Comparison of Brachial Artery Vasoreactivity in Elite Power Athletes and Age-Matched Controls

Abstract

Elite endurance athletes typically have larger arteries contributing to greater skeletal muscle blood flow, oxygen and nutrient delivery and improved physical performance. Few studies have examined structural and functional properties of arteries in power athletes.PurposeTo compare the size and vasoreactivity of the brachial artery of elite power athletes to age-matched controls. It was hypothesized brachial artery diameters of athletes would be larger, have less vasodilation in response to cuff occlusion, but more constriction after a cold pressor test than age-matched controls.MethodsEight elite power athletes (age = 23±2 years) and ten controls (age = 22±1 yrs) were studied. High-resolution ultrasonography was used to assess brachial artery diameters at rest and following 5 minutes of forearm occlusion (Brachial Artery Flow Mediated Dilation = BAFMD) and a cold pressor test (CPT). Basic fitness measures included a handgrip test and 3-minute step test.ResultsBrachial arteries of athletes were larger (Athletes 5.39±1.51 vs. Controls: 3.73±0.71 mm, p<0.05), had greater vasodilatory (BAFMD%: Athletes: 8.21±1.78 vs. Controls: 5.69±1.56%) and constrictor (CPT %: Athletes: -2.95±1.07 vs. Controls: −1.20±0.48%) responses, compared to controls. Vascular operating range (VOR = Peak dilation+Peak Constriction) was also greater in athletes (VOR: Athletes: 0.55±0.15 vs. Controls: 0.25±0.18 mm, p<0.05). Athletes had superior handgrip strength (Athletes: 55.92±17.06 vs. Controls: 36.77±17.06 kg, p<0.05) but similar heart rate responses at peak (Athletes: 123±16 vs. Controls: 130±25 bpm, p>0.05) and 1 minute recovery (Athletes: 88±21 vs. Controls: 98±26 bpm, p>0.05) following the step test.ConclusionElite power athletes have larger brachial arteries, and greater vasoreactivity (greater vasodilatory and constrictor responses) than age-matched controls, contributing to a significantly greater VOR. These data extend the existence of an ‘athlete’s artery’ as previously shown for elite endurance athletes to elite power athletes, and presents a hypothetical explanation for the functional significance of the ‘power athlete’s artery’.

Flow-Mediated Dilation in Athletes

“…Twenty-two studies comprised male subjects, three studies comprised female subjects (23,32,44), and four studies comprised female and male subjects (37,56,60 (20,36,37,59). Arterial endothelial function.…”

“…As for the duration of blood flow occlusion, 23 studies used a 5-min period, whereas six studies reported periods between 4 and 5 min (1,23,27,44,50,56). Peak brachial diameter after cuff deflation (i.e., during hyperemia) was determined via continuous ultrasound scan in 20 studies (1,3,(12)(13)(14)20,27,36,40,49,50,59,60) and single time point(s) ultrasound scan in seven studies (23,29,32,(44)(45)(46)56), and one study did not report such information (37). Time to peak brachial diameter after cuff deflation was reported in one study (3).…”

“…It has been proposed that long-term training may result in the enlargement of conduit arteries, which in turn could reduce (normalize) the effect of shear stress on the endothelium and thus diminish the stimulus for FMD enhancement in athletes (20,30). Alternative explanations for the discrepant FMD results in athletes may lie in the inherent limitations of cross-sectional comparisons and the small sample sizes of previous individual studies (1,3,(12)(13)(14)20,23,27,29,32,36,37,40,(44)(45)(46)49,50,56,59,60). In addition, longitudinal studies have been predominantly based on relatively short-to medium-term training interventions, hence plausibly assessing incomplete vascular adaptations (53).…”

Arterial dilator function in athletes: present and future perspectives

“…The fact that peripheral vascular conductance during submaximal exercise may not be increased in ATH (Fleg et al, 1994 ; Carrick-Ranson et al, 2014 ) suggests that enhanced arterial dilator function interacts with increased arterial constrictor function and/or sympathetic constrictor drive. In this respect, increased both arterial constrictor function and sympathetic (re)activity have been observed in ATH (Furlan et al, 1993 ; Welsch et al, 2013 ). Seemingly, the antagonism between dilator and constrictor forces may be futile unless associated with a more efficient perfusion in that part of the cardiac output is diverted from tissue with low oxygen demand toward active skeletal muscle.…”

“…The controversy arose as to whether vasodilator function was enhanced in ATH compared with untrained healthy peers (Green et al, 2013 ). This contention was justified by the conflicting report of decreased (Green et al, 2011 ; Phillips et al, 2011 ) and normal (Franzoni et al, 2005b ; Moe et al, 2005 ; Naylor et al, 2006 ; Ballard et al, 2008 ; Rognmo et al, 2008 ; Nualnim et al, 2011 ; Phillips et al, 2011 ; Rowley et al, 2012 ; Agrotou et al, 2013 ; Green et al, 2013 ) but also increased (Jensen-Urstad et al, 1999 ; Rywik et al, 1999 ; Rinder et al, 2000 ; Franzoni et al, 2005b ; Kasikcioglu et al, 2005 ; Rickenlund et al, 2005 ; Tanriverdi et al, 2005 ; Galetta et al, 2006 ; Hagmar et al, 2006 ; Walther et al, 2008 ; Florescu et al, 2010 ; Nualnim et al, 2011 ; Welsch et al, 2013 ) flow-mediated dilation (FMD), a common index of conduit artery dilator function, in ATH vs. age-matched controls. Likewise, the evidence on resistance artery dilator function was apparently heterogeneous (Green et al, 2012 ).…”