Theoretical Framework The investigators have determined that skeletal muscle tissue perfusion in healthy elderly is blunted compared to young. Additionally, local skeletal muscle vasodilation with sodium nitroprusside or exercise increased muscle perfusion in the elderly to more youthful levels, and when performed in combination with increased plasma amino acid availability, greatly amplified muscle protein synthesis. In the absence of physical activity, protein ingestion via traditional mixed nutrient meals is the primary means of stimulating muscle protein anabolism via an increase in precursor availability. However, anabolic efficiency and protein synthetic response to a mixed nutrient meal is often blunted in elderly. Therefore, they propose that a common vasodilatory drug, losartan, newly discovered to block TGF-β activation and signaling in skeletal muscle by antagonizing the angiotensin II type 1 receptor (AT1), will restore skeletal muscle nutritive flow via its vasodilatory actions and concomitantly prevent angiotensin II-induced muscle wasting. Notably, the vasodilatory effects of losartan are thought to be at least partially due to alleviation of oxidative stress (1) and the investigators previously found evidence for age-related oxidative stress in older individuals who exhibited resistance to the anabolic effects of amino acids (2). This latter finding is consistent with a previous report that antioxidant administration alleviates age-related anabolic resistance to leucine in rats (3). Accordingly, in the current study the investigators postulate that administration of the antioxidant N-acetylcysteine (NAC) will restore skeletal muscle nutritive blood flow and sensitivity to the anabolic effects of leucine. Thus, in the current study they propose to administer placebo, losartan or NAC in a group of healthy elderly to target key mechanisms responsible for inactivity-induced losses of lean body mass and function.