Cardiac output in a normal individual at rest ranges between 4 to 6 liters per minute, but during severe exercise the heart may be required to pump three to four times this amount. There are two primary modes by which the blood volume pumped by the heart, at any given moment, is regulated: 1) intrinsic cardiac regulation, in response to changes in the volume of blood flowing into the heart; and 2) control of heart rate and cardiac contractility by the autonomic nervous system.

The intrinsic ability of the heart to adapt to changing volumes of inflowing blood is known as the Frank-Starling mechanism (law) of the heart. In general, this response can simply be described as: the more the heart is stretched (increased blood volume), the greater will be the subsequent force of ventricular contraction and, thus, the amount of blood ejected through the aortic valve. In other words, within its physiological limits, the heart will pump out all the blood that enters it without allowing excessive damming of blood in veins. The underlying basis for this phenomenon is related to the optimization of the lengths of sarcomeres and the functional subunits of striate muscle; there is optimization in the potential for the contractile proteins (actin and myosin) to form crossbridges. It should also be noted that "stretch" of the right atrial wall (e.g., due to increased venous return) can directly increase the rate of the sinoatrial node by 10-20%; this also aids in the amount of blood that will ultimately be pumped per minute by the heart.

The pumping effectiveness of the heart is also effectively controlled by the autonomic nervous system by both the sympathetic and parasympathetic components of this system. There is extensive innervation of the myocardium by such. To get a feel for how effective the modulation of the heart by this innervation is, it has been reported that the cardiac output often can be increased by more than 100% by sympathetic stimulation and, by contrast, output can be nearly terminated by parasympathetic (vagal) stimulation.

Cardiovascular function is also modulated through reflex mechanisms that involve baroreceptors, the chemical composition of the blood, and via the release of various hormones. More specifically, baroreceptors, which are located in the walls of some arteries and veins, exist to monitor the relative blood pressure. Those specifically located in the carotid sinus help to reflexively maintain normal blood pressure in the brain, whereas those located in the area of the ascending arch of the aorta help to govern general systemic blood pressure (for more details, see the chapter on the Autonomic Nervous System). Chemoreceptors that monitor the chemical composition of blood are located close to the baroreceptors of the carotid sinus and arch of the aorta, in small structures known as the carotid and aortic bodies. The chemoreceptors within these bodies detect changes in blood levels of O2, CO2, and H+. Hypoxia (a low availability of O2), acidosis (increased blood concentrations of H+), and/or hypercapnia (high concentrations of CO2) stimulate the chemoreceptors to increase their action potential firing frequencies to the brain cardiovascular control centers. In response to this increased signaling, the central nervous system control centers, the hypothalamus, in turn, cause an increased sympathetic stimulation to arterioles and veins, producing vasoconstriction and a subsequent increase in blood pressure. In addition, the chemoreceptors simultaneously send neural input to the respiratory control centers in the brain, so to induce the appropriate control of respiratory function (e.g., increase O2 supply and reduce CO2 levels