THE INTERACTIVE EFFECTS OF CHRONIC ETHANOL CONSUMPTION AND EXERCISE TRAINING ON CARDIAC FUNCTION (HEART, ALCOHOL)

摘要

Chronic ethanol (ETOH) exposure results in severe morphological, biochemical and functional damage to the heart. In part, this damage appears to occur as the result of (1) reduced excitation-contraction coupling, and (2) reduced sarcolemmal catecholamine sensitivity. Endurance exercise training, on the other hand, enhances both of these myocardial characteristics, resulting in a more functionally competent heart. In order to determine how the functional capacity and the biochemistry of the rodent heart responds to the simultaneous imposition of both of these physiologic stressors, 60 female Sprague-Dawley rats were divided into 4 groups: run/control (R/C), run/ETOH (R/E), sedentary/control (S/C), sedentary/ETOH (S/E). ETOH was administered in a nutritionally balanced liquid diet of which 35% of the caloric content came from ETOH. Exercise training was carried out on a rodent treadmill using a progressive exercise protocol. After ten weeks of treatment, cardiac functional capacity was measured in an anesthetized, open-chest preparation. Following the completion of the functional measures, the left ventricle was isolated, and biochemically analyzed.;Cardiac functional capacity, as measured by peak left ventricular systolic pressure, rate of pressure development, and heart rate, remained unchanged by either experimental intervention. However, ETOH treatment significantly diminished the responsiveness of these measures to tyramine, a drug which induces the release of endogenous norepinephrine. Biochemical analysis included the determination of citrate synthase activity, cytochrome oxidase activity, myofibril ATPase activity, and protein content. No experimental treatment resulted in a significant change in any of these biochemical parameters.;The results of this study suggest that neither chronic ETOH treatment nor endurance exercise training appreciably affects either cardiac functional capacity as determined in an anesthetized preparation, or biochemical correlates of cardiac functional capacity. However, chronic ETOH exposure reduces the myocardium's ability to respond to a tyramine challenge, suggesting that chronic ETOH exposure reduces the heart's ability to respond to stress. Whether this is due to a reduced myocardial norepinephrine content or a reduced norepinephrine sensitivity remains to be determined. Endurance training was unable to attenuate this effect of ETOH on the heart.