Laboratory of Exercise Sciences, Fluminense Federal University, Niterói, Brazil.
Department of Surgery, Fluminense Federal University, Niterói, Brazil.
J Appl Physiol (1985). 2019 Nov 1;127(5):1491-1501. doi: 10.1152/japplphysiol.00401.2019. Epub 2019 Sep 23.
In animals, the blockade of acid-sensing ion channels (ASICs), cation pore-forming membrane proteins located in the free nerve endings of group IV afferent fibers, attenuates increases in arterial pressure (AP) and sympathetic nerve activity (SNA) during muscle contraction. Therefore, ASICs play a role in mediating the metabolic component (skeletal muscle metaboreflex) of the exercise pressor reflex in animal models. Here we tested the hypothesis that ASICs also play a role in evoking the skeletal muscle metaboreflex in humans, quantifying beat-by-beat mean AP (MAP; finger photoplethysmography) and muscle SNA (MSNA; microneurography) in 11 men at rest and during static handgrip exercise (SHG; 35% of the maximal voluntary contraction) and postexercise muscle ischemia (PEMI) before (B) and after (A) local venous infusion of either saline or amiloride (AM), an ASIC antagonist, via the Bier block technique. MAP (BAM +30 ± 6 vs. AAM +25 ± 7 mmHg, = 0.001) and MSNA (BAM +14 ± 9 vs. AAM +10 ± 6 bursts/min, = 0.004) responses to SHG were attenuated under ASIC blockade. Amiloride also attenuated the PEMI-induced increases in MAP (BAM +25 ± 6 vs. AAM +16 ± 6 mmHg, = 0.0001) and MSNA (BAM +16 ± 9 vs. AAM +8 ± 8 bursts/min, = 0.0001). MAP and MSNA responses to SHG and PEMI were similar before and after saline infusion. We conclude that ASICs play a role in evoking pressor and sympathetic responses to SHG and the isolated activation of the skeletal muscle metaboreflex in humans. We showed that regional blockade of the acid-sensing ion channels (ASICs), induced by venous infusion of the antagonist amiloride via the Bier block anesthetic technique, attenuated increases in arterial pressure and muscle sympathetic nerve activity during both static handgrip exercise and postexercise muscle ischemia. These findings indicate that ASICs contribute to both pressor and sympathetic responses to the activation of the skeletal muscle metaboreflex in humans.
在动物中，酸敏离子通道 (ASIC) 的阻断——位于 IV 类传入纤维游离神经末梢的阳离子孔形成膜蛋白——可减轻肌肉收缩时动脉压 (AP) 和交感神经活动 (SNA) 的增加。因此，ASIC 在介导动物模型中的运动加压反射的代谢成分（骨骼肌代谢反射）中起作用。在这里，我们测试了这样一个假设，即 ASIC 在引发人类骨骼肌代谢反射中也起作用，通过手指光体积描记法测量静息时和静态握力运动 (SHG；最大自主收缩的 35%) 和运动后肌肉缺血 (PEMI) 期间的每搏平均 AP (MAP；11 名男性的 MAP；) 和肌肉 SNA (MSNA；微神经记录)，并通过 Bier 阻断技术局部静脉输注生理盐水或阿米洛利 (AM)（一种 ASIC 拮抗剂）前后 (B 和 A)。在 ASIC 阻断下，SHG 的 MAP (BAM +30±6 对 AAM +25±7 mmHg， = 0.001) 和 MSNA (BAM +14±9 对 AAM +10±6 爆发/分钟， = 0.004) 反应减弱。阿米洛利还减弱了 PEMI 引起的 MAP 增加（BAM +25±6 对 AAM +16±6 mmHg， = 0.0001）和 MSNA（BAM +16±9 对 AAM +8±8 爆发/分钟， = 0.0001）。在生理盐水输注前后，SHG 和 PEMI 的 MAP 和 MSNA 反应相似。我们得出结论，ASIC 在引发 SHG 和孤立的骨骼肌代谢反射激活时的加压和交感反应中起作用。我们表明，通过 Bier 阻断麻醉技术局部静脉输注拮抗剂阿米洛利诱导的酸敏离子通道 (ASIC) 阻断减弱了静态握力运动和运动后肌肉缺血期间动脉压和肌肉交感神经活动的增加。这些发现表明，ASIC 有助于人类骨骼肌代谢反射激活时的加压和交感反应。
