Acute high-intensity exercise can affect cardiac health by altering substance metabolism. However, few metabolomics-based studies provide data on the effect of exercise along with myocardial metabolism. Our study aimed to identify metabolic signatures in rat myocardium during acute high-intensity exercise and evaluate their diagnostic potential for sports injuries. We collected rat myocardium samples and subjects’ serum samples before and after acute high-intensity exercise for metabolite profiling to explore metabolic alterations of exercise response in the myocardium. Multivariate analysis revealed myocardium metabolism differed before and after acute high-intensity exercise. Furthermore, 6 target metabolic pathways and 12 potential metabolic markers for acute high-intensity exercise were identified. Our findings provided an insight that myocardium metabolism during acute high-intensity exercise had distinct disorders in complex lipids and fatty acids. Moreover, an increase of purine degradation products, as well as signs of impaired glucose metabolism, were observed. Besides, amino acids were enhanced with a certain protective effect on the myocardium. In this study, we discovered how acute high-intensity exercise affected myocardial metabolism and exercise-related heart injury risks, which can provide references for pre-competition screening, risk prevention, and disease prognosis in competitive sports and effective formulation of exercise prescriptions for different people.
Acute high-intensity exercise is a harmful manner associated with a series of myocardial injuries. Metabolism disorder of myocardium is one of the most serious conditions. However, few metabolomics-based studies provide data on the effect of exercise along with myocardial metabolism. Our study aimed to identify metabolic signatures in rat myocardium during acute high-intensity exercise and evaluate their diagnostic potential to sports injuries. SD rats were divided into control group and acute high-intensity exercise group and their myocardium samples were analyzed by LC-MS to explore metabolic alterations of rats’ myocardium. This study showed myocardium metabolism clearly differed between the two groups. there were 6 target metabolic pathways and 12 potential metabolic markers for acute high-intensity exercise. Our findings provide an insight that myocardium metabolism during acute high-intensity exercise have distinct disorders in complex lipids and fatty acids. Moreover, an increase of purine degradation products as well as signs of impaired glucose metabolism were observed. However, the amino acid was enhanced, which had a certain protective effect on the myocardium.
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