RESPONSE

Abstract

Dear Editor-in-Chief: Thank you for the opportunity to respond. Although we welcome a critical analysis of our work, it appears that Lamberts and Noakes have misinterpreted what we wrote. We actually concluded, "Among well-trained subjects heterogeneous in V˙O2max and running performance, velocity at V˙O2max (vV˙O2max) is the best predictor of running performance because it integrates both maximal aerobic power and economy of running" (6). This is different than concluding that "the cardiovascular model (CVM) explains endurance performance better than the central governor model (CGM)," as they have claimed we did. Lamberts and Noakes label the classic model of physiological factors that determine endurance running performance "the cardiovascular model." We do not agree with this terminology because a number of factors (V˙O2max, running economy, and fractional utilization of V˙O2max) are involved (1,4,5). Lamberts and Noakes contend that "by recruiting the largest possible number of skeletal muscle fibers with the greatest contractile capacity, superior athletes will have the shortest foot contact times and the longest flight time, resulting in superior performance." However, sprinters should be able to recruit a larger number of muscle fibers with the greatest contractile ability because they possess the highest percentage type II muscle fibers. Sprinters also have shorter foot contact times and longer flight times than distance runners (2,3). If Lambert and Noakes were correct, then sprinters would be able to achieve higher peak treadmill velocities and would have faster 16-km run times than distance runners. Because this is not the case, it appears that something is wrong with their theory. We agree that cross-sectional studies cannot prove causation. However, alterations in O2 delivery (through blood doping, erythropoietin, beta blockade, induced anemia, and breathing hypoxic gas mixtures) will impact V˙O2max and endurance performance in predictable ways (1). These findings lend credibility to the claim that V˙O2max is a determinant of distance running performance. In addition, there are logical reasons why V˙O2max, running economy, and fractional utilization of V˙O2max are causally linked to distance running performance. Regarding the claim that we have not proven or disproven the central governor model (CGM), this is true. But the burden of proof for providing evidence to back up the CGM falls on Noakes et al. because they are the leading proponents of this model. Our study was not designed to test Dr. Noakes' CGM, which proposes that a central governor in the brain limits exercise performance to protect the heart and other organ systems from damage. Our study demonstrates that the same variables (V˙O2max and running economy) that are highly correlated with the 16-km run performance are also highly correlated with peak treadmill velocity. Lamberts and Noakes state, "Nor does [our] model predict that exercise performance is limited by oxygen delivery to the muscle…." This highlights the primary difference between the classic model for explaining distance running performance and the CGM. In our view, any model that does not acknowledge O2 delivery as a determinant of endurance exercise performance is severely flawed. James E. McLaughlin Exercise Physiology Department Lynchburg College Lynchburg, VA Edward T. Howley David R. Bassett, Jr. Department of Exercise, Sport, and Leisure Studies University of Tennessee Knoxville, TN