Myocardial Adaptation to Acute Oxygen Shortage

In this study, we examined the bioenergetic mechanisms underlying myocardial adaptation to O2-limited perfusion. Shortened O2 supply to contracting tissue results in nearly immediate metabolic and performance decline due to fast turnover rate of high-energy phosphates compared to their intracellular concentration.1 Thus, to maintain adequate ATP production, tissue is forced to divert from aerobic to anaerobic pathways: although less efficient than aerobic ones, glycolytic ATP production under hypoxic, high-flow conditions may account for up to half of total energy requirements.2 However, if low O2 supply is associated with reduced flow, the heart preferentially downregulates energy demand to meet supply.3 Whereas these processes were verified during sustained ischemia or hypoxia, it appears important to assess the mechanisms underlying acute regulation of performance. The main reason for this is the need to understand to a greater extent reperfusion injury and the generation of endogenous myocardial protection, both of which may be strictly linked to bioenergetic processes.