Myocardial oxidative metabolism (MVO2)

Myocardial oxidative metabolism is the fundamental physiological process by which the heart generates adenosine triphosphate (ATP) to sustain its continuous contractile activity. The heart is metabolically flexible, normally deriving 60-90% of its energy from the aerobic oxidation of fatty acids and the remainder from glucose, lactate, and ketones (Lopaschuk et al., 2010, Physiological Reviews). In pathological conditions such as heart failure or myocardial ischemia, this metabolic flexibility is compromised, leading to an "energy starvation" state where ATP production fails to meet demand (Neubauer, 2007, NEJM). Therapeutic strategies target this process by promoting glucose oxidation over fatty acid oxidation, a more oxygen-efficient pathway that helps protect the myocardium during periods of reduced oxygen supply (Stanley et al., 2005, Nature Clinical Practice Cardiovascular Medicine). While not a single molecular target, this metabolic network is modulated by several drugs that inhibit specific mitochondrial enzymes to improve cardiac function and symptoms in patients with chronic cardiovascular diseases (Kolwicz et al., 2013, Circulation Research).

Other names

Cardiac oxidative metabolismMyocardial energy metabolismCardiac mitochondrial respirationMyocardial oxygen consumption

Pharmacological modulation of myocardial oxidative metabolism typically involves shifting the heart's substrate preference from fatty acid oxidation to glucose oxidation. This shift is achieved by inhibiting enzymes such as long-chain 3-ketoacyl-CoA thiolase (3-KAT) or carnitine palmitoyltransferase 1 (CPT1), which reduces oxygen demand per unit of ATP produced and improves cardiac efficiency during ischemia or heart failure.