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