University of Arkansas, Fayetteville


Fatty acids are the primary fuel source for cardiac tissue in both humans and animals. These become especially important during times of starvation and long bouts of exercise. Fatty acids are broken down into smaller, useable acyl-CoA subunits through a process called beta-oxidation. The first step in this process must be catalyzed by one of four acyl-CoA dehydrogenase enzymes depending on the length of the fatty acid to be metabolized. The enzyme that catalyzes the break-down of long-chain fatty acids, long-chain acyl-CoA dehydrogenase (LCAD), was examined. The objective of this study was to determine how a single bout of endurance exercise impacts cardiac function in LCAD deficient mice as well as to assess whether recovery from exercise is adversely affected. Mice were separated into four groups for testing: LCAD, non-exercised; LCAD, exercised; control, non-exercised; and control, exercised. Mice were exercised by forced running at a speed of 31m/min with increasing grade (2%) each 20 min. Twenty-four hours post-exercise, the mice were anesthetized with sodium pentobarbital (40 ml/kg body weight,) and ejection fraction, fractional shortening, and cardiac output values were determined in both groups. It was determined that exercise had no effect on cardiac function or recovery in either the LCAD or control group. There was, however, a significant difference between the LCAD and control group for fractional shortening (p<0.05) and cardiac output (p<0.05). It was concluded that a single bout of endurance exercise had no significant effect on the cardiac function of LCAD deficient mice during recovery, although the disease did negatively affect cardiac function when compared to the control group.