Exercise training attenuates the myocardial dysfunction induced by endotoxin

Abstract

The purpose of this study was to determine whether exercise training protected against endotoxin-induced myocardial dysfunction. After a 12-wk treadmill training period, carotid catheters were implanted 24 h before saline or endotoxin administration into four groups of animals: trained saline-injected (TS), trained endotoxin-injected (TE), sedentary saline-injected (SS), and sedentary endotoxin-injected (SE). Heart rate and mean arterial pressure were monitored 4 h after in vivo endotoxin or saline injection. Mean arterial pressure decreased an average of 32 +/- 3 mmHg 1 h after endotoxin administration but was normal (109 +/- 6 mmHg) 2 h later. Plasma catecholamines, in vitro myocardial performance, and isolated myocyte adenosine 3′,5′-cyclic monophosphate (cAMP) production in response to isoproterenol were assessed 4 h after endotoxin injection. Plasma catecholamine levels were 5- to 15-fold higher in SE compared with the other groups. These data suggest that myocardial protection may be related to the lowered catecholamine levels elicited in TE compared with SE in response to endotoxin administration. The product of cardiac output and peak systolic pressure, an index of cardiac work, was 24–32% greater in TS compared with SS. Cardiac work was decreased 32% in TE compared with a 45% decrease in SE. cAMP was reduced in myocytes from SE in response to isoproterenol (-28%) and to forskolin (-44%) but not in myocytes from TE, compared with TS and SS. The difference in cAMP accumulation suggests that training maintains the integrity of the beta-adrenergic receptor adenylate cyclase system, which can be depressed by in vivo endotoxin administration.