Shibasaki Manabu, Rasmussen Peter, Secher Niels H, Crandall Craig G
Department of Environmental Health, Nara Women's University, Japan.
J Physiol. 2009 May 1;587(Pt 9):2101-7. doi: 10.1113/jphysiol.2009.169201. Epub 2009 Mar 23.
During heat stress, isometric handgrip (IHG) exercise causes cutaneous vasoconstriction, but it remains controversial whether neural mechanisms are responsible for this observation. The objective of this study was to test the hypothesis that cutaneous vasoconstriction during IHG exercise in heat stressed individuals occurs via a neural mechanism. An axillary nerve blockade was performed to block efferent nerve traffic to the left forearm in seven healthy subjects. Two intradermal microdialysis probes were placed within forearm skin of the blocked area. Forearm skin blood flow was measured by laser-Doppler flowmetry over the microdialysis probes as well as from skin of the contralateral (unblocked) forearm. Cutaneous vascular conductance (CVC) was calculated from the ratio of skin blood flow to mean arterial pressure. Effectiveness of nerve blockade was verified by the absence of tactile sensation, as well as an absence of sweating and cutaneous vasodilatation during a whole-body heat stress. Upon this confirmation, adenosine was perfused through one of the microdialysis probes to increase skin blood flow similar to that of the unblocked site. After internal temperature increased approximately 0.7 degrees C, subjects performed 2 min of IHG exercise at 35% of maximal voluntary contraction using the non-blocked arm. IHG exercise significantly decreased CVC at the unblocked site (82.3 +/- 5.7 to 70.9 +/- 5.4%max, P = 0.005, means +/- S.E.M.) and the adenosine treated site of the blocked arm (75.2 +/- 7.2 to 68.3 +/- 6.6%max, P = 0.005), whereas CVC was unchanged at the blocked site that did not receive adenosine (15.7 +/- 2.8 to 13.7 +/- 2.0%max, P = 0.10). Importantly, the reduction in CVC was greater at the unblocked site than at the adenosine treated site (11.4 +/- 2.6 vs. 6.9 +/- 1.6%max, respectively, P = 0.01). These findings suggest that neural and non-neural mechanisms contribute to the reduction in forearm CVC during IHG exercise in heat stressed humans.
在热应激期间,等长握力(IHG)运动可导致皮肤血管收缩,但神经机制是否对此现象负责仍存在争议。本研究的目的是检验以下假设:热应激个体在进行IHG运动时,皮肤血管收缩是通过神经机制发生的。对7名健康受试者进行腋神经阻滞,以阻断至左前臂的传出神经通路。在阻滞区域的前臂皮肤内放置两个皮内微透析探头。通过激光多普勒血流仪在前臂微透析探头处以及对侧(未阻滞)前臂皮肤测量前臂皮肤血流量。根据皮肤血流量与平均动脉压的比值计算皮肤血管传导率(CVC)。通过无触觉以及在全身热应激期间无出汗和皮肤血管舒张来验证神经阻滞的有效性。确认后,通过其中一个微透析探头灌注腺苷,以使皮肤血流量增加至与未阻滞部位相似的水平。在体温升高约0.7摄氏度后,受试者使用未阻滞的手臂以最大自主收缩的35%进行2分钟的IHG运动。IHG运动使未阻滞部位的CVC显著降低(从82.3±5.7%max降至70.9±5.4%max,P = 0.005,均值±标准误),以及阻滞手臂接受腺苷治疗部位的CVC显著降低(从75.2±7.2%max降至68.3±6.6%max,P = 0.005),而未接受腺苷的阻滞部位的CVC未改变(从15.7±2.8%max降至13.7±2.0%max,P = 0.10)。重要的是,未阻滞部位CVC的降低幅度大于腺苷治疗部位(分别为11.4±2.6%max和6.9±1.6%max,P = 0.01)。这些发现表明,神经和非神经机制均导致热应激人体在进行IHG运动时前臂CVC降低。