EFFECTS OF SKELETAL MUSCLE OXIDATIVE CAPACITY ON EXERCISE TOLERANCE FOLLOWING MYOCARDIAL INFARCTION

Abstract

1854 Past research has shown decreased exercise tolerance following myocardial infarction (MI). Numerous factors have been hypothesized to contribute to this decrement, including a decrease in the oxidative capacity of skeletal muscle. The purpose of this study was to determine whether muscle oxidative enzyme activity correlates with endurance performance, as measured by run time to exhaustion (RTE), in a rat model of MI. The animals were initially divided into two groups: sham-operated controls (SHAM) and animals in which a MI was surgically induced by ligating the left main coronary artery. MI rats were then subdivided into two groups according to left ventricular end diastolic pressure (LVEDP): <20mmHg [small MI (SMI)] and >20mmHg [large MI (LMI)]. After 6 wk of recovery, LVEDP differed among groups (p<0.05): SHAM (5±1 mmHg, n=19), SMI (11±1 mmHg, n=20), and LMI (30±3 mmHg, n=5). Exercise endurance was measured by performing a progressive RTE test. RTE was 54±2 min for SHAM, 49±3 min for SMI, and 34±6 min for LMI (p<0.05 for LMI vs SHAM, SMI). Citrate synthase activity (CS) was measured in six hindlimb muscles. No significant correlation was found between RTE and CS of any muscle in either the SHAM or SMI group. In contrast, in the LMI group, significant correlations were found between RTE and red gastrocnemius CS (r=0.95, p<0.05) and between RTE and plantaris CS (r=0.87, p<0.05). In addition, there was a tendency for a correlation between RTE and white vastus lateralis CS (r=0.86, 0.10<p<0.05). These data show that significant reductions in oxidative enzyme activity are associated with reduced endurance performance. It appears, however, that a large MI is required to produce significant alterations in endurance performance and oxidative capacity. Supported by NIH HL57226 and AHA-KS-97-GS-46