有氧运动可减少心肌梗死后乳酸积聚,改善心功能
Aerobic exercise reduces lactate accumulation and improves cardiac function after myocardial infarction.
Aerobic exercise reduces lactate accumulation and improves cardiac function after myocardial infarction.
本研究旨在探讨乳酸在心肌梗死(MI)后心功能障碍进展中的作用,并阐明有氧运动(AE)通过调节乳酸代谢改善梗死后心功能的效果,从而为临床改善MI后心功能提供实验依据。以NIH 3T3小鼠胚胎成纤维细胞和C57BL/6J小鼠为研究对象。用不同浓度的乳酸处理成纤维细胞,通过检测I型胶原(COL I)和α-平滑肌肌动蛋白(α-SMA)的表达水平评估成纤维细胞的活化状态。建立四种小鼠模型(SED-SHAM、AE-SHAM、SED-MI和AE-MI)。通过超声心动图评估左心室射血分数(LVEF)和左心室缩短分数(LVFS)以评价心功能。使用乳酸检测试剂盒检测心脏组织和血清中的乳酸水平,并通过代谢组学技术分析乳酸介导的血清代谢物变化。实验证实乳酸可显著诱导成纤维细胞活化。代谢组学结果显示,MI后乳酸水平升高导致花生四烯酰肉碱异常蓄积。实验揭示,SED-MI组心脏组织和血清中乳酸水平显著升高,而LVEF和LVFS降低。相反,AE-SHAM组心脏组织和血清中乳酸水平降低,LVEF和LVFS升高。AE-MI组心脏组织和血清中乳酸水平低于SED-MI组但高于AE-SHAM组,且AE-MI组的LVEF和LVFS显著高于SED-MI组。本研究证实乳酸蓄积参与心肌梗死后心功能障碍的病理过程,而有氧运动可通过降低心脏组织和血清中的乳酸水平改善MI后心功能。这些发现为靶向乳酸代谢防治梗死后心功能障碍提供了新的实验证据,也为有氧运动在心脏康复中的应用提供了理论支持。
This study aimed to investigate the role of lactate in the progression of cardiac dysfunction after myocardial infarction (MI) and clarify the effect of aerobic exercise (AE) on improving post-infarction cardiac function by regulating lactate metabolism, so as to provide experimental evidence for the clinical improvement of cardiac function after MI. NIH 3 T3 mouse embryonic fibroblasts and C57BL/6 J mice were used as research subjects. , fibroblasts were treated with different concentrations of lactate, and the activation state of fibroblasts was evaluated by detecting the expression levels of Collagen I (COL I) and -Smooth Muscle Actin (α-SMA). , four mouse models (SED-SHAM, AE-SHAM, SED-MI, and AE-MI) were established. Cardiac function was assessed by echocardiography for left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS). Lactate levels in cardiac tissue and serum were detected using a lactate assay kit, and serum metabolite changes mediated by lactate were analyzed via metabolomics technology. experiments confirmed that lactate could significantly induce fibroblast activation. Metabolomics results showed that elevated lactate levels after MI led to abnormal accumulation of arachidonoyl carnitine. experiments revealed that lactate levels in cardiac tissue and serum were significantly increased, while LVEF and LVFS were decreased in the SED-MI group. In contrast, lactate levels in cardiac tissue and serum were reduced, and LVEF and LVFS were elevated in the AE-SHAM group. Lactate levels in cardiac tissue and serum of the AE-MI group were lower than those of the SED-MI group but higher than those of the AE-SHAM group, and the LVEF and LVFS of the AE-MI group were significantly higher than those of the SED-MI group. This study confirmed that lactate accumulation is involved in the pathological process of cardiac dysfunction after myocardial infarction, and AE can improve cardiac function after MI by reducing lactate levels in cardiac tissue and serum. These findings provide new experimental evidence for the prevention and treatment of post-infarction cardiac dysfunction by targeting lactate metabolism, and also offer theoretical support for the application of AE in cardiac rehabilitation.
Ze Chen, Jimin Du, Shengkai Zuo, Chunxiao Wan. Aerobic exercise reduces lactate accumulation and improves cardiac function after myocardial infarction.. Frontiers in medicine. 2026; doi:10.3389/fmed.2026.1816790.
Ze Chen, Jimin Du, Shengkai Zuo, Chunxiao Wan (2026). Aerobic exercise reduces lactate accumulation and improves cardiac function after myocardial infarction.. Frontiers in medicine. https://doi.org/10.3389/fmed.2026.1816790
Ze Chen, Jimin Du, Shengkai Zuo, Chunxiao Wan. Aerobic exercise reduces lactate accumulation and improves cardiac function after myocardial infarction.[J]. Frontiers in medicine, 2026 doi:10.3389/fmed.2026.1816790.
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