Elucidating the optimal exercise intervention to improve arterial stiffness is a crucial vein of inquiry in the attempt to minimize cardiovascular morbidity and mortality. Alkatan et al. are therefore to be congratulated for assessing the impact of different prevalent exercise training (ET) modalities (swimming, cycling) on arterial stiffness in a high-risk population. Using well-established methods, they conclude that the magnitude of improvement in central (carotid) arterial stiffness is similar with swimming and cycling ET interventions. These findings contrast with previous evidence indicating a superior beneficial effect of cycling compared with swimming ET on carotid arterial stiffness. Herein, I would like to highlight 2 issues regarding the study of Alkatan et al. that commonly require particular consideration when addressing the impact of ET and may contribute to explain divergences.

The first issue refers to the apparent similarity of swimming and cycling ET interventions in terms of exercise intensity. Both swimming and cycling ET were planned to be performed at the same absolute exercise intensity (as quantified by heart rate monitoring), progressively increasing from 40% to 70% of maximal heart rate (HR _max ) reserve during 12 weeks. In this respect, it is known that HR _max is approximately 12 beats/min lower with swimming compared with land-based exercise. Accordingly, exercise intensity regarding swimming ET should be corrected when using land-based HR _max values. Because this adjustment is not reported in the study of Alkatan et al., swimming ET could have involved a greater relative exercise intensity than cycling ET. This may have influenced the impact of swimming versus cycling ET interventions, specifically taking into account the positive linear relation between relative exercise intensity and the effect of ET on arterial stiffness.

The second issue concerns the effect of subject randomization on the main outcome variables. In this regard, the swimming group presented higher baseline levels of carotid arterial stiffness compared with the cycling group (p <0.05) as determined from Figures 1 ( B stiffness) and 2 (distensibility) in the report by Alkatan et al. Given that the effect of ET on arterial stiffness is enhanced in subjects with increased baseline arterial stiffness, this could also have affected the comparison between swimming and cycling ET interventions. Nonetheless, the investigators can attenuate such potential confounding with additional analyses on ET groups matched by baseline arterial stiffness and/or including baseline arterial stiffness as a covariate. Taken together, a more precise estimate of the relative impact of distinct ET modalities on arterial stiffness may be obtained through the noteworthy work of Alkatan et al.