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Med Hypotheses. 2011 Aug;77(2):220-2. doi: 10.1016/j.mehy.2011.04.017. Epub 2011 May 7.
Sleep and muscle recovery: endocrinological and molecular basis for a new and promising hypothesis.
Dattilo M1, Antunes HK, Medeiros A, Mônico Neto M, Souza HS, Tufik S, de Mello MT.
Author information
Abstract
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.
Sleep and muscle recovery: endocrinological and molecular basis for a new and promising hypothesis.
Dattilo M1, Antunes HK, Medeiros A, Mônico Neto M, Souza HS, Tufik S, de Mello MT.
Author information
Abstract
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.
