To resist or to endure: exercise mode matters in arterial structure and function

Exercise training induces beneficial arterial adaptations in healthy individuals. The effects of exercise on arterial structure and function in healthy participants have been studied predominantly using cross-sectional comparisons of trained athletes and untrained healthy control participants. Few studies have investigated arterial adaptations with a randomized longitudinal exercise training design, which could account for within-subject responses to either endurance- or resistance-training stimuli. Comparisons between the long-term effects of endurance training (ET) versus resistance training (RT) may highlight structural and functional adaptations in the arteries. Spence et al. (2013) recently implemented a 6-month, prospective randomized longitudinal study to determine the effects of ET and RT on conduit artery adaptations in healthy humans. Their study revealed a divergent response in conduit arterial structural and functional adaptations following RT relative to ET. In the periphery, while RT training increased arterial diameter and function in the brachial artery, it did not elicit any changes in the femoral artery. Conversely, while ET training increased arterial diameter and function in the femoral artery, it did not elicit any changes in the brachial artery. Nonetheless, central arterial adaptations were present following both RT and ET training as measured by a decrease in carotid artery wall thickness. Their novel findings ultimately suggest that either exercise modality may be beneficial in reducing cardiovascular risk; however, exercise modality may influence specific peripheral arterial adaptations. Spence et al.'s study design provided a novel approach to evaluate arterial structure and function in RT and ET. Their protocols involved progressively increasing RT and ET workloads, thereby reducing the risk of participant drop-out resulting from injuries or fatigue. The RT and ET protocols were standardized to time, rather than energy expenditure. This may have led to differences in training workload and varying arterial adaptations. More specifically, ET was performed 3 days per week and included low- to moderate-intensity exercises focused on the lower body (i.e. walking, jogging and stretching). Low-volume sprint interval training (SIT; i.e. 30 s intervals interspersed with recovery) may further improve endothelial function and arterial distensibility, providing an attractive alternative to elicit arterial adaptations (Rakobowchuk et al. 2008). In comparison, RT was based on upper- and lower-body Olympic weightlifting exercises performed 3 days per week. Localized brachial artery adaptations occurred following RT, which may be related to consistent hand-grip during RT. Future studies are needed to determine the relative contribution of isometric hand-grip stimuli on conduit arterial adaptations. Investigations of exercise-induced arterial adaptation have focused predominantly on short-term (<12 weeks) training protocols. Notably, short-term exercise can produce both functional and structural changes in the conduit arteries, in part due to enhanced nitric oxide (NO) and endothelial nitric oxide synthase (eNOS) bioactivity (Tinken et al. 2008). Tinken et al. (2008) showed that functional changes in conduit arteries occur rapidly, with significant changes in brachial and popliteal artery flow-mediated dilatation occurring after just 2 weeks of endurance exercise training. Furthermore, it has been previously demonstrated that a 12-week endurance exercise intervention in previously sedentary healthy men resulted in significant increases in femoral artery lumen diameter (Dinenno et al. 2001). Few studies have investigated arterial adaptations with a longitudinal exercise training design to account for individual responses over an extended duration of training stimuli. Although arterial measures were obtained by Spence et al. (2013) prior to and following the 6-month intervention, a 3-month measure of arterial function and structure may have provided more insight into the arterial adaptations to the training stimuli. The inclusion of a 3 month data collection time point in the current study would have enabled comparisons between Spence et al.'s study and prior findings, as these other studies have used shorter-term exercise protocols and also observed significant arterial changes. Potential sex differences may limit the generalizability of the study findings, as Spence et al. (2013) used only male participants to examine arterial adaptation to RT or ET. In a recent review (Orshal & Khalil, 2004), sex differences in arterial tone were reported and attributed to direct arterial effects of sex hormones. Oestrogen and testosterone each bind to specific hormone receptors in the arteries. Oestrogen specifically induces vasodilatory effects via activation of eNOS and up-regulation of NO. Interestingly, total NO production and NO release from the endothelium was shown to be greater in premenopausal women than in men (Orshal & Khalil, 2004). Therefore, females may demonstrate improved adaptation to increased levels of shear stress than males. Sex differences may interact and mediate the relationship between changes in arterial function and structure following exercise training. Study findings (Spence et al. 2013) support the implementation of supervised long-term RT and ET programmes to improve arterial function among healthy participants. Long-term arterial adaptations following RT and ET programmes within clinical cohorts remain unclear. Future research may also include the role of RT and ET on arterial function within cardiovascular disease cohorts, including peripheral vascular disease, Kawasaki disease and Marfan syndrome cohorts. These clinical populations have characteristic deficiencies in arterial structure and function with limited research related to the benefits of exercise training. In fact, RT and ET may result in clinically relevant improvements in arterial structure and function, more so than healthy participants. Furthermore, RT protocols involving Olympic weightlifting may not be practical for a clinical cohort. Future studies should investigate more traditional RT training as it may be more suitable for the clinical population. Although the RT and ET protocols employed in the current study (Spence et al. 2013) may indeed elicit arterial benefits among clinical cohorts, continuous ET and traditional RT protocols may be too time consuming. In contrast, low-volume, high-intensity endurance exercise is an alternative approach proposed to improve arterial function and thus decrease cardiovascular risk (Gibala et al. 2012). In conclusion, this study (Spence et al. 2013) provided new insight into the longer-term effects of RT and ET on arterial structure and function. These novel findings need to be substantiated with future studies in healthy females and clinical cardiovascular cohorts to fully determine the clinical relevance of RT and ET on arterial structure and function.

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