Regular exercise is associated with a protective metabolic phenotype in the rat heart
Regular exercise is associated with a protective metabolic phenotype in the rat heart
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DOI：
10.1152/ajpheart.00925.2003
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发表时间：
2004-09-01
影响因子：
4.8
通讯作者：
Allard, MF
中科院分区：
文献类型：
--
作者：
Burelle, Y;Wambolt, RB;Allard, MF
心肌能量底物利用的适应性可能有助于定期运动对心脏的保护作用，有证据表明，药物代谢调节对缺血心脏再灌注有益。因此，我们验证了有规律的体育锻炼对缺血再灌注恢复的有益作用与保护性代谢表型相关的假设。对静坐对照(C)和跑步机训练（T: 10周，4天/周）的雌性Sprague-Dawley大鼠进行20分钟缺血和40分钟再灌注，在离体工作心脏中测量葡萄糖、乳酸和棕榈酸盐的功能、糖酵解和氧化。训练导致心肌肥厚（1.65 +/- 0.05 vs. 1.30 +/- 0.03 g heart wet wt, P < 0.001），缺血后功能恢复提高近50% （P < 0.05）。T型心脏缺血前后糖酵解降低25 ~ 30% (P < 0.05)，葡萄糖氧化率升高45% （P < 0.01）。结果，T型心脏缺血前后的葡萄糖氧化分数分别高出2倍和25% （P < 0.05）。缺血前后，T组棕榈酸酯氧化比C组高50 ~ 65% (P < 0.05)，乳酸氧化组间无显著差异。免疫印迹分析显示，所选酶和蛋白质含量的改变不能解释糖酵解的减少或葡萄糖和棕榈酸氧化的增加。结合对能量代谢的药理调节的有益作用的研究，本研究结果支持代谢适应在保护训练心脏免受缺血再灌注损伤中的作用。
Adaptation of myocardial energy substrate utilization may contribute to the cardioprotective effects of regular exercise, a possibility supported by evidence showing that pharmacological metabolic modulation is beneficial to ischemic hearts during reperfusion. Thus we tested the hypothesis that the beneficial effect of regular physical exercise on recovery from ischemia-reperfusion is associated with a protective metabolic phenotype. Function, glycolysis, and oxidation of glucose, lactate, and palmitate were measured in isolated working hearts from sedentary control ( C) and treadmill-trained ( T: 10 wk, 4 days/wk) female Sprague-Dawley rats submitted to 20 min ischemia and 40 min reperfusion. Training resulted in myocardial hypertrophy ( 1.65 +/- 0.05 vs. 1.30 +/- 0.03 g heart wet wt, P < 0.001) and improved recovery of function after ischemia by nearly 50% ( P < 0.05). Glycolysis was 25 - 30% lower in T hearts before and after ischemia ( P < 0.05), whereas rates of glucose oxidation were 45% higher before ischemia ( P < 0.01). As a result, the fraction of glucose oxidized before and after ischemia was, respectively, twofold and 25% greater in T hearts ( P < 0.05). Palmitate oxidation was 50 - 65% greater in T than in C before and after ischemia ( P < 0.05), whereas lactate oxidation did not differ between groups. Alteration in content of selected enzymes and proteins, as assessed by immunoblot analysis, could not account for the reduction in glycolysis or increase in glucose and palmitate oxidation observed. Combined with the studies on the beneficial effect of pharmacological modulation of energy metabolism, the present results provide support for a role of metabolic adaptations in protecting the trained heart against ischemia-reperfusion injury.