Purpose: Sleep is considered essential for muscle recovery, mainly due to its effect on hormone secretion. Total sleep deprivation or restriction is known to alter not only blood hormones but also cytokines that might be related to skeletal muscle recovery. This study aimed to evaluate whether total sleep deprivation after eccentric exercise-induced muscle damage (EEIMD) modifies the profiles of blood hormones and cytokines. Methods: In two separate conditions, with a crossover and randomized model, 10 men (age, 24.5 ± 2.9 yr; body mass index, 22.7 ± 2.3 kg·m⁻²) performed a unilateral EEIMD protocol that comprised 240 eccentric contractions of the knee extensor muscles using an isokinetic dynamometer. In one condition, a “muscle damage” protocol was followed by 48 h of total sleep deprivation and 12 h of normal sleep (DEPRIVATION). In the other condition, the same muscle damage protocol was conducted, followed by three nights of regular sleep (SLEEP). Isometric muscle voluntary contraction tests and blood samples were collected serially throughout the protocol and analyzed for creatine kinase, free and total testosterone, IGF-1, cortisol, tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6, receptor antagonist of IL-1 and IL-10. Results: Muscle voluntary contraction and serum creatine kinase increased equally over the study period in both conditions. From the cytokines evaluated, only IL-6 increased in DEPRIVATION. No differences were detected in testosterone levels between conditions, but IGF-1, cortisol, and cortisol/total testosterone ratio were higher in DEPRIVATION. Conclusions: Total sleep deprivation after EEIMD does not delay muscle strength recovery but modifies inflammatory and hormonal responses.

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 1 of 5 groups: control, sham, SD (for 96 h), RT, and RT+SD. The major outcomes of this study were muscle fiber cross-sectional area (CSA), anabolic and catabolic hormone profiles, and the abundance of select proteins involved in muscle protein synthesis and degradation pathways. SD resulted in muscle atrophy; however, when SD was combined with RT, the reduction in muscle fiber CSA was attenuated. The levels of IGF-1 and testosterone were reduced in SD animals, and the RT+SD group had higher levels of these hormones than the SD group. Corticosterone was increased in the SD group compared with the control group, and this increase was minimized in the RT+SD group. The increases in corticosterone concentrations paralleled changes in the abundance of ubiquitinated proteins and the autophagic proteins LC3 and p62/SQSTM1, suggesting that corticosterone may trigger these changes. SD induced weight loss, but this loss was minimized in the RT+SD group. We conclude that SD induced muscle atrophy, probably because of the increased corticosterone and catabolic signal. High-intensity RT performed before SD was beneficial in containing muscle loss induced by SD. It also minimized the catabolic signal and increased synthetic activity, thereby minimizing the body’s weight loss.

The aim was observe the influence of sleep deprivation (SD) and sleep recovery on muscle regeneration process in rats submitted to cryolesion. Thirty-two Wistar rats were randomly allocated in four groups: control (CTL), SD for 96 h (SD96), control plus sleep recovery period (CTL + R) and SD96h plus 96 h of sleep recovery (SD96 + R). The animals were submitted to muscle injury by cryolesioning, after to SD and sleep recovery. The major outcomes of this study were the reduction of muscular IGF-1 in both legs (injured and uninjured) and a delay in muscle regeneration process of animals submitted to SD compared to animals that slept, with increase connective tissue, inflammatory infiltrate and minor muscle fibers. SD impairs muscle regeneration in rats, moreover reduces muscular IGF-1 and sleep recovery was able to restore it to basal levels, but it was not enough to normalize the muscle regeneration.

Objective.Describe multicompartmental changes in the fat and various muscle fiber types, as well as the hormonal profile and metabolic rate induced by SD in rats.Methods.Twenty adult male Wistar rats were equally distributed into two groups: experimental group (EG) and control group (CG). The EG was submitted to SD for 96 h. Blood levels of corticosterone (CORT), total testosterone (TESTO), insulin like growth factor-1 (IGF-1), and thyroid hormones (T3 and T4) were used to assess the catabolic environment. Muscle trophism was measured using a cross-sectional area of various muscles (glycolytic, mixed, and oxidative), and lipolysis was inferred by the weight of fat depots from various locations, such as subcutaneous, retroperitoneal, and epididymal. The metabolic rate was measured using oxygen consumption (V˙O₂) measurement.Results.SD increased CORT levels and decreased TESTO, IGF-1, and T4. All fat depots were reduced in weight after SD. Glycolytic and mixed muscles showed atrophy, whereas atrophy was not observed in oxidative muscle.Conclusion.Our data suggest that glycolytic muscle fibers are more sensitive to atrophy than oxidative fibers during SD and that fat depots are reduced regardless of their location.