INTRODUCTION: Extreme forms of athlete's heart structurally resemble hypertrofic cardiomyopathy, which is a life-threatening disease associated with reduced myocardial blood flow (MBF) reserve (Camici & Crea 2007). However, it is not known how athlete's heart close to upper extremities (Maron & Pellicia 2006) showing any signs of maladaptive cardiac hypertrophy affects MBF and its reserve, and this was investigated in the present study. Additionally, it was sought to determine whether adenosine A2A receptors, which are regarded as important regulators of MBF, are affected in pronounced athlete's heart. METHODS: Ten healthy highly trained cross-country skiers (CCS) (24.6 ± 3.6 years, BMI 23.4 ± 0.9 kg/m2) and ten untrained men (UT) (25.7 ± 4.2 and 24.4 ± 2.9 kg/m2) were studied with positron emission tomography (PET). MBF was measured at rest and for MBF reserve determination also during intravenous adenosine Infusion (140 microg/kg/min). Finally, imaging of myocardial A2A receptors was performed with PET and 11C-TMSX tracer and structural left ventricular (LV) dimensions were measured with echocardiography. RESULTS: On average, CCS had 41% larger LV mass compared to UT (385 ± 43 g and 225 ± 34 g, respectively, p < 0.001). CCS had lower measured relative MBF at rest and during adenosine stress test. However, despite similar total and significantly lower relative LV work in CCS compared to UT, CCS had significantly higher total MBF in the whole LV. Furthermore, after MBF had been normalised with LV work (rest) and mean arterial pressure (adenosine), CCS showed significantly higher relative basal MBF and impaired MBF reserve compared to UT, although measured MBF values showed similar MBF reserve between the groups. Total adenosine A2A receptor volume was significantly higher in CCS, but A2A receptor density did not differ between the groups, and it did not correlate significantly with MBF either at rest, or during adenosine Infusion. However, it was found that the more fit the athlete was, the lower MBF he had during adenosine Infusion (r = - 0.64, p < 0.05). DISCUSSION AND CONCLUSIONS: The novel finding of the present study suggests that remarkable LV hypertrophy close to upper extremities observed in highly trained endurance athletes leads to myocardial 'overperfusion' at rest. This may be due to inefficiency caused by significantly hypertrophied LV in terms of blood flow, as observed in maladaptive cardiac hypertrophy, or more likely alterations in myocardial oxygen extraction. Moreover, endurance athletes seem not to have supranormal MBF reserve. In fact, if lower relative LV work in CCS is taken into account, CCS with pronounced athlete's heart actually show even impaired MBF capacity. This reduced MBF reserve may, however, be due to differences in adenosine kinetics in blood between the groups if MBF reserve is determined by adenosine stress test. Furthermore, adenosine receptor A2A density seems to increase along the increases in LV mass and contrary to animal studies, it appears not to be the sole adenosine receptor via adenosine-induced vasodilatation is mediated.
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