Rodent Skeletal Muscle Metabolomic Changes Associated With Static Cold Storage

Area of Science:

• Biochemistry
• Physiology
• Cellular Metabolism

Background:

• Skeletal muscle preservation is critical for transplantation and research.
• Understanding metabolic changes during preservation is essential for optimizing outcomes.
• Current preservation methods require evaluation for their impact on muscle viability.

Purpose of the Study:

• To investigate the effects of static cold storage on skeletal muscle metabolism.
• To compare cold storage with warm ischemia and warm storage conditions.
• To identify potential biomarkers of muscle injury and viability.

Main Methods:

• Utilized a rodent model with four experimental groups: naive control, warm ischemia, static warm storage, and static cold storage.
• Analyzed muscle energy status, performed metabolomics profiling, and conducted histopathological assessments.
• Quantified key metabolites including glycolytic pathway intermediates, Krebs cycle products, and purine degradation products.

Main Results:

• Warm ischemia and static warm storage led to decreased glycolytic metabolites and accumulation of succinate and hypoxanthine.
• Increased succinate and hypoxanthine levels correlated with higher muscle injury scores.
• Static cold storage maintained glycolytic pathway activity and energy status, with no significant changes in succinate or hypoxanthine compared to controls.

Conclusions:

• Warm ischemia significantly impairs skeletal muscle glycolysis and Krebs cycle activity.
• Static cold storage effectively preserves muscle glycolytic function and cellular energy.
• Succinate and hypoxanthine show potential as novel biomarkers for assessing skeletal muscle viability and injury severity.