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 Ca²⁺ in) and sarcoplasmic reticulum (SR)-releasable Ca²⁺ contents. These defects in Ca²⁺ regulation may contribute to abnormal contractility in MI myocytes. Because exercise training elicits positive adaptations in cardiac contractile function and myocardial Ca²⁺ regulation, the present study examined whether 6-8 wk of high-intensity sprint training (HIST) would ameliorate some of the cellular maladaptations observed in post-MI rats with limited exercise activity (Sed). In MI rats, HIST did not affect citrate synthase activities of plantaris muscles but significantly increased the percentage of cardiac α-myosin heavy chain (MHC) isoforms (57.2 ± 1.9 vs. 49.3 ± 3.5 in MI-HIST vs. MI-Sed, respectively; P ≤ 0.05). At the single myocyte level, HIST attenuated cellular hypertrophy observed post-MI, as evidenced by reductions in cell lengths (112 ± 4 vs. 130 ± 5 μm in MI-HIST vs. MI-Sed, respectively; P ≤ 0.005) and cell capacitances (212 ± 8 vs. 242 ± 9 pF in MI-HIST vs. MI-Sed, respectively; P ≤ 0.015). Reverse I(Na/Ca) was significantly lower (P ≤ 0.0001) in myocytes from MI-Sed rats compared with those from rats that were sham operated and sedentary. HIST significantly increased reverse I(Na/Ca) (P ≤ 0.05) without affecting the amount of Na⁺/Ca²⁺ exchangers (detected by immunoblotting) 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 ≤ 0.02) by HIST in MI myocytes. We conclude that the enhanced cardiac output and stroke volume in post-MI rats subjected to HIST are mediated, at least in part, by reversal of cellular maladaptations post-MI.