Sprint training restores normal contractility in postinfarction rat myocytes

The significance of 6-8 wk of high-intensity sprint training (HIST) on contractile abnormalities of myocytes isolated from rat hearts with prior myocardial infarction (MI) was investigated. Compared with the sedentary (Sed) condition, HIST attenuated myocyte hypertrophy observed post-MI primarily by reducing cell lengths but not cell widths. At high extracellular Ca2+ concentration (5 mM) and low pacing frequency (0.1 Hz), conditions that preferentially favored Ca2+ influx over efflux, MI-Sed myocytes shortened less than Sham-Sed myocytes did. HIST significantly improved contraction amplitudes in MI myocytes. Under conditions that favored Ca2+ efflux, i.e., low extracellular Ca2+ concentration (0.6 mM) and high pacing frequency (2 Hz), MI-Sed myocytes contracted more than Sham-Sed myocytes. HIST did not appreciably affect contraction amplitudes of MI myocytes under these conditions. Compared with MI-Sed myocytes, HIST myocytes showed significant improvement in time required to reach one-half maximal contraction amplitude shortening, maximal myocyte shortening and relengthening velocities, and half time of relaxation. Our results indicate that HIST instituted shortly after MI improved cellular contraction in surviving myocytes. Because our previous studies demonstrated that, in post-MI myocytes, HIST improved intracellular Ca2+ dynamics, enhanced sarcoplasmic reticulum Ca2+ uptake and Ca2+ content, and restored Na+/Ca2+ exchange current toward normal, we hypothesized that improvement in MI myocyte contractile function by HIST was likely mediated by normalization of cellular Ca2+ homeostatic mechanisms.