Circadian Rhythm and Sleep Disruption: Causes, Metabolic Consequences and Countermeasures.

Circadian (∼ 24 hour) timing systems pervade all kingdoms of life, and temporally optimize behaviour and physiology in humans. Relatively recent changes to our environments, such as the introduction of artificial lighting, can disorganize the circadian system, from the level of the molecular clocks that regulate the timing of cellular activities to the level of synchronization between our daily cycles of behaviour and the solar day. Sleep/wake cycles are intertwined with the circadian system, and global trends indicate that these too are increasingly subject to disruption. A large proportion of the world's population is at increased risk of environmentally-driven circadian rhythm and sleep disruption, and a minority of individuals are also genetically predisposed to circadian misalignment and sleep disorders. The consequences of disruption to the circadian system and sleep are profound and include myriad metabolic ramifications, some of which may be compounded by adverse effects on dietary choices. If not addressed, the deleterious effects of such disruption will continue to cause widespread health problems; therefore, implementation of the numerous behavioural and pharmaceutical interventions that can help restore circadian system alignment and enhance sleep will be important

Resistance training minimizes catabolic effect induced by sleep deprivation in rats

Sleep deprivation (SD) can induce muscle atrophy. We aimed to investigate the changes underpinning SD-induced muscle atrophy and the impact of this condition on rats that were previously submitted to resistance training (RT). Adult male Wistar EPM-1 rats were randomly allocated into one of five groups: control (CTRL), SHAM, SD (for 96 h) and groups that were submitted to resistance training (RT), and the combination of RT+SD. The major outcomes of this study were observed in muscle fiber cross-sectional area (CSA), anabolic and catabolic hormone profiles, and the abundance of select proteins involved in the muscle protein synthetic and protein degradation pathways. SD resulted in muscle atrophy; when combined with RT, the reduction in muscle fiber CSA was attenuated. The level of IGF-1 and testosterone was reduced in SD animals, and the RT+SD had higher levels of these variables than SD group. Corticosterone was increased in the SD group compared with the CTRL, and this increase was minimized in the RT+SD group. The increases in corticosterone concentrations between groups paralleled the abundance of the autophagic proteins LC3, p62/SQSTM1, and ubiquitinated proteins, suggesting that corticosterone may trigger these changes. SD induced weight loss, but the previously trained group had minimized this loss. We report that SD induced muscle atrophy, probably due to the increased corticosterone and catabolic signal. High intensity RT performed before SD was beneficial in containing muscle loss rate induced by SD. It also minimized the catabolic signal and increased the synthetic activity, thereby minimizing the body's weight loss.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author