Sprint training normalizes Ca2+ transients and SR function in postinfarction rat myocytes

Previous studies have shown that myocytes isolated from sedentary (Sed) rat hearts 3 wk after myocardial infarction (MI) undergo hypertrophy, exhibit altered intracellular Ca2+ concentration ([Ca2+](i)) dynamics and abnormal contraction, and impaired sarcoplasmic reticulum (SR) function manifested as prolonged half-time of [Ca2+](i) decline. 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 restore [Ca2+](i) dynamics and SR function in MI myocytes toward normal. In MI rats, HIST ameliorated myocyte hypertrophy as indicated by significant (P less than or equal to 0.05) decreases in whole cell capacitances [Sham-Sed 179 +/- 12 (n = 20); MI-Sed 226 +/- 7 (n = 20); MI-MIST 183 +/- 11 pF (n = 19)]. MIST significantly (P < 0.0001) restored both systolic [Ca2+](i), [Sham-Sed 421 +/- 9 (n = 79); MI-Sed 350 +/- 6 (n = 70); MI-MIST 399 +/- 9 nM (n = 70)] and half-time of [Ca2+](i) decline (Sham-Sed 0.197 +/- 0.005; MI-Sed 0.247 +/- 0.006; MI-MIST 0.195 +/- 0.006 s) toward normal. Compared with Sham-Sed myocytes, SR Ca2+-ATPase expression significantly (P < 0.001) decreased by 44% in MI-Sed myocytes. Surprisingly, expression of SR Ca2+-ATPase was further reduced in Aa-HIST myocytes to 26% of that measured in Sham-Sed myocytes. There were no differences in calsequestrin expression among the three groups. Expression of phospholamban was not different between Sham-Sed and MI-Sed myocytes but was significantly (P < 0.01) reduced in MI-HIST myocytes by 25%. Our results indicate that HIST instituted shortly after MI improves [Ca2+](i) dynamics in surviving myocytes. Improvement in SR function by HIST is mediated not by increased SR Ca2+-ATPase expression but by modulating phospholamban regulation of SR Ca2+ ATPase activity.