Following acute myocardial infarction the functional load of the surviving heart muscle does increase considerably, leading to an increased release of adrenergic neurotransmitters with a consequent decrease in endogenous catecholamine stores. Within the first 24 h following infarction, a temporary decline in the high-energy phosphate content is observed in the surviving heart muscle; futhermore, a reduction in lactate extraction is noted. In the intact organism an increased shortening of the surviving heart muscle is noted as a consequence of the altered ventricular geometry and the increased release of catecholamines. If these effects are excluded by means of isolation and analysis in vitro, a decrease in contractile function could be demonstrated in the surviving heart muscle in the early phase following infarction; the response to positive inotropic interventions was depressed as well. These changes are reversible; six weeks following infarction a normal contractile behaviour is observed.