Frontiers in medicine · 2026
Aerobic exercise reduces lactate accumulation and improves cardiac function after myocardial infarction.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Chen Ze, Du Jimin, Zuo Shengkai, Wan Chunxiao
Аннотация
OBJECTIVE: 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.
METHODS: NIH 3 T3 mouse embryonic fibroblasts and C57BL/6 J mice were used as research subjects. In vitro, 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 α-Smooth Muscle Actin (α-SMA). In vivo, 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.
RESULTS: In vitro 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. In vivo 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.
CONCLUSION: 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.
METHODS: NIH 3 T3 mouse embryonic fibroblasts and C57BL/6 J mice were used as research subjects. In vitro, 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 α-Smooth Muscle Actin (α-SMA). In vivo, 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.
RESULTS: In vitro 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. In vivo 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.
CONCLUSION: 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.