Resistance exercise: a non-pharmacological strategy to minimize or reverse sleep deprivation-induced muscle atrophy.

Sleep is important for maintenance of skeletal muscle health. Sleep debt can induce muscle atrophy by increasing glucocorticoids and decreasing testosterone, growth hormone and insulin-like growth factor-I. These hormonal alterations result in a highly proteolytic environment characterized by decreased protein synthesis and increased degradation. Given that sleep deprivation is increasingly prevalent in modern society, strategies to minimize or reverse its adverse effects need to be investigated. Resistance exercise has been suggested as an intervention that would benefit the muscle health. The practice of this type of exercise can increase the concentration of testosterone, growth hormone and insulin-like growth factor I and stimulate the protein synthesis through a key signaling molecule, mammalian target of rapamycin. Thus, we hypothesized that resistance exercise is an important non-pharmacological strategy to counteract deleterious effects of sleep debt on skeletal muscle.

Sleep and muscle recovery: endocrinological and molecular basis for a new and promising hypothesis.

Sleep is essential for the cellular, organic and systemic functions of an organism, with its absence being potentially harmful to health and changing feeding behavior, glucose regulation, blood pressure, cognitive processes and some hormonal axes. Among the hormonal changes, there is an increase in cortisol (humans) and corticosterone (rats) secretion, and a reduction in testosterone and Insulin-like Growth Factor 1, favoring the establishment of a highly proteolytic environment. Consequently, we hypothesized that sleep debt decreases the activity of protein synthesis pathways and increases the activity of degradation pathways, favoring the loss of muscle mass and thus hindering muscle recovery after damage induced by exercise, injuries and certain conditions associated with muscle atrophy, such as sarcopenia and cachexia.