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SPECIAL COMMUNICATIONS: Letters to the Editor-in-Chief

RESPONSE

Green, Daniel PhD

Author Information
Medicine & Science in Sports & Exercise: June 2013 - Volume 45 - Issue 6 - p 1220
doi: 10.1249/MSS.0b013e31828d6016
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Dear Editor-in-Chief

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

Nedlands, Australia

REFERENCES

1. Atkinson G, Batterham AM, Thijssen DHJ, Green DJ. A new approach to improve the specificity of flow-mediated dilation for indicating endothelial function. J Hypertens. 2013; 31: 287–91.
2. Green DJ, Fowler DT, O’Driscoll JG, Blanksby BA, Taylor RR. Endothelium-derived nitric oxide activity in forearm vessels of tennis players. J Appl Physiol. 1996; 81: 943–8.
3. Naylor LH, George K, O’Driscoll G, Green DJ. The athlete’s heart: a contemporary appraisal of the “Morganroth hypothesis”. Sports Med. 2008; 38: 69–90.
4. Spence AL, Carter HH, Naylor LH, Green DJ. A prospective randomised longitudinal study involving 6-months of endurance or resistance exercise on conduit artery adaptation in humans. J Physiol (Lond). 2013; 591 (Pt 5): 1265–75.
5. Thijssen DHJ, Black MA, Pyke K, et al. Assessment of flow mediated dilation (FMD) in humans: a methodological and physiological guideline. Am J Physiol. 2011; 300: 2–12.
6. Thijssen DHJ, Dawson EA, Black MA, Hopman MTE, Cable NT, Green DJ. Heterogeneity in conduit artery function in humans: impact of arterial size. Am J Physiol. 2008; 295: H1927–34.
7. Tinken TM, Thijssen DHJ, Black MA, Cable NT, Green DJ. Conduit artery functional adaptation is reversible and precedes structural changes to exercise training in humans. J Physiol (Lond). 2008; 586: 5003–12.
8. Tinken TM, Thijssen DHJ, Hopkins ND, Dawson EA, Cable NT, Green DJ. Shear stress mediates vascular adaptations to exercise training in humans. Hypertension. 2010; 55: 312–8.
©2013The American College of Sports Medicine