Enhanced Conduit Artery Flow-Mediated Dilation in Elite Atheletes

Abstract

Dear Editor-in-Chief Recently, Green et al. (1) reported structural enlargement and similar or even decreased flow-mediated dilation (FMD) in conduit arteries of elite athletes compared with sedentary counterparts. A previous handgrip exercise intervention study in active young males had provided evidence for the dependence of vascular adaptations on exercise-induced shear stress (7). In accordance with a theory first proposed by Laughlin (3), Green et al. suggested that lack of enhanced FMD in elite athletes might be a common feature of long-term training-induced vascular adaptations related to structural remodeling and normalization of exercise-induced shear stress. Given the relevance of that statement for the future interpretation of FMD data in both exercise science and clinical contexts, we would like to contribute to the discussion. Studies in elite endurance athletes performed by several research groups have shown conflicting FMD results (2,4–6,8). Indeed, there is a balance between studies reporting decreased (1) or normal (1,4,5), and enhanced FMD (2,6,8) in highly trained athletes compared with their sedentary counterparts. A previous study from our group demonstrated higher FMD in predominantly and nonpredominantly trained limbs of national and international class cyclists and swimmers (8). Moreover, we observed signs of structural remodeling such as larger baseline diameters in conduit arteries and also higher muscle perfusion and vascular conductance during isolated exercise in both groups of athletes (8). Interestingly, despite larger baseline artery diameters, peak exercise-induced shear stress was not normalized but increased in the cyclists and swimmers compared with their sedentary controls (8), contrasting with the rationale of the aforementioned statement (1). This finding is a key point to discuss arterial adaptations in highly trained athletes. To the best of our knowledge, no other study reported shear stress during exercise in highly trained athletes, and accordingly, the hypothesis that arterial remodeling necessarily causes normalization of shear stress during exercise training bouts remains to be explored, especially at the high exercise intensity levels reached by elite athletes. On the other hand, we do not discard that a partial normalization of shear stress may occur in highly trained athletes at some stages during their training program, thus decreasing the stimulus for FMD enhancement. Nonetheless, taking together, the literature does not support the existence of a steady arterial adaptation state characteristic of highly trained athletes as implied before (1). Although speculative, it is conceivable that arterial endothelial function adaptations could be strongly dynamic and related to variations in training intensity, volume, frequency, and modality of periodized training programs commonly followed by elite athletes to reach peak performance at particular time points during the competitive season. In conclusion, few research groups and thus few studies have investigated FMD in highly trained athletes. Therefore, until more evidence becomes available, we suggest to keep this interesting and consequential question open to further discussion. David Montero, Hons Philippe Obert, PhD Guillaume Walther University of Avignon Laboratoire de Pharm-Ecologie Cardiovasculaire Avignon, France