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Abstract

  1. Top of page
  2. Abstract
  3. Do athletes possess enlarged conduit and resistance arteries?
  4. Do athletes exhibit wall thickness changes?
  5. Do athletes exhibit enhanced vascular function?
  6. Summary
  7. References
  8. Acknowledgements

Whilst the existence of a specific phenotype characterized as ‘athlete's heart’ is generally acknowledged, the question of whether athletes exhibit characteristic vascular adaptations has not been specifically addressed. To do so in this symposium, studies which have assessed the size, wall thickness and function of elastic, large muscular and smaller resistance arteries in athletes have been reviewed. Notwithstanding the caveats pertaining to cross-sectional comparisons between athletes and ‘matched’ control subjects, these studies reveal increased conduit artery size, including enlargement of epicardial arteries and those supplying skeletal muscle. Evidence that peak limb blood flow responses are enhanced in athletes further suggests that resistance arteries undergo increases in total cross-sectional area. Such increases can be localized to those arteries supplying active muscle leading to speculation, supported by exercise training studies in humans and animal and cellular data, that arterial enlargement is associated with repetitive episodic increases in arterial shear stress which elicit endothelium-mediated remodelling. Such structural remodelling at conduit and resistance artery level may play a role in accommodating the substantial increase in cardiac output apparent in endurance athletes; arterial pressure is not increased at rest or during exercise in athletes (versus control subjects). Arterial wall remodelling also occurs in athletes but, in contrast to the impact of shear stress on remodelling of arterial lumenal dimensions, the impact of endurance athletic status on wall thickness may be a systemic, rather than localized, phenomenon. Finally, the question of whether the arteries of athletes exhibit enhanced function is moot. Somewhat paradoxically, measures of conduit and resistance artery endothelial function may not be enhanced, compared with healthy control subjects. This may relate to the inherent difficulty of improving arterial function which is already normal, or the time course and transient nature of functional change. It may also relate to the impact of compensatory structural remodelling, as arterial lumen size and wall thickness both affect functional responsiveness. In summary, there is clear evidence for an impact of athletic status on arterial structure and function, at least with respect to the impact of endurance training. Arterial adaptation may, to some extent, emulate that evident in the hearts of endurance athletes, and it is tempting to speculate that similar mechanisms may be at play.

‘Athlete's heart’ is now a generally accepted term and, indeed, has been used as a benchmark to characterize athletic status (Maron, 1986). This concept evolved from early observations by percussion and subsequent evidence from radiography, two-dimensional echocardiography and recent magnetic resonance and computed tomography studies (George et al. 1991; Naylor et al. 2008). Although there may be some limits (Naylor et al. 2008; Spence et al. 2011) to the Morganroth schema of athletic adaptation in the heart (Morganroth et al. 1975), it is now generally accepted that chamber volume and mass adapt to prolonged and intense physical effort in a manner related to the loading of the ventricles.

In contrast, the impact of athletic status on arterial characteristics has not been fully characterized, due in part to the historical difficulty of assessing the size, structure and function of different arteries in vivo. In this symposium report, we examine the question of the existence of a characteristic ‘athlete's artery’, by reviewing studies of resistance and conduit vessel adaptation in elite-level athletes. In most cases, such studies have recruited a matched control group, and we frankly acknowledge the limitations of cross-sectional comparisons when addressing the question of the impact of exercise training, as previously described (Naylor et al. 2008). Nonetheless, much can be achieved by observing an athletic benchmark (Chakravarthy & Booth, 2004) and in many cases we provide supporting evidence from longitudinal training studies and those in animals and cellular models.

Do athletes possess enlarged conduit and resistance arteries?

  1. Top of page
  2. Abstract
  3. Do athletes possess enlarged conduit and resistance arteries?
  4. Do athletes exhibit wall thickness changes?
  5. Do athletes exhibit enhanced vascular function?
  6. Summary
  7. References
  8. Acknowledgements

Whilst the impact of aerobic exercise training on capillary growth is well established (Andersen & Henriksson, 1977; Brown, 2003), vascular resistance and blood pressure regulation are primarily the province of upstream arterioles and (small) arteries, many of which lie outside the muscle interstitium (Snell et al. 1987; Segal, 1992; Thijssen et al. 2010). Such arterial vessels can adapt to training functionally or by outward structural remodelling (Thijssen et al. 2010).

Resistance vessel remodelling in athletes

Historical perspectives

In his Physiological Review of 1977, J.-P. Clausen pointed out, on the basis of studies using arterial cannulation and dye-dilution techniques, that maximal cardiac output increases as a result of training, whereas maximal mean arterial pressure does not (Clausen, 1977). He stated that ‘…it seems justified to conclude that training reduces total peripheral resistance at maximal exercise’. This makes the point that any hypotensive impact of exercise training must be predicated on functional or structural arterial adaptation, which accommodates enhanced output reserve (Green et al. 2008). Furthermore, studies that attempted to determine whether training-induced increases in oxygen uptake were associated with increased central (cardiac output) or peripheral (vasodilator capacity) adaptations, using one-legged training models (Saltin, 1969; Klausen et al. 1982), suggested that the capacity for vasodilatation in skeletal muscle after training exceeds that of cardiac output to maintain blood pressure, a finding recently endorsed by Calbet and Saltin (Calbet et al. 2004; Saltin & Calbet, 2006). This literature emphasizes the plasticity of the vasculature in response to exercise training and suggests that arterial adaptation is sine qua non for exercise performance in endurance athletes.

Remodelling of lumen dimension

Changes in the collective cross-sectional area of the resistance vasculature have been studied in athletes by measuring peak vasodilator responses elicited by prolonged ischaemia, or ischaemic exercise (Thijssen et al. 2010). The assumption is that, while at rest and in submaximal exercise conditions there are a number of competitive functional influences on vascular tone that conspire to determine flow, peak stimuli reveal the structural ‘capacity’ of a vascular bed (Conway, 1963; Takeshita & Mark, 1980; Naylor et al. 2005). Athletes typically exhibit enhanced peak vasodilator capacity in such studies (Martin et al. 1987; Snell et al. 1987). In 1986, Sinoway and colleagues reported significantly higher peak reactive hyperaemic forearm blood flow responses in the preferred limbs of elite tennis players, relative to their non-preferred arm and those of non-athletic control subjects (Sinoway et al. 1986). This study established that resistance arterial remodelling specific to the active muscle bed occurs in athletes. A subsequent hand-grip training study indicated that localized resistance vessel remodelling occurs, largely independent of skeletal muscle hypertrophy, sympathetic or circulatory influences (Sinoway et al. 1987). Taken together, these findings, later independently confirmed (Green et al. 1994, 1996; Rowley et al. 2011a), indicated that resistance artery remodelling is apparent in athletes and can occur as a result of localized and intrinsic vascular stimuli.

It must also be acknowledged that studies involving single-legged exercise indicate that peak blood flows can be enhanced with hypoxia or haemodilution, suggesting that excess dilator capacity exists in untrained subjects and that sympathetic restraint may play a role in active muscle blood flow control during exercise (Secher & Richardson, 2009). Nonetheless, much higher peak vasodilatation is apparent in trained subjects than in untrained control subjects (Richardson et al. 1995; Green et al. 1994), and the localized exercise training studies presented above indicate that adaptations in vasodilator capacity as well as arterial remodelling contribute to the athletic phenotype.

Conduit artery remodelling in athletes

Coronary arteries

Autopsy studies were the first to suggest structural conduit artery enlargement, in particular of the coronary arteries, in athletes (Currens & White, 1961) and fit individuals (Rose et al. 1967; Mann et al. 1972). However, these studies may be polluted by the lack of active tone and the potential impact of post-mortem tissue change. An in vivo angiographic study by Haskell et al. (1993) demonstrated that coronary artery dilator capacity (in response to nitroglycerine) was enhanced in runners, whereas no differences in coronary dimensions were evident at rest. This finding emphasizes the importance of eliciting dilator responses to uncover differences between athletes and control subjects, confirmed by others (Kozàkovàet al. 2000; Nguyen et al. 2011). It also suggests that basal arterial tone may be enhanced in athletes, a finding endorsed by the study of Sugawara et al. (2007), who illustrated that leg exercise training enhanced α-adrenoceptor-mediated vasoconstrictor tone and resting plasma noradrenaline concentrations, partly in compensation for enhanced vasodilator capacity. Interestingly, repeat coronary angiographic studies involving exercise training interventions generally confirm that functional coronary adaptations are apparent, but are less consistent with respect to the impact on vasodilator capacity (Windecker et al. 2002) or, by association, arterial remodelling. This may relate to the study time course, with studies involving shorter interventions being less likely to demonstrate structural remodelling (see ‘Athlete paradox: why is arterial function not enhanced?’; Hambrecht et al. 2000, 2003). The studies of Hambrecht and co-workers also suggest that coronary flow reserve (indicative of resistance vessel adaptation) increases in response to short-term training, in the absence of changes in epicardial dilator responses to nitroglycerine or adenosine, suggesting that adaptation of resistance arteries may precede that associated with conduit vessels. Finally, transthoracic echocardiographic studies in which epicardial diameters were imaged (Pelliccia et al. 1990; Hildick-Smith et al. 2000) have also reported similar resting, but enhanced nitroglycerine-induced, coronary vasodilatation in athletes compared with control subjects.

Peripheral conduit arteries

Several studies have used ultrasound techniques to compare large artery size in athletes relative to control subjects. Zeppilli et al. (1995) reported enlarged aortic, carotid and subclavian arteries in track cyclists and long-distance runners, relative to matched sedentary control subjects, which persisted after correction for body surface area. Aortic arch and subclavian artery size were enhanced in wheelchair athletes, whereas abdominal aorta and mesenteric artery values were lower in these subjects. In 2000, Schmidt-Trucksass and co-workers reported that cyclists, middle-distance runners and triathletes had wider femoral, but not carotid, arteries than control subjects and paraplegics (Schmidt-Trucksass et al. 2000). This was followed by a similar study in which larger femoral arteries were observed in cyclists than in healthy control subjects, paraplegic subjects and below-knee amputees (Huonker et al. 2003). Paraplegic subjects exhibited larger subclavian diameters than control subjects. There were no differences between any of the groups in this study in the size of the aorta, suggesting that muscular conduit arteries are subject to changes in diameter more than larger elastic vessels.

In another recent study, brachial artery diameters were significantly larger in elite canoe paddlers and wheelchair athletes compared with control subjects, and superficial femoral artery diameters were significantly larger in runners/cyclists than in control subjects and paraplegic subjects (Rowley et al. 2011b). The plasticity of arteries in elite athletes was further suggested in a study of elite rowers, in whom significantly enlarged brachial arteries exhibited further expansion following the resumption of regular training (Naylor et al. 2006). Finally, the preferred limb of tennis players exhibited larger subclavian diameter than the contralateral limb (Huonker et al. 2003), a finding reinforced by the observation of larger racquet arm brachial artery diameters in elite squash players (Rowley et al. 2011a).

Remodelling of arterial size: mechanisms

Strong evidence supports the role of repetitive shear stress and the endothelium in chronic changes in arterial size. Arterial ligation in rabbits, which decreases flow, also decreases arterial size, and this effect is endothelium dependent (Langille & O’Donnell, 1986). Manipulation of flow and shear stress leads to similar findings (Kamiya & Togawa, 1980; Tuttle et al. 2001), indicating that wall shear is homeostatically regulated in a nitric oxide-dependent manner (Tronc et al. 1996). In recent studies in humans, unilateral manipulation of blood flow and shear stress using partial cuff occlusion during bilateral hand-grip exercise training bouts resulted in changes in hyperaemic flows and conduit artery dilatation that were shear stress dependent (Tinken et al. 2010). Similar findings were also apparent after exercise-independent increases in flow induced by repetitive forearm heating (Green et al. 2010a; Naylor et al. 2011). These studies implicate changes in shear as a principal physiological stimulus to adaptation and vascular remodelling in response to exercise training in healthy humans.

Summary: remodelling of arterial size in athletes

Collectively, evidence from resistance and conduit artery studies strongly supports the notion that athletes possess larger arteries than control subjects. Whilst some evidence suggests that diameter may not be obviously enlarged in all circumstances at rest, this may be due to compensatory increases in vasoconstrictor tone to maintain blood pressure (Sugawara et al. 2007). Responses to peak vasodilator stimuli consistently reveal enhanced vasodilator reserve in athletes, strongly suggesting that athletes possess structurally enlarged conduit and resistance vessels. It is likely that this vascular enlargement is related to repeated increases in shear stress associated with chronic exercise, but other haemodynamic and humoral stimuli may be involved and have not, to date, been thoroughly investigated in humans. Whilst a consensus exists that peripheral conduit and coronary arteries exhibit arterial remodelling, evidence for enlargement of carotid arteries and the aorta in athletes is less consistent. Caveats regarding arterial remodelling include the lack of data available in weight- or power-trained individuals; most data are derived from endurance sports.

Do athletes exhibit wall thickness changes?

  1. Top of page
  2. Abstract
  3. Do athletes possess enlarged conduit and resistance arteries?
  4. Do athletes exhibit wall thickness changes?
  5. Do athletes exhibit enhanced vascular function?
  6. Summary
  7. References
  8. Acknowledgements

Using high-resolution ultrasound techniques it is possible to image the wall of large and muscular conduit arteries in humans and recent automated edge-detection approaches have improved the reliability and validity of this approach (Woodman et al. 2001; Potter et al. 2007, 2008). Wall remodelling may also have implications for atherosclerotic risk, because wall thickness measures in carotid and peripheral arteries predict cardiovascular events (see Thijssen et al. 2012). Changes in arterial wall thickness also impact upon peak vasodilator capacity and functional responses to vasodilator stimuli (Thijssen et al. 2011b).

Information regarding the wall thickness characteristics of athletes is scarce and somewhat conflicting. Dinenno et al. (2001) reported lower femoral artery wall thickness in endurance-trained middle-aged men versus control subjects, a finding supported by Galetta et al. (2006) in male runners (∼66 years old). In contrast, Abergel et al. (1998) reported increased wall thickness in the carotid artery of young elite cyclists, and Schmidt-Trucksass et al. (2003) observed increased femoral artery wall thickness in young male cyclists, triathletes and weight lifters, relative to control subjects. In a separate study, however, the same authors reported no difference between femoral or carotid artery wall thickness in endurance athletes and control subjects (Schmidt-Trucksass et al. 2000).

We recently attempted to clarify this literature by assessing carotid, brachial and superficial femoral artery diameter and wall thickness in elite athletes engaged in predominantly lower limb (runners/cyclists) or upper limb exercise (canoe paddlers) and matched able-bodied, recreationally active control subjects. We also studied wheelchair control subjects and athletes. Decreased wall thickness was observed in all arteries of able-bodied athletes compared with control subjects, including wheelchair athletes compared with wheelchair control subjects (Rowley et al. 2011b). A further study of elite squash players also confirmed decreased brachial artery wall thickness, which, in contrast to the effects on lumen diameter reported above, was apparent in both limbs (Rowley et al. 2011a). This finding may suggest that the mechanisms responsible for localized adaptations in arterial diameter may differ from those associated with changes in wall thickness in athletes, which appears to be a systemic phenomenon. In support of this notion, our recent experiments implicate shear stress as a mechanism in the response of arterial function and diameter to exercise training (Tinken et al. 2010; Naylor et al. 2011), whereas manipulation of shear stress during exercise training had no impact of arterial wall thickness (Thijssen et al. 2011a).

Cross-sectional studies of athletes which suggest a decrease in wall thickness are, on the whole, supported by data which indicate that physical activity and fitness levels are inversely related to carotid artery wall thickness (see reviews: Green et al. 2011; Thijssen et al. 2012) in humans. Finally, longitudinal training studies suggest that, whilst the effects of exercise training on atherosclerosis of the carotid artery may require intense exercise or interventions performed over prolonged time periods, relatively short-term studies of peripheral arterial wall thickness indicate that an aerobic exercise training programme decreases femoral (Dinenno et al. 2001), popliteal and brachial intima–media thickness (Green et al. 2010b).

Remodelling of arterial wall thickness: mechanisms

Our recent study in elite squash players indicated that, whilst brachial artery diameter was unilaterally affected, arterial wall thickness was similar between the limbs (Rowley et al. 2011a). These data were confirmed in other athletic groups, who performed predominantly upper or lower limb events, but had generalized decreases in conduit artery wall thickness (Rowley et al. 2011b). These findings suggest that, whilst the arterial lumen dimension can be modified by local mechanisms (such as shear stress), wall thickness may be affected by systemic factors. One such factor that is known to affect the artery wall is transmural pressure, which is modulated during exercise as a result of generalized changes in blood pressure (Laughlin et al. 2008; Newcomer et al. 2011). Chronic and sustained increases in blood pressure have pro-atherogenic effects on endothelial cells (Laughlin et al. 2008), including lower bioavailability of nitric oxide and higher levels of VCAM-1, ICAM-1, endothelin-1 and reactive oxygen species. In addition, hypertension is associated with arterial wall thickening in large and small arteries (Folkow et al. 1958; Dinenno et al. 2000). However, exercise generates intermittent increases in blood pressure. Whilst speculative, it may be that the nature of the pressure stimulus, chronic versus intermittent, may modify the adaptive arterial response. This will be an interesting area for further research.

Summary: remodelling of carotid and peripheral conduit artery wall thickness

Taken together, studies performed in athletes and healthy subjects who were exercise trained indicate that arterial wall thickness decreases as a result of prolonged training interventions, particularly in peripheral arteries supplying active skeletal muscle (Thijssen et al. 2012). As these studies were undertaken in athletes and healthy younger subjects, the decrease in wall thickness should not necessarily be taken to reflect atherosclerotic change, but rather a physiological impact on wall remodelling in healthy arteries, the long-term health implications of which are currently unknown.

Do athletes exhibit enhanced vascular function?

  1. Top of page
  2. Abstract
  3. Do athletes possess enlarged conduit and resistance arteries?
  4. Do athletes exhibit wall thickness changes?
  5. Do athletes exhibit enhanced vascular function?
  6. Summary
  7. References
  8. Acknowledgements

Although several short-term exercise training studies, usually in patients with coronary disease, have reported enhanced vascular (endothelial) function (Hambrecht et al. 2000, 2003; Windecker et al. 2002), to our knowledge there have been no reports of coronary endothelial function in athletic populations. Studies of athletes have predominantly been undertaken in peripheral arterial beds. Resistance vessel function has been assayed via infusion of vasoactive agents into peripheral arteries and measurement of vasodilator responses, whilst conduit artery function has often been studied by measuring the responses of larger arteries to increases in blood flow (shear stress) or pharmacological activation.

Peripheral resistance arteries

The first study of athletes and resistance vessel function used the between-limb model in elite tennis players (Green et al. 1996). This study confirmed previous findings (see section ‘Remodelling of lumen dimension’) that peak dilator responses were enhanced in the racquet arm. However, endothelium-dependent and -independent vasodilator responses to acetylcholine and sodium nitroprusside were not enhanced in the preferred limb, and the impact of inhibition of nitric oxide on basal forearm flows was also unaltered. Unilateral forearm hand-grip training was, likewise, not associated with improvement in resistance vessel responses to intrabrachial vasoactive drug infusion (Green et al. 1994). In a study using similar methodology, cyclists and triathletes demonstrated enhanced forearm vascular resistance in responses to one dose of acetylcholine, but not to NG-monomethyl-l-arginine or sodium nitroprusside (Kingwell et al. 1996), whilst cycle training did not modify responses to acetylcholine (Kingwell et al. 1997). Likwise, forearm responses to acetylcholine and sodium nitroprusside were similar between young sedentary and endurance-trained runners (DeSouza et al. 2000). Interestingly, older athletes exhibited enhanced responses to acetylcholine compared with older sedentary subjects, and exercise training in older sedentary subjects improved acetylcholine-mediated vasodilatation, suggesting that athletic status may retard the effects of ageing on the vasculature (DeVan & Seals, 2012), findings which are generally supported by those of Galetta et al. (2006). These studies suggest, somewhat paradoxically, that peripheral resistance vessel function may not be enhanced in athletes, a conclusion broadly in keeping with findings from exercise training studies (Thijssen et al. 2010).

Peripheral conduit arteries

In studies of elite rowers, paddlers, runners and cyclists, we have not observed enhanced flow-mediated conduit artery vasodilatation in the limbs (Rowley et al. 2011b; Fig. 1). Likewise, Petersen et al. (2006) in a cine-magnetic resonance imaging study, observed that endothelial function in the brachial artery was not enhanced in rowers. In contrast, Walther et al. (2008) reported higher flow-mediated dilator responses in cyclists and swimmers, compared with control subjects. However, smooth muscle sensitivity to nitric oxide was also increased, suggesting that endothelial function may not, in fact, be enhanced in these athletes (Walther et al. 2008). Overall, these studies suggest that vascular function may not be enhanced in athletes, a finding which is consistent with the lack of consensus regarding the impact of exercise training interventions in healthy volunteers (Thijssen et al. 2010; Green et al. 2011).

image

Figure 1. Representation of data derived from distinct groups of elite athletes Conduit artery function, in this case femoral artery flow-mediated dilatation (FMD%) is, somewhat paradoxically, not enhanced in elite athletes. This may be due to the inherent problem of ‘supra-normalizing’ function of a priori healthy arteries, or a consequence of structural changes in the artery which negate the ‘need’ for functional upregulation. For example, arteries of athletes are larger in lumen dimension (diameter) and also possess distinctly different wall thickness-to-lumen ratios than arteries of healthy matched control subjects. Both wall thickness-to-lumen ratio and size of the artery impact on arterial function. The arteries of athletes may, therefore, be normal in function, but at different structural remodelling ‘set points’ from the arteries of healthy non-athletic control subjects.

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Athlete paradox: why is arterial function not enhanced?

Whilst it is tempting to speculate that vascular function should be enhanced in arteries of athletes, evidence derived from the resistance and conduit artery studies, described above, using a variety of technical approaches, generally suggests that athletes possess functionally ‘normal’ arteries. There are several possible reasons for this apparent ‘athlete paradox’.

Time course of functional versus structural adaptations

Based on their extensive animal studies, Laughlin and colleagues suggested that functional arterial adaptations may precede those in arterial size and structure (Laughlin, 1995). Conceptually, this suggests that rapid and transient changes occur in arterial function in response to exercise training, which may then be superseded by structural remodelling, which normalizes shear stress and negates the need for ongoing functional enhancement. Whilst this notion remains hypothetical, evidence for differences in the time course of changes in arterial function and structure exists, including recent human data showing initial improvement, and subsequent return to baseline, of flow-mediated dilatation in humans in response to exercise training (Tinken et al. 2008, 2010). In one of these studies, changes in arterial function were not observed in the absence of exercise-related manipulation of shear stress (Tinken et al. 2010). These data suggest that the lack of apparent increase in vascular function in athletes may be related to arterial remodelling. In other words, it is possible that functional changes have resolved in athletes who have already undergone a process of structural arterial remodelling.

Impact of structural adaptations on functional responses

Conduit artery dilator responses are indirectly related to arterial diameter (Celermajer et al. 1992; Silber et al. 2005). Although this relationship has been attributed, in part, to the relationship between smaller arteries and shear stress (Silber et al. 2005), we recently demonstrated that lumen dimension correlates highly with flow-mediated dilatation responses, independent of shear (Thijssen et al. 2008, 2009) and that arterial size and shear-independent nitroglycerine responses are also inversely related. Whatever the mechanism responsible for the relationship between arterial size and functional responses, athletes have characteristically enlarged arteries and this may have implications for the interpretation of vasodilator responses. A further consideration is the impact of wall thickness changes. Folkow and co-workers established that arteries with enlarged wall thickness, relative to lumen size, exhibit exaggerated functional responses to a range of stimuli (Folkow et al. 1958). We recently confirmed this phenomenon across conduit arteries of different size in humans (Thijssen et al. 2011b). It is conceivable, therefore, that changes in the wall thickness of arteries in athletes may impact on functional vasodilator responses in athletes.

Summary

Functional responses in arteries are complex and influenced by the myriad humoral, paracrine and neural mechanisms that impact on arterial tone. All of these can be, and probably are, affected by athletic status (Green et al. 2011). For example, changes in autonomic balance may affect vasomotor tone in athletes, although conflicting evidence is apparent in reduced sympathoexitation in the medulla (Mueller, 2010) versus enhanced basal vasoconstrictor tone (Sugawara et al. 2007) and muscle sympathetic nerve activity (Alvarez et al. 2005) as a result of training. In any event, the evidence presented above suggests that arterial function, and in particular but not exclusively endothelial function, is not necessarily enhanced in athletes. This apparent ‘athlete paradox’ may be at least partly explained on the basis of structural adaptations in the arteries that impact upon function.

Summary

  1. Top of page
  2. Abstract
  3. Do athletes possess enlarged conduit and resistance arteries?
  4. Do athletes exhibit wall thickness changes?
  5. Do athletes exhibit enhanced vascular function?
  6. Summary
  7. References
  8. Acknowledgements

Despite the many lessons that can be derived from the study of athletes as a model of physiological adaptation, far less attention has been devoted to changes that occur in their arteries than in their hearts. At this time, sufficient evidence exists to conclude that endurance athletes possess enlarged arteries, which may also exhibit decreased wall thickness (Fig. 2). These structural changes may impact on arterial function, because there is limited evidence for enhanced arterial responsiveness to pharmacological or physiological stimulation in athletes. Haemodynamic signals may contribute to arterial remodelling, with shear stress implicated in localized effects of repeated exercise bouts on conduit and resistance artery enlargement. Changes in wall thickness may be systemic rather than localized in nature, and the mechanisms responsible are not well defined. The impact of distinct forms of exercise on arteries, exemplified in comparisons between strength/power and endurance athletes, have not been specifically investigated but may provide important insights. Just as there is ‘athlete's heart’, we provide evidence for the existence of ‘athlete's artery’ in humans.

image

Figure 2. Representation of an ‘athlete's artery’, which comprises larger lumen dimension and decreased wall thickness, relative to an artery from a healthy non-athletic control subject Caveats include the predominant derivation of data from endurance athletes; not a great deal is known about the systematic effects of resistance or power athleticism on arterial size or function. In addition, it is not always apparent that athletes’ arteries are larger based on resting lumen dimensions; this is due to the possible compensatory increase in basal constrictor tone in larger arteries.

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References

  1. Top of page
  2. Abstract
  3. Do athletes possess enlarged conduit and resistance arteries?
  4. Do athletes exhibit wall thickness changes?
  5. Do athletes exhibit enhanced vascular function?
  6. Summary
  7. References
  8. Acknowledgements
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