Elsevier

Medical Hypotheses

Volume 77, Issue 2, August 2011, Pages 220-222
Medical Hypotheses

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

https://doi.org/10.1016/j.mehy.2011.04.017Get rights and content

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.

Section snippets

Background

Several pieces of evidence point to sleep as an important regulator of numerous biological aspects, maintaining vital physiological functions, homeostasis, learning and memory, by promoting the development of the central nervous system and physical recovery [1], [2].

However, in recent years, a reduction in the duration of sleep time is becoming evident in the populations of industrialized countries, motivating a search for a better understanding of the potential health hazards arising from

Hormonal changes resulting from sleep deprivation/restriction and its impact on skeletal muscle metabolism

Considering the physiological properties that the hormones testosterone, IGF-1 and cortisol/corticosterone have on the body, a potentially catabolic and proteolytic environment may be present in sleep debt conditions. Although this condition appears to be associated with increased body mass in humans, the mechanisms responsible for this association need to be better understood, considering that individuals deprived of sleep for 72 h showed higher urinary excretion of urea, suggesting greater

Pathways involved in protein synthesis and degradation, and its possible modulation in response to sleep deprivation/restriction

IGF-1-mediated signaling is a central element in the stimulation of muscle protein synthesis, best characterizing muscle growth and relating to adaptive processes in skeletal muscle [24]. In muscle, the binding of IGF-1 to its receptor promotes the activation of phosphatidylinositol 3-kinase (PI3K) and Akt, which induces muscle hypertrophy. This is primarily mediated by stimulation of protein translation via regulation of glycogen synthase kinase-3β (GSK-3β) and mammalian Target of Rapamycin

Can the process of muscle recovery be damaged by sleep deprivation/restriction?

Sleep, and the lack thereof, should be stressed as contributing an important role in the process of muscle recovery after certain kinds of damage, whether induced by exercise or injury. It is well established that muscle has highly plastic properties and is capable of recovering from several types of damage. However, significant molecular changes are required to allow damaged cells to recover or be replaced by new cells, involving steps that depend on the proliferation, fusion and

Conflict of interest

None declared.

Acknowledgements

The authors thank Everald Van Cooler, Patricia Chakur Brum, the Laboratory of Cellular and Molecular Physiology of Excercise, School of Physical Education and Sport, University of São Paulo (USP), and the support of the Associação Fundo de Incentivo á Pesquisa (AFIP), the Centro de Estudos em psicobiologia e Exercicio Acidentes (CEPE), the Centro de Estudo Multidisciplinar em Sonolencia e Acidentes (CEMSA), CEPID/SONO-FAPESP (#98/14303-3), CNPq, CAPES, FAPESP (2009/11056-1), UNIFESP, FADA,

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