Arterial Diameter and WT
Brachial artery diameter was significantly greater in UL athletes and wheelchair subjects (both controls and athletes) compared with able-bodied inactive controls (Fig. 1A). WT measures were, however, significantly smaller in all three athletic groups (UL, LL and wheelchair athletes) compared with the control groups (Fig. 1B). Brachial wall-to-lumen ratio (W/L) data were significantly smaller in all groups compared with able-bodied controls (Fig. 1C). A positive correlation between FFM and brachial diameter was significant across all groups (r = 0.50, P < 0.001), but no relationship was apparent between FFM and brachial artery WT (r = −0.08, P = 0.6).
LL athletes had the largest SF diameters, which were significant larger than those observed in able-bodied controls (Fig. 2A). Wheelchair users (both controls and athletes) had significantly smaller SF diameters than able-bodied controls and athletes (Fig. 2A). However, WT of able-bodied athletes (UL and LL) and wheelchair athletes was significantly lower than that in the control groups (Fig. 2B). W/L in the able-bodied athletes was significantly smaller than in the able-bodied control. The wheelchair control subjects possessed significantly higher W/L ratios than able-bodied controls and athletes (Fig. 2C). Lower limb FFM correlated with SF artery diameter across all groups (r = 0.77, P < 0.001), and a modest inverse correlation also existed between leg FFM and SF artery WT (r = −0.4, P < 0.05).
Resting diameter was comparable between all five groups (Table 2). However, WT and W/L in the athlete groups (UL, LL, and wheelchair athletes) were significantly lower compared with both able-bodied and wheelchair controls (Table 2).
The purpose of this study was to better understand local versus systemic effects of chronic exercise and inactivity on arterial diameter and WT by studying upper and lower limb–dominant athletic populations and subjects with spinal cord injury. We observed larger brachial artery diameters in canoeists and wheelchair subjects, whereas lower limb dominant athletes (i.e., runners and cyclists) possessed larger femoral arteries. Markedly reduced femoral diameters were evident in both wheelchair groups. These differences between groups are consistent with local effects of physical (in)activity on remodeling of conduit arterial lumen. We also observed lower WT in the carotid, brachial, and SF arteries in all athletic groups compared with their less active peers. These data suggest that, in contrast to localized remodeling of diameter, physical (in)activity is associated with systemic effects on conduit artery WT in humans in vivo.
We studied distinct groups to provide insight into the effect of chronic exposure to physical (in)activity of the upper or lower limbs. Consistent with previous cross-sectional (10,18,25) and longitudinal (2,18) observations, we found that chronic exercise training was associated with localized effect on arterial remodeling. Although we have adopted a cross-sectional design that may involve some selection bias, our data concur with findings of significantly larger vessels in the dominant limbs of elite racquet players (6,23,27).
A potential explanation for the localized remodeling of arterial diameter relates to the shear stress stimulus acting on the endothelium (30). In agreement with observations in animal studies (11,12,31), we recently found that adaptations in brachial artery function and size after handgrip exercise training in humans were prevented by decreasing exercise-induced shear stress (30). Other studies have provided mechanistic evidence relating shear stress to changes in vascular function and structure (9,31). Whereas this evidence implicates shear stress in changes in arterial size, there are numerous factors that influence arterial tone in humans and we cannot exclude the possibility that other stimuli, such as local changes in hemodynamic, metabolic, and vasoactive substances, may partly contribute, although limited evidence currently exists regarding such mechanisms and effects on arterial remodeling in humans. It should also be noted that arterial diameter correlated with FFM in both the upper and lower limbs in our subjects, suggesting that conduit artery diameter and lean tissue mass are related, perhaps by virtue of the increase in shear stress after metabolic vasodilation of a larger mass of muscle. At the very least, our data suggest the existence of localized changes in arterial diameter in response to physical (in)activity.
There are relatively few studies of the direct effect of exercise on artery WT in healthy humans (2,8,16,28,29). Most of these studies suggest an effect of exercise training on WT in vessels supplying the active muscle beds, whereas studies examining the effect of exercise on carotid artery are conflicting (22,28), possibly because of the duration of training and a priori WT. Few studies have directly examined local and systemic effects of exercise training on WT. Recently, we reported reduced brachial arterial WT in both the dominant and the nondominant forearms of elite squash players (24), in contrast to the differences apparent between the limbs in arterial diameter. These findings can be interpreted as evidence for a generalized or systemic effect of exercise training of wall remodeling (19). This is endorsed by the observation in the present study that lower WT was present in the carotid, brachial, and SF arteries of both upper and lower limb–trained athletes compared with their less active able-bodied controls. Wheelchair athletes also demonstrated lower carotid and brachial arterial WT compared with able-bodied and wheelchair controls. These novel observations further support the view that systemic effects of physical (in)activity may drive changes in conduit arterial WT.
The mechanisms responsible for changes in arterial WT in humans are not well described in humans. Increased shear stress is associated with arterial remodeling, at least of lumen diameter (11,31), and it may have contributed to the observations in the present study. However, it is notable that arteries in both physiologically active and less active vessel beds in the athletic groups, which would logically be chronically exposed to different shear stress forces, both exhibited lower WT. In a recent study, we also reported similar reductions in brachial artery WT after 8 wk of bilateral handgrip training, despite unilateral manipulation of the brachial artery shear stress (29). It is likely that systemic effects of exercise contribute to exercise-related changes in WT and systemic effects of shear stress cannot be entirely excluded as a mechanism. Alternate mechanistic explanations for changes in WT in response to exercise training include generation of circulating biochemical species, hormonal activation, or inflammation, although limited evidence currently exists relating these factors to arterial remodeling in humans. Brief, cyclic exposure to pressure/circumferential strain, such as that associated with exercise bouts, may contribute to antiatherogenic adaptation in the artery wall (13,14,32). Finally, the significant inverse correlation between leg FFM and femoral artery thickness is notable in our study and, to our knowledge, a novel observation. The relationship between skeletal muscle mass and artery WT deserves further investigation to determine which change occurs first and whether there is causation.
Our observation of systemic effects of exercise and inactivity may have potential clinical implications. Measurement of conduit arterial WT is a popular and frequently adopted surrogate measure of atherosclerosis, and previous studies have demonstrated the strong predictive capacity of the carotid arterial WT for future cardiovascular events (15,26). Our findings suggest that exercise, even in subjects with a complete (motor) lesion of the lower limbs, may produce beneficial effects on arterial WT above and below the lesion. This suggests that exercise training may have beneficial effects on the arterial wall, even in those regions that are not physically active. Such changes in the arterial wall may contribute to the cardioprotective effects of exercise training. Increases in artery diameter may also possess potential clinical relevance, and we have previously proposed that such changes in artery diameter and function may inform the design of exercise training interventions (3,5).
There are several limitations of the present study. Future studies should include longitudinal training designs to better study the role of localized and systemic mechanisms on arterial remodeling in athletic populations. To this end, we recently reported WT changes in response to localized (29), and whole body exercise (8), and other key studies have assessed the effect of training per se (2,28). Because advanced age is associated with an increase in WT (1), a potential limitation of this article is the age difference between wheelchair controls and athletes for the comparison of arterial WT between these groups. However, carotid, brachial, and femoral arterial WT in the wheelchair controls were comparable to (young) able-bodied controls, whereas WT in the wheelchair athletes was consistently lower than the able-bodied controls. Therefore, the age difference between wheelchair controls and athletes unlikely explain the difference in WT between groups.
In conclusion, the finding of the present study suggests that exercise and inactivity lead to opposite effects on remodeling of the arterial lumen, likely driven by local mechanisms. In contrast, remodeling of arterial WT is evident in the carotid, brachial, and SF arteries, suggesting the presence of a systemic effect of exercise on the conduit WT. Future studies should further elucidate the mechanisms and stimuli that underlie these novel observations.
Ms. Rowley is funded by Cardiac Risk in the Young UK. Professor Green is supported by a grant from the Australian Research Council and the National Heart Foundation of Australia. Dr. Thijssen is financially supported by the Netherlands Heart Foundation (E. Dekker stipend 2009T064).
The authors thank the British Canoe Union coaches and athletes, especially English Institute of Sport physiotherapist Julie Pearce and physiologist Dr. Jamie Pringle.
The authors gratefully thank the GBWBA for their assistance with this study.
None of the authors have conflict to disclosures.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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Keywords:©2012The American College of Sports Medicine
EXERCISE; ARTERIAL DIAMETER; INTIMA MEDIA THICKNESS; ATHLETES