Background: A study was conducted to determine if prolonged exercise could provoke sympathetic neuronal alteration in an athlete's heart through assessment of myocardial distribution of 123I-metaiodobenzylguanidine (MIBG) in nine ultramarathon runners at baseline and after a 4-hour race.
Methods and results: After injection of 370 MBq of 123I-MIBG, the athletes ran for 4 hours, covering 45 +/- 8 km. Planar and single-photon emission computed tomography (SPECT) images of the thorax were acquired at the end of the race. Two weeks later, studies at baseline were performed. A heart:mediastinum ratio (HMR) was calculated to quantify MIBG uptake. Basal MIBG studies showed normal myocardial tracer uptake, on both planar and SPECT images, and the HMR was 1.84 +/- 0.16. After the 4-hour race, MIBG studies showed decreased myocardial uptake in all athletes, and the HMR was 1.70 +/- 0.18 (p < 0.005). A positive correlation between the percentage of decrease of HMR after the race and the distance covered was observed (r = .910, p < 0.001).
Conclusions: Myocardial MIBG activity is decreased by prolonged exercise in long-distance runners. The degree of reduction of myocardial MIBG activity is related to the distance covered. Prolonged exercise, as sustained sympathetic stimulus, may alter myocardial distribution of MIBG.