Some aspects on the regulation of carbohydrate and lipid metabolism in cardiac tissue.

FFA are the main substrate of biological oxidation in cardiac muscle under normal conditions. But it could be shown in man and animal that during heavy exercise there is a shift to preferential oxidation of lactate. During oxygen deficiency in hypoxic or ischemic situations which may occur lightly in distinct areas of hypertrophic hearts after exercise, lactate, alpha-glycerol phosphate and acyl-CoA as well as triglyceride levels in cardiac tissue may increase, whereas FFA are less oxidized. Unoxidized intracellular FFA and acyl-CoA, which are not esterified in a sufficient way to triglycerides, may impair oxidative phosphorylation in mitochondria, the P/O quotient as well as cardiac function perhaps by an interference with Ca++ movements during the contraction cycle. With the examples of anoxia and complete ischemia as the two extreme situations of O2 deficiency some principles of the alteration of cardiac metabolism are pointed out, and furthermore attempts to improve anoxic tolerance of cardiac tissue.