Dr. Robert Fitts earned his B.S. in 1967 from the State University of New York-Cortland, his M.A.in 1969 from the University of Buffalo, and his Ph.D. in 1972 from the University of Wisconsin in Madison. He did Postdoctoral Fellow studies at Washington University. His laboratory's primary goal is to understand how muscles generate force and elucidate what processes control excitation and contraction (E-C) coupling. In addition to these basic questions, we are evaluating how weightlessness (and models of weightlessness) and fatigue alter muscle function. Finally, we are interested in the effects of regular exercise-training with particular emphasis on its role in preventing the deleterious effects of zero-g and fatigue on skeletal muscle function. We have recently begun to study the role of regular exercise in improving the functional capacity of the whole heart and isolated single myocytes. Our research effort is directed primarily on three projects: (1) the etiology of muscle fatigue, and (2) the role of high resistance and endurance exercise in improving heart cell function, and (3) the effect of microgravity on the structure-function relationship in skeletal muscle. Currently, we are evaluating the effects of long-term flight aboard the International Space Station. Our goal is to determine the time course of the deleterious alterations in muscle with microgravity so that we can model the expected changes that would occur on a very long duration flight such as a trip to Mars. Related projects are studying the causes of the increased susceptibility to muscle damage (and resulting muscle soreness) that is experienced by all crew members post-flight, and work designed to assess the effectiveness of current exercise countermeasures. Our fatigue studies have centered on 2 processes: 1) the role of excitation-contraction coupling (ECC) in muscle fatigue; and 2) the effect of inorganic phosphate (Pi) and H+ on the force and power production of isolated single fibers. The ECC studies utilize voltage clamped rat fibers to elucidate the cellular causes of a particular type of fatigue know as low frequency fatigue (where force is lost selectively at low frequencies). Preliminary data suggests the main problem involves a disruption of the SR Ca2+ release channel. Our studies on the role of Pi and H+ in muscle fatigue have concentrated on the role of these ions in directly inhibiting the force production of the contracting fiber.