Shortened and fragmented sleeping patterns occupying modern industrialized societies may promote metabolic disturbances accompanied by increased risk of weight gain and skeletal muscle degradation. Short-term sleep restriction may alter energy homeostasis by modifying dopamine brain receptor signaling, leading to hyperpalatable food consumption and risk of increased adiposity. Concomitantly, the metabolic damage caused by lower testosterone and higher cortisol levels may stimulate systemic inflammation, insulin resistance, and suppress pathways involved in muscle protein synthesis. These changes may lead to dysregulated energy balance and skeletal muscle metabolism, increasing the risk of sarcopenic obesity, an additional public health burden. Future trials controlling for food intake and exploring further the influence of sleep deprivation on anabolic and catabolic signaling, and gut peptide interaction with energy balance are warranted.