Noakes T D
Department of Exercise and Sports Science, Medical Research Council, University of Cape Town, Sports Science Institute of South Africa, Newlands.
Med Sci Sports Exerc. 1998 Sep;30(9):1381-98. doi: 10.1097/00005768-199809000-00007.
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 (VO2max) is limited by the development of anaerobiosis in the active muscle, and 3) endurance performance is also determined by skeletal muscle anaerobiosis because the VO2max 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 VO2max of 4 L x min(-1). His error resulted from his incorrect belief that the real VO2 unmeasurable because it includes a large "anaerobic component," rose exponentially at running speeds greater than 13.2 km x 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 VO2 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 VO2 "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 VO2, 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 precede 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.
巴西特和豪利认为1996年J. B. 沃尔夫讲座是错误的，原因如下：1）A. V. 希尔确实证实了“平台现象”的存在；2）最大摄氧量（VO2max）受活跃肌肉中无氧代谢发展的限制；3）耐力表现也由骨骼肌无氧代谢决定，因为VO2max是运动能力的最佳预测指标。因此，4）心血管而非骨骼肌因素决定耐力表现。他们进一步认为希尔的“科学直觉是正确的”，在过去70年里“只需相对较小的改进”。但本反驳中所呈现的证据表明，希尔既没有寻求也不相信“平台现象”或个体最大摄氧量的概念。这两个概念是泰勒等人在1955年提出的，并错误地归因于希尔。相反，希尔认为人类存在一个普遍的VO2max为4 L×min⁻¹。他的错误源于他错误地认为实际的VO2因包含大量“无氧成分”而无法测量，并且在跑步速度大于13.2 km×h⁻¹时呈指数上升。但希尔及其同事确实是第一个意识到心输出量（CO）进而VO2出现平台对心脏本身构成危险的人。因为与骨骼肌不同，心脏的泵血能力既依赖于自身的血液供应，同时也是其自身血液供应的决定因素。因此，如果CO达到峰值导致“平台现象”，那么该峰值的直接原因将是心肌氧输送出现平台，进而导致心肌缺血逐渐加重。随着运动持续超过假定的VO2“平台”，缺血必然会恶化。为了应对这一困境，希尔及其同事提出在“心肌或神经系统中”存在一种调节机制，以防止在最大运动期间发生心肌缺血。这种调节机制会使最大运动在冠状动脉血流、CO或VO2出现平台之前或骨骼肌无氧代谢开始之前就终止。因此，提出了一种新的生理模型，其中骨骼肌的募集由一个中枢“调节机制”进行调节，专门用于防止在最大运动期间骨骼肌无氧代谢发展之前出现进行性心肌缺血。结果，心血管功能“限制”了最大运动能力，这可能是由于心肌氧输送受限所致。该模型与在低压低氧环境下运动期间心血管功能的所有已发表研究结果相符，在这种环境下心肌缺氧更有可能发生。
