Molecular Cardiac Physiology Group, Simon Fraser University , Burnaby, British Columbia , Canada.
Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah , Salt Lake City, Utah.
Am J Physiol Heart Circ Physiol. 2018 Feb 1;314(2):H285-H292. doi: 10.1152/ajpheart.00405.2017. Epub 2017 Nov 3.
The ability of cardiomyocytes to recover from a proton load was examined in the hearts of exercise-trained and sedentary control rats in CO/[Formula: see text]-free media. Acidosis was created by the NHCl prepulse technique, and intracellular pH (pH) was determined using fluorescence microscopy on carboxy-SNARF-1 AM-loaded isolated cardiomyocytes. CO-independent pH buffering capacity (β) was measured by incrementally reducing the extracellular NHCl concentration in steps of 50% from 20 to 1.25 mM. β increased as pH decreased in both exercise-trained and sedentary control groups. However, the magnitude of increase in β as a function of pH was found to be significantly ( P < 0.001) greater in the exercise-trained group compared with the sedentary control group. The rate of pH recovery from an imposed proton load was found to not be different between the exercise-trained and control groups. The Na/H exchanger-dependent H extrusion rate during the recovery from an imposed proton load, however, was found to be significantly greater in the exercise-trained group compared with the control group. By increasing β and subsequently the Na/H exchanger-dependent H extrusion rate, exercise training may provide cardiomyocytes with the ability to better handle an intracellular excess of H generated during hypoxia/ischemic insults and may serve in a cardioprotective role. These data may be predictive of two positive outcomes: 1) increased exercise tolerance by the heart and 2) a protective mechanism that limits the degree of myocardial acidosis and subsequent damage that accompanies ischemia-reperfusion stress. NEW & NOTEWORTHY The enhanced ability to deal with acidosis conferred by exercise training is likely to improve exercise tolerance and outcomes in response to myocardial ischemia-reperfusion injury.
在不含 CO 的培养基中，研究了运动训练和久坐对照组大鼠心肌细胞从质子负荷中恢复的能力。通过 NHCl 预脉冲技术产生酸中毒，并使用加载有羧基-SNARF-1 AM 的分离心肌细胞的荧光显微镜测定细胞内 pH（pH）。通过从 20 到 1.25 mM 以 50%的步长逐渐降低细胞外 NHCl 浓度来测量 CO 独立的 pH 缓冲能力（β）。在运动训练和久坐对照组中，随着 pH 值的降低，β 值均增加。然而，与久坐对照组相比，β 值随 pH 值增加的幅度在运动训练组中显著增加（P < 0.001）。从施加的质子负荷中恢复 pH 的速度在运动训练组和对照组之间没有差异。然而，从施加的质子负荷中恢复时，Na/H 交换器依赖性 H 外排率在运动训练组中显著高于对照组。通过增加β值，继而增加 Na/H 交换器依赖性 H 外排率，运动训练可能使心肌细胞具有更好地处理缺氧/缺血损伤期间细胞内过多 H 的能力，并可能发挥心脏保护作用。这些数据可能预示着两种积极的结果：1）心脏的运动耐量增加，2）限制伴随缺血再灌注应激的心肌酸中毒和随后损伤程度的保护机制。新观点和重要发现运动训练赋予的增强处理酸中毒的能力可能会改善对心肌缺血再灌注损伤的运动耐量和结果。
