“ fixed-case”> CVC 低于具有L‐ style =“ fixed-case”> NAME 的Control。 > OCC 以 style =“ fixed-case”> HHS (P≤0.05),但不是 style =“ fixed-case”> LHS (P> 0.05) 。我们显示,通过刺激 style =“ fixed-case”> NOS 和腺苷受体,metaboreceptor激活可调节 style =“ fixed-case”> CVC ,而 style =“固定情况下的> NOS ,而不是 style =“ fixed-case”> COX 或腺苷受体,在所有加热水平下都会出汗。

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