We thank our good friends from Avignon for their interest in our article, which is only natural given their important contributions to this field.
As stated in the Discussion of our article, and reiterated by Montero et al., there are articles that suggest that conduit arterial function is enhanced, unchanged, and even lower in athletes than controls. The literature is mixed, and the purpose of our article was to address this and provide some possible physiological explanations, on the basis of imputation from our recent work relating to the effects of training on artery remodeling (7) and the known effect of baseline diameter on flow-mediated dilation (FMD) interpretation (6). The latter may be a mathematical artifact (1) rather than any effect of shear normalization, and perhaps our colleagues have misunderstood us on this point. Nonetheless, we accept that we provided speculative explanations. Indeed, it was our intention to raise new hypotheses.
The idea that vascular function should be enhanced in athletes is charismatic, because these individuals experience episodic increases in shear, a known stimulus to enhance endothelial function (8). However, several studies, including our own, suggest that such enhancement is not always apparent. Indeed, the majority of FMD studies (as quoted by Montero et al.) indicates that athletes, paradoxically, do not exhibit enhanced function. Furthermore, the observation of lack of enhancement in vascular function is not limited to FMD. There are also data on lack of enhancement in blood flow responses to NO agonists measured by plethysmography in the preferred limb, relative to contralateral forearm, of elite tennis players (2). We proposed that one reason for the absence of enhanced function may relate to the effect of structural changes in arteries (7). We agree with Montero et al. that the relation between function and structure may exist in dynamic equilibrium, affected by training volume and other factors. Indeed, we recently proposed such an explanation ourselves: “vascular adaptation is highly dynamic and set-points that evolve to balance adaptations in function and structure can be continually adjusted in response to modifications in the exercise stimulus” (4).
Perhaps another part of the explanation is in the ubiquitous assumption in exercise science that differences between athlete’s and controls can be attributed to the effects of exercise rather than the myriad between-subject factors that can affect physiology and generate “noise.” This assumption has led to potential errors in the interpretation of training data pertaining to cardiac adaptation (3). Finally, the extant studies of athletes and FMD have used techniques of varying quality and veracity. Future studies that adopt recent guidelines should produce more consistency (5).
Paradoxical findings provide for a rich vein of inquiry. We are grateful to share the company of such thoughtful and accomplished colleagues in our journey toward understanding.
Daniel Green, PhD
School of Sports Science, Exercise and Health
The University of Western Australia
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