Lactate modulates cardiac gene expression in mice during acute physical exercise

Area of Science:

• Cardiovascular Physiology
• Exercise Metabolism
• Molecular Biology

Background:

• Lactate is traditionally viewed as a metabolic waste product.
• Emerging evidence suggests lactate may function as a signaling molecule.
• Its role in cardiac tissue during physiological stress, like exercise, requires further investigation.

Purpose of the Study:

• To investigate the role of cardiac lactate as a signaling molecule during acute exercise.
• To determine the relationship between cardiac lactate levels and metabolic gene expression.
• To assess the impact of lactate transporter inhibition on cardiac metabolism.

Main Methods:

• Mice (C57BL6/J) underwent treadmill running at varying intensities (30-90% Smax).
• Lactate transporter blocker (α-cyano-4-hydroxycynnamate - CINN) was administered.
• Cardiac lactate levels, glycolytic/oxidative enzyme activities (HK, LDH, CS), and gene expression (LDH, NRF-2, COX-IV, PGC-1α) were measured.

Main Results:

• High-intensity exercise (90% Smax) elevated cardiac lactate, HK, CS activity, and PGC-1α/COX-IV mRNA.
• Lower exercise intensities did not alter cardiac lactate levels.
• CINN administration reduced cardiac lactate, HK/CS activity, and PGC-1α/COX-IV mRNA in high-intensity runners.
• Cardiac lactate positively correlated with PGC-1α and COX-IV gene expression.

Conclusions:

• Cardiac lactate levels are associated with gene transcription during high-intensity exercise.
• Lactate may act as a signaling molecule influencing cardiac metabolism and gene expression.
• Targeting lactate transport could modulate exercise-induced metabolic adaptations in the heart.