Sarcopenia is a constant in aging. Observed over long periods, it can reach 1% per year. But it is such a tenuous phenomenon that it cannot be observed over short periods at steady state. The aging phenomenon mainly hits fibers, Type II but on aged muscle thin, normal, and hypertrophic fibers cohabit with sclerosis and fat increases. Sarcopenia is difficult to study, due to the lack of simple clinical, biochemical, or imaging measures. Anthropometric data are largely dependent on water content. DEXA gives better information on appendicular muscle loss. Measures of strength analyze functional outcomes of sarcopenia. Sarcopenia appears largely multifactorial. Hormonal changes, e.g., drop in growth hormone, menopause, and andropause, explain impaired protein synthesis. Disuse (sedentary, bed rest) may explain chronical protein lysis. But the main factors for muscle lysis imply life events and occurring diseases. Cytokines (IL6, TNF alpha) and stress hormones (cortisol) induce quick protein lysis in muscle. Rapid and intensive successive aggressions during life cannot be compensated by slowed synthesis. Harmful consequences of sarcopenia explain many disabilities of old age: loss of strength, inducing itself loss of mobility, falls, equilibrium disorders, poor ADL: loss of nutritional reserves (protein and glycogen) impairing capacities of immune response. Muscle loss spoils vital functions as respiration. Treatment remains rather limited to resistance exercise. Although, these results are thin, they are the only ones to be validated in all the elderly even the frail or the old. However it is not efficient during the evolution of an inflammatory process. The powerful action of cytokine and cortisol on muscular hypermetabolism must be incited for early treatment of any infectious or inflammatory event. Nutritional supplementation has no efficiency in the absence of malnutrition and without exercise. Although mobility impairments mainly due to sarcopenia are the first cause of disablement in the elderly, we lack information on etiology, evolution, and measurement of sarcopenia. We also lack controlled therapeutical studies.