Maximal oxygen uptake: "classical" versus "contemporary" viewpoints: a rebuttal. Med. Sci. Sports Exerc., Vol. 30, No. 9, pp. 1381-1398, 1998. Bassett and Howley contend that the 1996 J. B. Wolffe lecture is erroneous because: 1) A. V. Hill did establish the existence of the "plateau phenomenon," 2) the maximum oxygen consumption (V˙O2max) is limited by the development of anaerobiosis in the active muscle, and 3) endurance performance is also determined by skeletal muscle anaerobiosis because the V˙O2max is the best predictor of athletic ability. As a result, 4) cardiovascular and not skeletal muscle factors determine endurance performance. They further contend that Hill's "scientific hunches were correct," requiring "only relatively minor refinements" in the past 70 yr. But the evidence presented in this rebuttal shows that Hill neither sought nor believed in either the "plateau phenomenon" or the concept of the individual maximum oxygen consumption. These twin concepts were created by Taylor et al. (97) in 1955 and erroneously attributed to Hill. Rather Hill believed that there was a universal human V˙O2max of 4 L·min−1. His error resulted from his incorrect belief that the real V˙O2, unmeasurable because it includes a large "anaerobic component," rose exponentially at running speeds greater than 13.2 km·h−1. But Hill and his colleagues were indeed the first to realize the danger that a plateau in cardiac output (CO) and hence in V˙O2 would pose for the heart itself. For unlike skeletal muscle, the pumping capacity of the heart is both dependent on, but also the determinant of, its own blood supply. Thus, if the CO reaches a peak causing the "plateau phenomenon," the immediate cause of that peak will have been a plateau in myocardial oxygen delivery, causing a developing myocardial ischemia. The ischemia must worsen as exercise continues beyond the supposed V˙O2 "plateau." To accommodate this dilemma, Hill and his colleagues proposed a governor "either in the heart muscle or in the nervous system" necessary to prevent myocardial ischemia developing during maximal exercise. This governor would cause maximal exercise to terminate before the development of a plateau in either coronary flow, CO, or V˙O2, or the onset of skeletal muscle anaerobiosis. Accordingly, a new physiological model is proposed in which skeletal muscle recruitment is regulated by a central "governor" specifically to prevent the development of a progressive myocardial ischemia that would preceed the development of skeletal muscle anaerobiosis during maximum exercise. As a result cardiovascular function "limits" maximum exercise capacity, probably as a result of a limiting myocardial oxygen delivery. The model is compatible with all the published findings of cardiovascular function during exercise in hypobaric hypoxia, in which there is a greater likelihood that myocardial hypoxia will develop.
Department of Exercise and Sports Science and Bioenergetics of Exercise Research Unit of the Medical Research Council, University of Cape Town, Sports Science Institute of South Africa, Newlands, 7700, SOUTH AFRICA
Submitted for publication February 1998.
Accepted for publication June 1998.
The author's research is supported by the dedicated financial support of the University of Cape Town, the Medical Research Council of South Africa, the Liberty Life Insurance Company, the Foundation for Research and Development, the Founding Donors of the Sports Science Institute of South Africa, Bromor Foods, and a variety of other nutritional and pharmaceutical companies.
Address for correspondence: Professor Tim Noakes, Liberty Life Professor of Exercise and Sports Science and Director, Bioenergetics of Exercise Research Unit of the Medical Research Council at the University of Cape Town, Sports Science Institute of South Africa, Boundary Road, Newlands, 7700, South Africa.