SPRINT TRAINING ATTENUATES MYOCYTE HYPERTROPHY AND IMPROVES CA2+ HOMEOSTASIS IN POSTINFARCTION MYOCYTES

Myocytes isolated from rat hearts 3 wk after myocardial infarction (MI ) had decreased Na+/Ca2+ exchange currents (I-Na/Ca; 3 Na+ out:1 Ca2in) and sarcoplasmic reticulum (SR)-releasable Ca2+ contents. These de fects in Ca2+ regulation may contribute to abnormal contractility in M I myocytes. Because exercise training elicits positive adaptations in cardiac contractile function and myocardial Ca2+ regulation, the prese nt study examined whether 6-8 wk of high-intensity sprint training (KI ST) would ameliorate some of the cellular maladaptations observed in p ost-MI rats with Limited exercise activity (Sed). In MI rats, KIST did not affect citrate synthase activities of plantaris muscles but signi ficantly increased the percentage of cardiac cr-myosin heavy chain (MH C) isoforms (57.2 +/- 1.9 vs. 49.3 +/- 3.5 in MI-KIST vs. MI-Sed, resp ectively; P less than or equal to 0.05). At the single myocyte level, KIST attenuated cellular hypertrophy observed post-MI, as evidenced by reductions in cell lengths (112 +/- 4 vs. 130 +/- 5 mu m in MI-KIST v s. MI-Sed, respectively; P less than or equal to 0.005) and cell capac itances (212 +/- 8 vs. 242 +/- 9 pF in MI-KIST vs. MI-Sed, respectivel y; P less than or equal to 0.015). Reverse I-Na/Ca was significantly l ower (P less than or equal to 0.0001) in myocytes from MI-Sed rats com pared with those from rats that were sham operated and sedentary. KIST significantly increased reverse I-Na/Ca (P less than or equal to 0.05 ) without affecting the amount of Na+/Ca2+ exchangers (detected by imm unoblotting) in MI myocytes. SR-releasable Ca2+ content, as estimated by integrating forward I-Na/Ca during caffeine-induced SR Ca2+ release , was also significantly increased (P less than or equal to 0.02) by H IST in MI myocytes. We conclude that the enhanced cardiac output and s troke volume in post-MI rats subjected to KIST are mediated, at least in part, by reversal of cellular maladaptations post-MI.