Delliaux Stephane, Ichinose Masashi, Watanabe Kazuhito, Fujii Naoto, Nishiyasu Takeshi
Aix-Marseille University, MD, DS-ACI, UMR 2, Marseille, France; APHM, Hôpital Nord, Pôle cardiovasculaire et thoracique, Laboratoire de Physiologie Respiratoire-Explorations à l'Exercice, Marseille, France; Assistance Publique, Hôpitaux de Marseille, Hôpital Nord, Pôle cardiovasculaire et thoracique, Laboratoire de Physiologie Respiratoire-Explorations à l'Exercice, Marseille, France; Laboratory of Physiology-Circulation, Institute of Health and Sport Sciences, University of Tsukuba, Tsukuba, Japan; and Japan Society for the Promotion of Science, Tokyo, Japan
School of Business and Administration, Meiji University, Tokyo, Japan; Laboratory of Physiology-Circulation, Institute of Health and Sport Sciences, University of Tsukuba, Tsukuba, Japan; and.
Am J Physiol Regul Integr Comp Physiol. 2015 Jul 1;309(1):R43-50. doi: 10.1152/ajpregu.00402.2014. Epub 2015 Apr 22.
We characterized the cardiovascular responses to forearm muscle metaboreflex activation during hypercapnia. Ten healthy males participated under three experimental conditions: 1) hypercapnia (HCA, PetCO2 : +10 mmHg, by inhalation of a CO2-enriched gas mixture); 2) muscle metaboreflex activation (MMA, by 5 min of local circulatory occlusion after 1 min of 50% maximum voluntary contraction isometric handgrip under normocapnia); and 3) HCA+MMA. We measured mean arterial pressure (MAP), heart rate (HR), and cardiac output (CO); calculated stroke volume (SV), and total peripheral resistance (TPR); and evaluated myocardial oxygen consumption (MV̇o2) and cardiac work (CW) noninvasively. MAP increased in the three experimental conditions but HCA+MMA led to the highest MAP, CO, and HR. Moreover, HCA+MMA increased SV and was associated with the highest MV̇o2 and CW. HCA and MMA exhibited inhibitory interactions with MAP, HR, TPR, MV̇o2, and CW, increases of which were smaller during HCA+MMA than the sum of the increases during HCA and MMA alone (MAP: +28 ± 2 vs. +34 ± 2 mmHg, P < 0.001; HR: +15 ± 2 vs. +22 ± 3 bpm, P < 0.01; TPR: +1.1 ± 1.4 vs. +3.0 ± 1.5 mmHg·l·min(-1), P < 0.05; MV̇o2: +50.25 ± 4.74 vs. +59.48 ± 5.37 mmHg·min(-1)·10(-2), P < 0.01; CW: +59.10 ± 7.52 vs. +63.67 ± 7.71 ml mmHg·min(-1)·10(-4), P < 0.05). Oppositely, HCA and MMA interactions were linearly additive for CO (+2.3 ± 0.4 l/min) and SV (+13 ± 4 ml). We showed that muscle metaboreflex and hypercapnia interact in healthy humans, reducing vasoconstriction but enhancing SV.
我们对高碳酸血症期间前臂肌肉代谢性反射激活的心血管反应进行了特征描述。十名健康男性在三种实验条件下参与研究：1）高碳酸血症（HCA，通过吸入富含二氧化碳的混合气体使呼气末二氧化碳分压（PetCO2）升高10 mmHg）；2）肌肉代谢性反射激活（MMA，在正常碳酸血症下进行50%最大自主收缩等长握力1分钟后，进行5分钟局部循环阻断）；3）HCA + MMA。我们测量了平均动脉压（MAP）、心率（HR）和心输出量（CO）；计算了每搏输出量（SV）和总外周阻力（TPR）；并无创评估了心肌耗氧量（MV̇o2）和心脏作功（CW）。在三种实验条件下MAP均升高，但HCA + MMA导致最高的MAP、CO和HR。此外，HCA + MMA增加了SV，并与最高的MV̇o2和CW相关。HCA和MMA对MAP、HR、TPR、MV̇o2和CW表现出抑制性相互作用，在HCA + MMA期间这些指标的升高幅度小于单独HCA和MMA期间升高幅度之和（MAP：+28±2 vs. +34±2 mmHg，P < 0.001；HR：+15±2 vs. +22±3次/分钟，P < 0.01；TPR：+1.1±1.4 vs. +3.0±1.5 mmHg·l·min⁻¹，P < 0.05；MV̇o2：+50.25±4.74 vs. +59.48±5.37 mmHg·min⁻¹·10⁻²，P < 0.01；CW：+59.10±7.52 vs. +63.67±7.71 ml mmHg·min⁻¹·10⁻⁴，P < 0.05）。相反，HCA和MMA对CO（+2.3±0.4 l/min）和SV（+13±4 ml）的相互作用呈线性相加。我们表明，在健康人体中肌肉代谢性反射和高碳酸血症相互作用，减少血管收缩但增加SV。
