Excess functional capacity is a fundamental characteristic of biological systems. Reserve capacity allows the system to respond, at least temporarily, to marked increases in demand without failing. In the heart, for example, cardiac output can increase from 5 l/min at rest to 15–20 l/min at stress, a functional reserve capacity of 300–400% . Disease interferes with an organ’s function, reducing reserve capacity. As a result, testing maximum performance often allows early detection of disease, before the disorder is clinically apparent. Exercise testing with electrocardiographic monitoring was suggested almost 100 years ago to detect coronary disease. It was considered too dangerous for safe diagnostic use, however, because patients became symptomatic with exertion. Developing techniques for continuous patient monitoring and standardizing the stress test procedure made the procedure creditable for diagnostic use. In the 1920s, Arthur Master, a cardiologist in New York City2 [2, 3], and the subsequent work of many investigators , fostered the evolution of exercise electrocardiographic stress testing. The “stress test” that Master employed consisted of a two-step platform. The patient held the EKG leads and walked up and down the two steps for 3 min (the “double Master” test). The number of trips (climbing and descending the steps) during the 3-min interval varied with age, gender, and weight, from a maximum of 64 for a 15to 19-year-old to a minimum of 24 for a 75to 79-year-old. The EKG was recorded at rest, during stress, at the termination of stress, and at 2 min and 6 min post stress. Following 40 years of experience with stress electrocardiography, two radionuclide procedures were developed as diagnostic techniques in the 1970s: (a) myocardial perfusion imaging at rest and stress  and (b) stress gated blood pool and first-pass radionuclide ventriculography [6, 7]. In addition to the heart, nuclear medicine procedures have incorporated this “loss of reserve” concept to identify early-phase disease in many organs. Some of the clinically useful stress procedures are summarized in Table 1. Estorch and colleagues report an extension of the “reserve function” concept to determine the reserve capacity of sympathetic innervation in the myocardium. In the normal heart, sympathetic stimuli increase the force and rate of contraction  associated with a marked increase in coronary blood flow. This stimulus can arise either by stimulation of sympathetic nerves innervating the heart or via an increase in the circulating levels of catecholamines. The sympathetic neurons innervating the heart originate in the intermediolateral column of the spinal cord, primarily in the upper thoracic segments . The fibers emerge from the cord and synapse, and the This Editorial Commentary refers to the article http://dx.doi.org/10.1007/s00259-004-1520-2.