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      Myocardial blood flow and adenosine A2A receptor density in endurance athletes and untrained men.

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          Abstract

          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 A(2A)R 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(-2) versus 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.

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          Author and article information

          Journal
          J. Physiol. (Lond.)
          The Journal of physiology
          Wiley
          1469-7793
          0022-3751
          Nov 01 2008
          : 586
          : 21
          Affiliations
          [1 ] Turku PET Centre, Departments of Clinical Physiology and Nuclear Medicine, University of Turku, Turku, Finland. ilkka.heinonen@tyks.fi
          Article
          jphysiol.2008.158113
          10.1113/jphysiol.2008.158113
          2652164
          18772204
          71c03a8e-2217-4ee2-9c2c-b12aa3fcbfa2
          History

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