Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa , Ottawa, ON , Canada.
Faculty of Health and Sport Sciences, University of Tsukuba , Tsukuba City , Japan.
J Appl Physiol (1985). 2019 Apr 1;126(4):1129-1137. doi: 10.1152/japplphysiol.00657.2018. Epub 2019 Jan 17.
Age-related impairments in cutaneous vascular conductance (CVC) and sweat rate (SR) during exercise may result from increased arginase activity, which can attenuate endogenous nitric oxide (NO) production. We therefore evaluated whether arginase inhibition modulates these heat-loss responses in young ( = 9, 23 ± 3 yr) and older ( = 9, 66 ± 6 yr) men during two 30-min bouts of moderate-intensity cycling (Ex1 and Ex2) in the heat (35°C). CVC and SR were measured at forearm skin sites perfused with ) lactated Ringer's (control), ) -nitro--arginine methyl ester (L-NAME; NO synthase-inhibited), or ) N-hydroxy-nor-arginine and S-(2-boronoethyl)-l-cysteine (Nor-NOHA + BEC; arginase-inhibited). In both groups, CVC was reduced at L-NAME relative to control and Nor-NOHA + BEC (both < 0.01). Likewise, SR was attenuated with L-NAME compared with control and Nor-NOHA + BEC during each exercise bout in the young men (all ≤ 0.05); however, no influence of treatment on SR in the older men was observed ( = 0.14). Based on these findings, we then evaluated responses in 7 older men (64 ± 7 yr) during passively induced elevations in esophageal temperature (∆T) equal to those in Ex1 (0.6°C) and Ex2 (0.8°C). L-NAME reduced CVC by 18 ± 20% CVC at a ∆T of 0.8°C ( = 0.03) compared with control, whereas Nor-NOHA + BEC augmented CVC by 20 ± 18% CVC, on average, throughout heating (both ≤ 0.03). SR was not influenced by either treatment ( = 0.80) Thus, arginase inhibition does not modulate CVC or SR during exercise in the heat but, consistent with previous findings, does augment CVC in older men during passive heating. In the current study, we demonstrate that local arginase inhibition does not influence forearm cutaneous vasodilatory and sweating responses in young or older men during exercise-heat stress. Consistent with previous findings, however, we observed augmented cutaneous blood flow with arginase inhibition during whole-body passive heat stress. Thus, arginase differentially affects cutaneous vasodilation depending on the mode of heat stress but does not influence sweating during exercise or passive heating.
年龄相关的运动时皮肤血管传导率（CVC）和出汗率（SR）的降低可能是由于精氨酸酶活性增加所致，而精氨酸酶活性可减弱内源性一氧化氮（NO）的产生。因此，我们评估了在高温（35°C）下，年轻（= 9，23±3 岁）和老年（= 9，66±6 岁）男性进行两次 30 分钟中等强度骑行（Ex1 和 Ex2）期间，精氨酸酶抑制是否会调节这些热损失反应。在前臂皮肤部位测量 CVC 和 SR，该部位用）乳酸林格氏液（对照）、）-硝基--精氨酸甲酯（L-NAME；一氧化氮合酶抑制剂）或）N-羟基-N-硝基-L-精氨酸和 S-（2-硼乙基）-L-半胱氨酸（Nor-NOHA + BEC；精氨酸酶抑制剂）灌注。在两组中，与对照和 Nor-NOHA + BEC 相比，L-NAME 使 CVC 降低（均 < 0.01）。同样，与对照和 Nor-NOHA + BEC 相比，年轻男性在每次运动过程中 L-NAME 使 SR 降低（均 ≤ 0.05）；然而，在老年男性中，治疗对 SR 没有影响（= 0.14）。基于这些发现，我们随后评估了 7 名老年男性（64±7 岁）在食管温度升高（ΔT）等于 Ex1（0.6°C）和 Ex2（0.8°C）时的反应。与对照相比，L-NAME 在 ΔT 为 0.8°C 时使 CVC 降低 18±20%（=0.03），而 Nor-NOHA + BEC 使 CVC 在整个加热过程中平均增加 20±18%（均 ≤ 0.03）。两种治疗均不影响 SR（=0.80）。因此，精氨酸酶抑制在高温下运动时不会调节 CVC 或 SR，但与先前的发现一致，它会在老年人被动加热时增加 CVC。在当前研究中，我们证明了在运动-热应激期间，局部精氨酸酶抑制不会影响年轻或老年男性的前臂皮肤血管扩张和出汗反应。然而，与先前的发现一致，我们观察到在全身被动热应激期间，精氨酸酶抑制使皮肤血流量增加。因此，精氨酸酶根据热应激的模式不同而对皮肤血管舒张产生不同的影响，但不会影响运动时的出汗或被动加热时的出汗。
