6533b82dfe1ef96bd12911d0

RESEARCH PRODUCT

Myocardial blood flow and adenosine A2Areceptor density in endurance athletes and untrained men

Pauliina VirsuVesa OikonenJuhani KnuutiPirjo NuutilaHeikki KainulainenKaisa LiukkoKari K. KalliokoskiJukka KemppainenUrho M. KujalaKjell NågrenRobert BoushelRobert BoushelS. V. NesterovIlkka HeinonenMatti Luotolahti

subject

medicine.medical_specialtybiologyHuman studiesPhysiologyAthletesbusiness.industryAdenosine A2A receptorBlood flowbiology.organism_classificationAdenosineHyperaemiaEndocrinologyInternal medicinemedicinemedicine.symptombusinessPerfusioncirculatory and respiratory physiologymedicine.drug

description

Previous human studies have shown divergent results concerning the effects of exercise training on myocardial blood flow (MBF) at rest or during adenosine-induced hyperaemia in humans. We studied whether these responses are related to alterations in adenosine A2A receptor (A2AR) density in the left-ventricular (LV) myocardium, size and work output of the athlete's heart, or to fitness level. MBF at baseline and during intravenous adenosine infusion, and A2AR density at baseline were measured using positron emission tomography, and by a novel A2AR tracer in 10 healthy male endurance athletes (ET) and 10 healthy untrained (UT) men. Structural LV parameters were measured with echocardiography. LV mass index was 71% higher in ET than UT (193 ± 18 g m−2versus 114 ± 13 g m−2, respectively). MBF per gram of tissue was significantly lower in the ET than UT at baseline, but this was only partly explained by reduced LV work load since MBF corrected for LV work was higher in ET than UT, as well as total MBF. The MBF during adenosine-induced hyperaemia was reduced in ET compared to UT, and the fitter the athlete was, the lower was adenosine-induced MBF. A2AR density was not different between the groups and was not coupled to resting or adenosine-mediated MBF. The novel findings of the present study show that the adaptations in the heart of highly trained endurance athletes lead to relative myocardial ‘overperfusion’ at rest. On the other hand hyperaemic perfusion is reduced, but is not explained by A2AR density.

https://doi.org/10.1113/jphysiol.2008.158113