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Degree

Doctor of Philosophy, Ohio State University, Educational Services and Research, 2004.

Abstract

It was the purpose of this study to investigate effects of exercise training on post-ischemia/reperfusion (I/R) contractile function. I/R induced significant contractile dysfunction in hearts from sedentary control animals; left ventricular developed pressure (LVDP) and maximal rate of pressure development and relaxation (±dP/dt) decreased, while end-diastolic pressure (EDP) increased. However, this dysfunction was attenuated 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 and level of myocardial adenine nucleotide, such that I/R reduced myocardial ATP and ADP levels 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. 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/m2), 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, I/R reduced V0 by 34% in both control and trained trabeculae (2.64 ± 0.15 vs. 1.74 ± 0.17 trabecula lengths/sec). Exercise training increased the expression of the beta isoform of myosin heavy chain (MHC-beta) in trabeculae, as well as, in the ventricular free wall. 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.

Keywords

Myocardial stunning; Exercise training; Ischemia/reperfusion

Advisor

George E Billman

Pages

xviii, 132 p. :ill

Document number: osu1078942640
Permalink: http://rave.ohiolink.edu/etdc/view?acc_num=osu1078942640

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