Data inconsistencies and inaccuracies combined with methodological problems render physiological interpretation suspect

Excerpt

We wish to applaud Jenkins, Mauger, and Hopker (2016) for following previous encouragement to address the mechanistic bases by which the self-paced \(\dot{V}{{\text{O}}_{2\max }}\) protocol (SPV) test may increase \(\dot{V}{{\text{O}}_{2\max }}\) (Poole et al. 2014). Previously, Mauger et al. (2013) reported that the SPV (performed on a non-motorized treadmill) increased \(\dot{V}{{\text{O}}_{2\max }}\) to ~119% of that achievable on a graded motorized treadmill test. Their claim that this occurred via improved conditions for O₂ extraction in the exercising muscle(s) was found wanting based upon the established relationship between cardiac output and \(\dot{V}{{\text{O}}_{2\max }}\) which dictates a hyperbolic increase in a-vO₂ difference (i.e., O₂ extraction) as a function of \(\dot{V}{{\text{O}}_{2}}\). This relationship severely constrains further increases in fractional O₂ extraction during high intensity exercise (i.e., at high \(\dot{V}{{\text{O}}_{2}}\)), because O₂ reserves in the venous blood are far too limited to increase \(\dot{V}{{\text{O}}_{2\max }}\) by 19%. Thus, in Jenkins et al. (2016), cardiac output estimation via bioimpedance is employed to resolve whether whole body O₂ transport might be higher during the SPV and provide a mechanism for such an elevated \(\dot{V}{{\text{O}}_{2\max }}\) which does not depend principally on increased fractional O₂ extraction. …