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 a s prolonged half-time of [Ca2+](i) decline. Because exercise training elici ts positive adaptations in cardiac contractile function and myocardial Ca2 regulation, the present study examined whether 6-8 wk of high-intensity sp rint training (HIST) would restore [Ca2+](i) dynamics and SR function in MI myocytes toward normal. In MI rats, HIST ameliorated myocyte hypertrophy a s indicated by significant (P less than or equal to 0.05) decreases in whol e 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) restore d 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 expressio n significantly (P < 0.001) decreased by 44% in MI-Sed myocytes. Surprising ly, 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 ca lsequestrin expression among the three groups. Expression of phospholamban was not different between Sham-Sed and MI-Sed myocytes but was significantl y (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 m yocytes. Improvement in SR function by HIST is mediated not by increased SR Ca2+-ATPase expression but by modulating phospholamban regulation of SR Ca 2+ ATPase activity.