Sprint training shortens prolonged action potential duration in postinfarction rat myocyte: mechanisms

Two electrophysiological manifestations of myocardial infarction (MI)-induc ed myocyte hypertrophy are prolongation of action potential duration (APD) and reduction of transient outward current (I-to) density. Because high-int ensity sprint training (HIST) ameliorated myocyte hypertrophy and improved myocyte Ca2+ homeostasis and contractility after MI, the present study eval uated whether 6-8 wk of HIST would shorten the prolonged APD and improve th e depressed I-to in post-MI myocytes. There were no differences in resting membrane potential and action potential amplitude (APA) measured in myocyte s isolated from sham-sedentary (Sed), MI-Sed, and MI-HIST groups. Times req uired for repolarization to 50 and 90% APA were significantly (P < 0.001) p rolonged in MI-Sed myocytes. HIST reduced times required for repolarization to 50 and 90% APA to values observed in Sham-Sed myocytes. The fast and sl ow components of I-to were significantly (P < 0.0001) reduced in MI-Sed myo cytes. HIST significantly (P < 0.001) enhanced the fast and slow components of I-to in MI myocytes, although not to levels observed in Sham-Sed myocyt es. There were no significant differences in steady-state I-to inactivation and activation parameters among Sham-Sed, MI-Sed, and MI-HIST myocytes. Li kewise, recovery from time-dependent inactivation was also similar among th e three groups. We suggest that normalization of APD after MI by HIST may b e mediated by restoration of I-to toward normal levels.