Previous studies demonstrated an enhanced ₂-adrenoceptor (₂-AR) responsiveness in animals susceptible to ventricular fibrillation (VF) that was eliminated by exercise training. The present study investigated the effects of endurance exercise training on ₁-AR and ₂- AR expression in dogs susceptible to VF. Myocardial ischemia was induced by a 2 min occlusion of the left circumflex artery during the last min of exercise in dogs with healed infarctions: 20 had VF (susceptible, S) and 13 did not (resistant, R). These dogs were randomly assigned to either 10-wk exercise training (treadmill running, S n = 9, R n = 8) or an equivalent sedentary period (S n = 11, R n = 5). Left ventricular tissue -AR protein and mRNA were quantified by Western Blot analysis and RT-PCR, respectively. As ₂-ARs are located in caveolae, caveolin-3 was also quantified. ₁-AR gene expression decreased (~ 5 fold), ₂-AR gene expression was not changed, and the ratio of ₂-AR to ₁-AR gene expression was significantly increased in susceptible compared to resistant dogs. ₁-AR protein decreased (~ 50%) and ₂-AR protein increased (400%) in non-caveolar fractions of the cell membrane in susceptible dogs. Exercise training returned ₁-AR gene expression to levels seen in resistant animals, but did not alter ₂-AR protein levels in susceptible dogs. These data suggest that ₁-AR gene expression was decreased in susceptible animals compared to the resistant dogs and, further, that exercise training improves ₁-AR gene expression, thereby restoring a more normal -AR balance.