Exercise training effects on myocardial stunning

It was the purpose of this study to investigate effects of exercise training on post-ischemia/reperfusion (I/R) contractile function. Phenotype of stunned myocardium was experimentally induced in an isolated Langendorff heart perfusion model (15 min global ischemia/30 min reperfusion) using male Sprague-Dawley rats that had undergone 10--12 week treadmill exercise training. I/R induced significant (ANOVA, p < .05) contractile dysfunction in hearts from sedentary control animals; left ventricular developed pressure (LVDP) and maximal rate of pressure development and relaxation (+/-dP/dt) decreased (p < .05), while end-diastolic pressure (EDP) increased. However, this dysfunction (as expressed as % change from the last min before ischemia) was attenuated (p < .05) in the myocardium from exercise-trained animals (LVDP, sedentary -60.8 +/- 6.4%, vs. trained -15.6 +/- 8.6%; +dP/dt, sedentary -54.1 +/- 4.7%, vs. trained -16.7 +/- 8.4%; -dP/dt, sedentary -44.4 +/- 2.5%, vs. trained -17.9 +/- 7.2%; EDP, sedentary 539.5 +/- 147.6%, vs. trained 71.6 +/- 30.6%). In contrast, exercise training did not alter Troponin I (TnI) degradation. Myocardial adenine nucleotide level was not affected by exercise training, such that I/R reduced (p > .05) myocardial ATP (sedentary 29% vs. trained 22%) and ADP levels (sedentary 34% vs. trained 29%) to a similar extent in both sedentary and trained animals. Exercise training increased the amplitude of Ca2+ transients and the maximal rate of Ca2+ decline. Ischemia/reperfusion had no effect on these parameters.; The maximal normalized isometric force measured in isolated, skinned ventricular trabeculae (force/cross-sectional area; P0/CSA) was increased by an average 26% in trained trabeculae (25.8 +/- 1.6 kN/m 2), compared to controls (20.5 +/- 1.3 kN/m2) and this increase was not affected by ischemia/reperfusion. Exercise training had no effect on maximal shortening velocity (V0); in contrast, ischemia/reperfusion reduced V0 by 34% (p < 0.05) in both control and trained trabeculae (2.64 +/- 0.15 vs. 1.74 +/- 0.17 trabecula lengths/sec). Exercise training increased (p < 0.05) the expression of the beta isoform of myosin heavy chain (MHC-beta) in trabeculae (49 +/- 5%, trained; 21 +/- 2%, control; expressed as percent of total MHC protein), as well as, in the ventricular free wall (23 +/- 3%, trained; 10 +/- 1%, control). Thus, despite the similar degree of ischemic response shown as a reduction in myocardial adenine nucleotide and V0 and proteolytic damage to TnI, myocardium from exercise-trained animals had better contractile functional recovery following a brief period of ischemia. The potential adaptive factors that might contribute to this improvement in contractile function include an enhanced Ca2+ handling mechanism, an increase in P0/CSA, and a possible increase in the economy, as inferred from increased expression of MHC-beta.