Following a transient increase in relative mitochondrial volume which lasts but a few days, cardiac hypertrophy in response to pressure- or volume-overload is characterized by a preferential growth of contractile elements resulting in a decreased mitochondria/myofibrils volume ratio. At least under some conditions, the number of mitochondria/unit area increases as does the organelles surface/volume ratio. If the functional overload persists for a long period of time, e.g. 12-15 months, relative mitochondrial volume is decreased further. Unlike the imbalance in growth of mitochondria and myofibrils, the total surface area (sarcolemma plus T-System) enlarges in proportion to the increase in cell volume. While most of the components which are altered during hypertrophy become normalized as cardiac hypertrophy regresses, the process is slower than the imbalance associated with cellular enlargement. Most models of cardiac hypertrophy differ from normal growth in that the latter is characterized by proportional growth of all cellular components. In contrast, hypertrophy associated with exercise results in proportional growth in cellular components. The idea that growth of various cellular organelles is regulated by separate mechanisms is gaining support. Both sympathectomy and noreprinephrine depletion normalize the growth of mitochondria and myofibrils, while thyroxine treatment stimulates a preferential growth of mitochondria. Current evidence, therefore, suggests that myocardial cell growth probably involves complex processes which may vary with different conditions associated with the stimulus invoking enhanced cellular enlargement.