Low birth weight in humans is associated with an increased risk of cardiovascular disease. Humans with heart failure have a reduced beta-adrenergic response. The aim of this study was to investigate the hemodynamic response to the beta-adrenergic agonist isoproterenol and to identify molecular deficiencies that may be predictive of cardiac failure in a low birth weight rodent model which develops insulin resistance and type-2 diabetes in adulthood. Wistar rats were fed a control or a low protein diet throughout pregnancy and lactation. The resting heart rate and blood pressure of the 3 month old male offspring of these dams, termed "control" and "Low Protein" (LP) groups respectively, and their responses to isoproterenol (ISO) infusion were monitored by radiotelemetry. The protein expression of beta-adrenergic signalling components was also measured by western blotting. Basal heart rate was increased in LP offspring (p<0.04), although mean arterial pressure was comparable with controls. Chronotropic effects of ISO were blunted in LP offspring with significant delays to maximal response (p=0.01), a shorter duration of response (p=0.03) and a delayed return to baseline (p=0.01) at the lower dose (0.1 µg/kg/min). At the higher dose (1.0 µg/kg/min ISO), inotropic response was blunted (p=0.03) but quicker (p=0.001). In heart tissue of LP offspring, 1-adrenergic receptor expression (1-AR) was reduced (p<0.03). 1-adrenergic receptor kinase (1-ARK) and both stimulatory (G_s) and inhibitory G-protein (G_i) levels remained unchanged, while -arrestin levels were higher (p<0.03). Finally, insulin receptor- expression was reduced in LP offspring (p<0.012). Low protein offspring have reduced beta-adrenergic responsiveness and attenuated adrenergic and insulin signalling, suggesting that intrauterine undernutrition alters heart failure risk.