During exercise, the skeletal muscle pumps will increase venous return to levels at which the Starling mechanism is insufficient, as there is an upper limit to stroke volume. This is when the two other mechanisms come into play, both mediated by the sympathetic system. Increasing the heart rate (the chronotropic response) will allow an increased output, and increased contractility (the inotropic response) will allow the stoke volume to be maintained at high heart rates and will help minimize the rise in EDP. These responses are triggered by exercise, the anticipation of exercise, and emotional stress. Also, the failing heart will be under considerable sympathetic drive.
Now if the heart simply reacts to variations in venous return, what mechanism ensures an adequate rate of return at rest? The kidneys are central to this; if the cardiac output is insufficient for adequate renal perfusion then the kidneys retain salt and water via the renin/angiotensin mechanism, the circulating volume is thus increased and the rate of venous return is augmented as a direct consequence. Hence, salt retention is a feature of cardiac failure.