Libonati J R, Gaughan J P, Hefner C A, Gow A, Paolone A M, Houser S R
Department of Cardiopulmonary Sciences, Bouve' College of Pharmacy and Health Sciences, Northeastern University, Boston, MA 02115, USA.
Med Sci Sports Exerc. 1997 Apr;29(4):509-16. doi: 10.1097/00005768-199704000-00013.
We examined the effects of two exercise training modalities, i.e., low-intensity endurance and sprint running, on in vitro, isovolumic myocardial performance following ischemia and reperfusion. Rats ran on a treadmill 5 d.wk-1 for 6 wk at the following levels: endurance; 20 m.min-1, 0% grade, 60 min.d-1 and sprint; five 1-min runs at 75 m.min-1, 15% grade interspersed with 1-min active recovery runs at 20 m.min-1, 15% grade. Both endurance and sprint training significantly improved exercise tolerance relative to control (P < 0.05) on two graded exercise tests. Buffer perfused hearts of control (N = 18), endurance (N = 20), and sprint (N = 13) trained animals underwent no-flow ischemia (20 min) and reperfusion (30 min) in a Langendorff mode. During reperfusion, left ventricular developed pressure and its first derivative were 20% higher in sprint (P < 0.05) than either endurance or control hearts. Left ventricular end-diastolic pressure was lowest in sprint during reperfusion (sprint, 10 +/- 1 mm Hg vs endurance, 14 +/- 2 mm Hg; and control, 14 +/- 2 mm Hg, at 30 min reperfusion). Hearts were then used for biochemical studies or dissociated into single cells for measurement of contraction, cell calcium, and action potential duration. Single cell contractions were greatest in sprint despite similar calcium transients in all groups. Ischemia/reperfusion caused action potential prolongation in control but not trained myocytes. Hearts from sprint had the greatest glyceraldehyde-3-phosphate dehydrogenase activity (P < 0.05) and a tendency towards increased superoxide dismutase activity. These results suggest that sprinting increases myocardial resistance to ischemia/reperfusion. This protection may be secondary to increased myofilament calcium sensitivity and/or myocardial expression of glyceraldehyde-3-phosphate dehydrogenase.
我们研究了两种运动训练方式，即低强度耐力训练和短跑训练，对缺血再灌注后体外等容心肌性能的影响。大鼠每周在跑步机上跑5天，持续6周，强度如下：耐力训练，速度20米/分钟，坡度0%，每天60分钟；短跑训练，以75米/分钟的速度进行5次1分钟跑，坡度15%，每次之间穿插以20米/分钟、坡度15%进行1分钟的主动恢复跑。在两项分级运动测试中，耐力训练和短跑训练均显著提高了运动耐力（相对于对照组，P < 0.05）。对对照组（N = 18）、耐力训练组（N = 20）和短跑训练组（N = 13）的动物心脏进行缓冲灌注后，在Langendorff模式下进行无血流缺血（20分钟）和再灌注（30分钟）。再灌注期间，短跑训练组左心室舒张末压及其一阶导数比耐力训练组和对照组高20%（P < 0.05）。再灌注期间，短跑训练组左心室舒张末压最低（再灌注30分钟时，短跑训练组为10±1毫米汞柱，耐力训练组为14±2毫米汞柱，对照组为14±2毫米汞柱）。然后将心脏用于生化研究，或解离为单细胞以测量收缩、细胞钙和动作电位持续时间。尽管所有组的钙瞬变相似，但短跑训练组的单细胞收缩最大。缺血/再灌注导致对照组心肌细胞动作电位延长，但训练组心肌细胞未出现这种情况。短跑训练组心脏的甘油醛-3-磷酸脱氢酶活性最高（P < 0.05），超氧化物歧化酶活性有增加趋势。这些结果表明，短跑可增加心肌对缺血/再灌注的耐受性。这种保护作用可能继发于肌丝钙敏感性增加和/或甘油醛-3-磷酸脱氢酶在心肌中的表达增加。
