Ischemia-modified albumin (IMA) has been proposed as a biological marker of myocardial ischemia (1)(2). Exposure to ischemic myocardium modifies circulating albumin at its NH2 terminus by different mechanisms, and this modification is the basis of IMA measurement by the albumin cobalt binding (ACB) test (3). The tissue-specific nature of the mechanism by which ischemia modifies albumin remains undetermined. Together with a nondiagnostic electrocardiogram and negative troponin values, IMA concentrations within the reference interval have high negative predictive value of myocardial ischemia in patients with suspected acute coronary syndromes (1)(2). However, IMA cardiospecificity has not been validated and needs an evidence base before routine clinical use. A recent report showed significant IMA increases 24–48 h after a marathon race, with exercise-promoted gastrointestinal and/or delayed skeletal muscle ischemia being evoked as possible causes of such increases (4). However, because IMA has shown rapid kinetics of increase (in minutes) and return to baseline no longer than 12 h after angioplastic procedures (5), long-duration skeletal muscle ischemia (i.e., occurring during marathons) does not appear to be the most appropriate model to investigate the effect of such ischemia on IMA values or the kinetics of IMA occurring during acute coronary syndromes. The aim of this work was to analyze the possible contribution of skeletal muscle ischemia to IMA by investigating its short-term kinetics in an isolated skeletal-muscle ischemia model. Because lactate and ammonia concentrations increase sharply after a forearm ischemia test, their possible influence in the ACB assay was studied. Ten healthy volunteers (4 men and 6 women) from our laboratory staff (age range, 48–61 years; median, 53 years) with no personal or family history of cardiovascular disease and no known cardiovascular risk factors after a medical examination underwent a forearm ischemia test (6). Briefly, after an overnight fast (10–12 …