**5. Conclusion**

Myocardial energy metabolism in non-cyanotic CHD was basically sustained by fatty acids oxidation whether or not with increasing workloads. The glucose use was accelerated with overload with cellular hypoxia although very variable. Lactate seemed to play an important role to maintain lactate-pyruvate redox potential. When myocardial workloads were mild as in ASD group, the NADH demand was complemented by lactate oxidation. On the other hand, when workloads were as strong as producing a myocardial hypoxic state as in PH group, lactate production was accelerated to maintain the cellular redox state.
