Helton de Sá Souza

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

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.

Short sleep duration and obesity: mechanisms and future perspectives

A reduction of sleep time has become common over the last century, and growing evidence from both epidemiological and laboratory‐based studies suggests sleep curtailment is a new risk factor for the development of obesity. On this basis, the present review examines the role of sleep curtailment in the metabolic and endocrine alterations, including decreased glucose tolerance and insulin sensitivity, increased evening concentrations of cortisol, increased levels of ghrelin, decreased levels of leptin and increased hunger and appetite. It will be discussed how sleep restriction may lead to increase in food intake and result in greater fatigue, which may favour decreased energy expenditure. Altogether, evidences point to a possible role of decreased sleep duration in the current epidemic of obesity and therefore present literature highlights the importance of getting enough good sleep for metabolic health. Many aspects still need to be clarified and intervention studies also need to be conducted. Copyright

Paradoxical sleep deprivation induces muscle atrophy

Introduction: Because paradoxical sleep deprivation (PSD) induces a catabolic hormone profile, we sought to evaluate the morphology of the tibialis anterior (TA) muscle and testosterone and corticosterone levels of paradoxical sleep–deprived rats.Methods: Three study groups of rats were established: the first group was sleep deprived for 96 h; the second group was also sleep deprived for 96 h, but then returned to their home‐cage and allowed to sleep for the next 96 h; and the third group was the control group, with a normal sleep cycle. Results: PSD reduced the weight and fiber cross‐sectional area of the TA muscle. Moreover, PSD enhanced plasma corticosterone and reduced serum testosterone levels. The 96 h of sleep after PSD was sufficient to restore partially the morphology of TA, while hormones returned to basal levels. Conclusion: PSD induces hormonal alterations that may mediate muscle atrophy. Muscle Nerve, 2012

Resistance training minimizes catabolic effects 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 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 bodys weight loss.

Exercise deprivation increases negative mood in exercise-addicted subjects and modifies their biochemical markers.

The aim of this study was to identify the possible association between biochemical markers of exercise addiction and affective parameters in a sample of athletes during 2weeks of withdrawal exercise. Eighteen male runners were distributed into a control group (n=10) composed of runners without exercise addiction symptoms and an exercise addiction group (n=8) composed of runners with exercise addiction symptoms. The volunteers performed a baseline evaluation that included affective questionnaires, blood samples, body composition and an aerobic test performed at ventilatory threshold I. After the baseline evaluation, the groups started an exercise withdrawal period that was sustained for 2weeks. During exercise withdrawal, an actigraph accelerometer was used to monitor the movement index, and CK and LDH were measured in blood samples to validate the non-exercise practice. At the end of the exercise withdrawal period, a blood collection, aerobic test and mood scale was performed in the re-test. The results showed that at the end of the experimental protocol, when compared with the control group, the exercise addiction group showed an increase in depression, confusion, anger, fatigue and decreased vigor mood that improved post-exercise, along with low levels of anandamide at all time-points evaluated and a modest increase in β-endorphin post-exercise. Moreover, the exercise addiction group showed a decrease in oxygen consumption and respiratory exchange ratio after the exercise withdrawal period, which characterized a detraining phenomenon. Our data suggest that a 2-week withdrawal exercise period resulted in an increase of negative mood in exercise addiction; additionally, exercise addiction showed low levels of anandamide.

Resistance exercise: A non-pharmacological strategy to minimize or reverse sleep deprivation-induced muscle atrophy

Sleep is important for maintenance of skeletal muscle health. Sleep debt can induce muscle atrophy by increasing glucocorticoids and decreasing testosterone, growth hormone and insulin-like growth factor-I. These hormonal alterations result in a highly proteolytic environment characterized by decreased protein synthesis and increased degradation. Given that sleep deprivation is increasingly prevalent in modern society, strategies to minimize or reverse its adverse effects need to be investigated. Resistance exercise has been suggested as an intervention that would benefit the muscle health. The practice of this type of exercise can increase the concentration of testosterone, growth hormone and insulin-like growth factor I and stimulate the protein synthesis through a key signaling molecule, mammalian target of rapamycin. Thus, we hypothesized that resistance exercise is an important non-pharmacological strategy to counteract deleterious effects of sleep debt on skeletal muscle.

Negative Energy Balance Induced by Paradoxical Sleep Deprivation Causes Multicompartmental Changes in Adipose Tissue and Skeletal Muscle

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.

Chronic Exercise Promotes Alterations in the Neuroendocrine Profile of Elderly People

Aging and physical inactivity are 2 factors that favour the development of cardiovascular disease, metabolic syndrome, obesity, and diabetes. In contrast, adopting a habitual moderate exercise routine may be a nonpharmacological treatment alternative for neuroendocrine aging disorders. We aimed to assess the effects of moderate exercise training on the metabolic profiles of elderly people with sedentary lifestyles. Fourteen sedentary, healthy, elderly male volunteers participated in a moderate training regimen for 60 min/day, 3 days/week for 24 weeks at a work rate equivalent to their ventilatory aerobic threshold. The environment was maintained at a temperature of 23±2°C, with a humidity of 60±5%. Blood samples for analysis were collected at 3 intervals: at baseline (1 week before training began), and 3 and 6 months after training. The training promoted increased aerobic capacity (relative VO(2), and time and velocity to VO(2)max; (p<0.05)) and reduced serum α-MSH (p<0.05) after 3 months of training when compared with the baseline data. In addition, serum thyroid hormone (T3 and T4) was reduced after 6 months of training compared with baseline levels. Our results demonstrate that a moderate exercise training protocol improves the metabolic profile of older people, and metabolic adaptation is dependent on time.

CrossFit Overview: Systematic Review and Meta-analysis

BackgroundCrossFit is recognized as one of the fastest growing high-intensity functional training modes in the world. However, scientific data regarding the practice of CrossFit is sparse. Therefore, the objective of this study is to analyze the findings of scientific literature related to CrossFit via systematic review and meta-analysis.MethodsSystematic searches of the PubMed, Web of Science, Scopus, Bireme/MedLine, and SciELO online databases were conducted for articles reporting the effects of CrossFit training. The systematic review followed the PRISMA guidelines. The Oxford Levels of Evidence was used for all included articles, and only studies that investigated the effects of CrossFit as a training program were included in the meta-analysis. For the meta-analysis, effect sizes (ESs) with 95% confidence interval (CI) were calculated and heterogeneity was assessed using a random-effects model.ResultsThirty-one articles were included in the systematic review and four were included in the meta-analysis. However, only two studies had a high level of evidence at low risk of bias. Scientific literature related to CrossFit has reported on body composition, psycho-physiological parameters, musculoskeletal injury risk, life and health aspects, and psycho-social behavior. In the meta-analysis, significant results were not found for any variables.ConclusionsThe current scientific literature related to CrossFit has few studies with high level of evidence at low risk of bias. However, preliminary data has suggested that CrossFit practice is associated with higher levels of sense of community, satisfaction, and motivation.

Paradoxical Sleep Deprivation Causes Cardiac Dysfunction and the Impairment Is Attenuated by Resistance Training

Background Paradoxical sleep deprivation activates the sympathetic nervous system and the hypothalamus-pituitary-adrenal axis, subsequently interfering with the cardiovascular system. The beneficial effects of resistance training are related to hemodynamic, metabolic and hormonal homeostasis. We hypothesized that resistance training can prevent the cardiac remodeling and dysfunction caused by paradoxical sleep deprivation. Methods Male Wistar rats were distributed into four groups: control (C), resistance training (RT), paradoxical sleep deprivation for 96 hours (PSD96) and both resistance training and sleep deprivation (RT/PSD96). Doppler echocardiograms, hemodynamics measurements, cardiac histomorphometry, hormonal profile and molecular analysis were evaluated. Results Compared to the C group, PSD96 group had a higher left ventricular systolic pressure, heart rate and left atrium index. In contrast, the left ventricle systolic area and the left ventricle cavity diameter were reduced in the PSD96 group. Hypertrophy and fibrosis were also observed. Along with these alterations, reduced levels of serum testosterone and insulin-like growth factor-1 (IGF-1), as well as increased corticosterone and angiotensin II, were observed in the PSD96 group. Prophylactic resistance training attenuated most of these changes, except angiotensin II, fibrosis, heart rate and concentric remodeling of left ventricle, confirmed by the increased of NFATc3 and GATA-4, proteins involved in the pathologic cardiac hypertrophy pathway. Conclusions Resistance training effectively attenuates cardiac dysfunction and hormonal imbalance induced by paradoxical sleep deprivation.