Identification of the serum metabolomic profile for acute ischemic preconditioning in athletes

In recent years, ischemic preconditioning (IPC) has emerged as an effective strategy to increase tissue resistance against long-term ischemic damage and has been increasingly integrated into exercise regimens. However, further research is needed to explore the impact of IPC-mediated metabolic alterations from an exercise standpoint to conduct a comprehensive exploration of metabolic alterations and their exercise-related mechanisms during acute IPC.

Nontarget metabolomics was performed on blood samples obtained from 8 male athletes both before and after IPC. The studies included the identification of differentially abundant metabolites, analysis of receiver operating characteristic (ROC) curves, Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis for differentially abundant metabolites, and metabolite set enrichment analysis (MSEA).

Nineteen differentially abundant metabolites were identified, with increasing levels of five metabolites, such as O-desmethyltramadol and D-gluconate, whereas 14 metabolites, including 9-hydroxy-10e, 12z-octadecadienoic acid (9-HODE), tetradione, 2-hexenal, (2,4-dichlorophenoxy)acetic acid (2,4-D), and phosphatidylserine (PS), decreased. ROC curve analysis revealed an AUC of 0.9375 for D-gluconate. Both KEGG enrichment analysis and MSEA revealed enrichment in the pentose phosphate pathway (PPP).

This study revealed that PPP, D-gluconate, O-desmethyltramadol, and D-2-aminobutyric acid could be upregulated within 5 min after acute IPC, whereas 2,4-D, PS, 9-HODE, 2-hexenal, and tetradinone could be downregulated. These identified metabolites show promise for improving physical functional status and could be harnessed to enhance athletic performance.