The Potential Role of Sleep in Promoting a Healthy Body Composition: Underlying Mechanisms Determining Muscle, Fat, and Bone Mass and Their Association with Sleep

Abstract

Sleep plays an essential role in human life. While sleep is a state elicited by the brain, its vital role reaches beyond maintaining brain health. Unhealthy sleeping habits have been associated with increased risk for inflammation, obesity, or diabetes. Evidence is emerging that sleep guides processes playing an important role in promoting the regulation of endocrine function involved in tissue regeneration and tissue remodelling. Thereby, sleep presumably is a critical factor contributing to the balance of core body tissues: bone, fat, and muscle mass. Given the increasing prevalence of various chronic diseases and comorbidities due to unhealthy lifestyle choices, sleep could be a key target to promote a healthy body composition up until old age. Here, we review the potential role of sleep and its underlying brain oscillations in body core tissues turnover. Specifically, we discuss potential underlying mechanisms linking sleep to body composition, both during rest and under challenging conditions. Among other described pathways, we highlight the possible role of the growth hormone that was found to be involved in the homeostasis of all core body tissues and has been strongly linked to brain activity dominating deep sleep, the so-called slow waves. Finally, we formulate important questions to be addressed in future research on the effect of sleep on body composition and specifically emphasize the importance of intervention studies to move from correlative to causal evidence.

Effects of auditory sleep modulation approaches on brain oscillatory and cardiovascular dynamics

“…Sleep represents a powerful system for promoting brain and body health. It is suggested to play a role in a plethora of functions such as cleaning away toxic by-products [1][2][3], synaptic homeostasis [4], memory consolidation [5][6][7][8][9][10][11], metabolic [12], and cardiovascular functions [13][14][15][16], and body core tissue turnover [17]. Particularly, nonrapid eye movement (NREM) sleep with its large-amplitude, low-frequency slow waves has been proposed to guide those beneficial effects (e.g.…”

Chronic Sleep Deprivation Impaired Bone Formation in Growing Rats and Down-Regulated PI3K/AKT Signaling in Bone Tissues

“…However, it is difficult to explain the reduced osteoblast differentiation and imbalance in bone turnover status, which was likely unrelated to the negligible decrease in body mass. Furthermore, if these changes were mediated by other possible effects of the SD, such as increased inflammation 30 , 31 and vitamin D deficiency, then an increase in bone resorption would have been expected; 30 , 32 however, this was not observed. Our finding of marked alterations in transcriptome of bone tissue shows that the SD directly acts on osteocytes rather than via central nervous system function and further suggests that sleep may play an equally important role in peripheral energy metabolism, as previous reported.…”

Phenotyping obesity: A focus on metabolically healthy obesity and metabolically unhealthy normal weight

“…178,179 Sleep restriction also results in the loss of the beneficial effects of GH on muscle mass and fat distribution. 180 Sleep debt is also associated with an increased prediction towards the consumption of high-fat or carbohydrate-rich foods as well as reduced physical activity, 181 as a result of the aforementioned endocrine changes 181 and enhanced activation of brain reward and foodsensitive centres in response to unhealthy food. 182…”

“…153 Studies evaluating T2DM risk in MHO identified an approximate 4-fold increased risk compared with MHNW. 179,180,197,212,213,227 Subjects who progressed to MUHO were at higher risk for developing T2DM compared to those who retained the MHO status, yet this risk was lower when compared to those with stable MUHO. 228 On the other hand, Wang et al reported that individuals with persistent MHO were not at increased risk compared with stable MHNW after 6 years of follow-up 229 but with very wide 95% confidence intervals in the odds ratio (0.20-1.40).…”