The Akt family of intracellular protein kinases regulates cellular growth, proliferation, survival and metabolism. Postnatal growth of the heart chiefly involves non‐proliferative cardiac myocyte enlargement analogous to skeletal muscle growth. Cardiac hypertrophy exists in a ‘physiological’ form that is an adaptive response to long‐term exercise training, and as a ‘pathological’ form that is often a maladaptive response to hypertension or valvular heart disease. By use of an Akt1‐deficient mouse model system, we determined that Akt1 activity is required for physiologic cardiac growth in response to insulin‐like growth factor 1 stimulation or exercise training. In contrast, Akt1 activity was found to antagonize pathologic cardiac growth that occurs in response to endothelin 1 stimulation or pressure overload. Evaluation of an Akt2‐deficient mouse model system demonstrated that this family member plays an important role in insulin‐stimulated glucose uptake and metabolism, and may not regulate physiologic or pathologic cardiac growth. Therefore, Akt1 selectively promotes physiological cardiac growth while Akt2 selectively promotes insulin‐stimulated cardiac glucose metabolism.