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The skeletal muscle was always seen from biomechanical and biochemical views. It is well-established that an active muscle brings many benefits for different body organs and tissues, including the immune system. Since the 1970s, many studies have shown the importance of regular exercise and physical activity in increasing the body's ability to fight opportunist infections, as well as a strategy to fight established diseases. This interaction was mainly attributed to the glutamine, a non-essential amino acid produced by the active skeletal muscle and primarily consumed by rapidly dividing cells, including lymphocytes and monocytes/macrophages, as their main source of energy. Therefore, these cells' function would be significantly improved by the presence of a bigger glutamine pool, facilitating phagocytosis, antigen-presentation, proliferative capacity, cytokine synthesis and release, among other functions. Despite its importance, glutamine is not the only molecule to connect these two tissues. The presence of cytokines is crucial for a proper immune system function. Many of them have well-established pro-inflammatory properties, while others are known for their anti-inflammatory role. Interleukin-6 (IL-6), however, has been in the center of many scientific discussions since it can act as pro- and anti-inflammatory cytokine depending on the tissue that releases it. Skeletal muscle is an essential source of IL-6 with anti-inflammatory properties, regulating the function of the immune cells after tissue injury and the healing process. Therefore, this review aims to discuss further the role of these four components (glutamine, and interleukin-6, and its interface with monocytes/macrophages, and lymphocytes) on the communication between the skeletal muscle and the immune system.

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Probiotic supplementation arises as playing an immune-stimulatory role. High-intensity and -volume exercise can inhibit immune cell function, which threatens athletic performance and recovery. We hypothesized that 30 days of probiotic supplementation could stabilize the immune system of athletes preventing immune suppression after a marathon race. Twenty-seven male marathonists were double-blinded randomly into probiotic (Bifidobacterium-animalis-subsp.-Lactis (10 × 109) and Lactobacillus-Acidophilus (10 × 109) + 5 g of maltodextrin) and placebo (5 g of maltodextrin) group. They received 30 sachets and supplemented 1 portion/day during 30 days before the race. Blood were collected 30 days before (rest), 1 day before (pre), 1 h after (post) and 5 days after the race (recovery). Both chronic and acute exercise modulated a different T lymphocyte population (CD3+CD4-CD8- T-cells), increasing pre-race, decreasing post and returning to rest values at the recovery. The total number of CD8 T cell and the memory subsets statistically decreased only in the placebo group post-race. Pro-inflammatory cytokine production by stimulated lymphocytes decreased in the probiotic group after the supplementation period. 30 days of probiotic supplementation maintained CD8 T cell and effector memory cell population and played an immunomodulatory role in stimulated lymphocytes. Both, training and marathon modulated a non-classical lymphocyte population regardless of probiotic supplementation.

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Skeletal muscle strength and mass, major contributors to sprint/power athletic performance, are influenced by genetics. However, to date, only a handful of genetic variants have been associated with sprint/power performance. The ACVR1B A allele (rs rs2854464) has previously been associated with increased muscle-strength in non-athletic cohort. However, no follow-up and/or replications studies have since been conducted. Therefore, the aim of the present study was to compare the genotype distribution of ACVR1B rs2854464 between endurance athletes (E), sprint/power (S/P) athletes, mixed athletes (M), and non-athletic control participants in 1672 athletes (endurance athletes, n = 482; sprint/power athletes, n = 578; mixed athletes, n = 498) and 1089 controls (C) of both European Caucasians (Italian, Polish and Russians) and Brazilians. We have also compared the genotype distribution according to the athlete's level of competition (elite vs. sub-elite). DNA extraction and genotyping were performed using various methods. Fisher's exact test (adjusted for multiple comparisons) was used to test whether the genotype distribution of rs2854464 (AA, AG and GG) differs between groups. The A allele was overrepresented in S/P athletes compared with C in the Caucasian sample (adjusted p = 0.048), whereas there were no differences in genotype distribution between E athletes and C, in neither the Brazilian nor the Caucasian samples (adjusted p > 0.05). When comparing all Caucasian athletes regardless of their sporting discipline to C, we found that the A allele was overrepresented in athletes compared to C (adjusted p = 0.024). This association was even more pronounced when only elite-level athletes were considered (adjusted p = 0.00017). In conclusion, in a relatively large cohort of athletes from Europe and South America we have shown that the ACVR1B rs2854464 A allele is associated with sprint/power performance in Caucasians but not in Brazilian athletes. This reinforces the notion that phenotype-genotype associations may be ethnicity-dependent.

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The purpose of this study was to verify the association between ACTN3 polymorphism and physiological parameters related to endurance performance. A total of 150 healthy male volunteers performed a maximal incremental running test to determine the speeds corresponding to ventilatory threshold (VT) and respiratory compensation point (RCP). Participants were genotyped and divided into terciles based on the analysed variables. Genotype frequencies were compared through χ(2) test between lower and higher terciles, with the lowest or highest values of each analysed variable. ACTN3 XX genotype was over-represented in higher tercile for VT and RCP. Odds ratio also showed significantly higher chances of XX individuals to be in higher tercile compared to RR (7.3) and RR + RX (3.5) for VT and compared to RR genotype (8.1) and RR + RX (3.4) for RCP. Thus, XX individuals could attain the VT and RCP at higher speeds, suggesting that they are able to sustain higher running speeds in lower exercise intensity domains. It could result in higher lipid acids oxidation, saving muscle glycogen and delaying the fatigue during prolonged exercises, which could be the advantage mechanism of this genotype to endurance performance.

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This study explored the effects of Health at Every Size(®)-based intervention on obese women by qualitatively evaluating participants' perception toward the program and quantitatively evaluating changes related to psychological, behavioral, and body composition assessments. A prospective 1-year quasi-experimental mixed-method trial was conducted. The mixed-method design was characterized by a spiral method, and quantitative and qualitative findings were combined during the interpretation phase. The qualitative data involved three focus groups; and quantitative data comprised physiological, psychological, and behavioral assessments. Initially, 30 participants were recruited; 14 concluded the intervention. From the focus groups, the following interpretative axes were constructed: the intervention as a period of discoveries; shifting parameters: psychological, physical, and behavioral changes; eating changes, and; redefining success. Body weight, body mass index, total body fat mass, and body fat percentage were significantly decreased after the intervention (-3.6, -3.2, -13.0, and -11.1%, respectively; p ≤ 0.05, within-time effect). Participants reported to be more physically active and perceiving better their bodies. Eating-wise, participants reported that the hunger and satiety cues and the consumption of more frequent meals facilitated their eating changes. Finally, participants reported that they could identify feelings with eating choices and refrain from the restrained behavior. These qualitative improvements were accompanied by modest but significant improvements in quantitative assessments. Clinicaltrials.gov registration: NCT02102061.

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Sarcopenia describes an age-related decline in skeletal muscle mass, strength, and function that ultimately impairs metabolism and leads to poor balance, frequent falling, limited mobility, and a reduction in quality of life. Here we investigate the pathogenesis of sarcopenia through a proteomic shotgun approach. In brief, we employed tandem mass tags to quantitate and compare the protein profiles obtained from young versus old rat slow-twitch type of muscle (soleus) and a fast-twitch type of muscle (extensor digitorum longus, EDL). Our results disclose 3452 and 1848 proteins identified from soleus and EDL muscles samples, of which 78 and 174 were found to be differentially expressed, respectively. In general, most of the proteins were structural related and involved in energy metabolism, oxidative stress, detoxification, or transport. Aging affected soleus and EDL muscles differently, and several proteins were regulated in opposite ways. For example, pyruvate kinase had its expression and activity different in both soleus and EDL muscles. We were able to verify with existing literature many of our differentially expressed proteins as candidate aging biomarkers and, most importantly, disclose several new candidate biomarkers such as the glioblastoma amplified sequence, zero ß-globin, and prolargin.

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BACKGROUND: Studies failing to show a negative effect of rapid weight loss (RWL) on performance have been conducted in athletes who have been cycling weight for years. It has been suggested that chronic weight cycling could lead combat athletes to become resistant to the stresses associated with weight loss. To investigate the effects of RWL up to 5% of body mass on high-intensity intermittent performance in weight cyclers (WC) and non-weight cyclers (non-WC). METHODS: Eighteen male combat athletes (WC: n=10; non-WC: n=8) reduced up to 5% of their body mass in 5 days. Body composition, high-intensity performance and plasma lactate were assessed preweight loss and postweight loss. Athletes had 4 h to re-feed and rehydrate following the weigh-in. Food intake was recorded during the weight loss and the recovery periods. RESULTS: Athletes significantly decreased body mass, lean body mass (most likely due to fluid loss) and fat mass following weight loss. No significant changes in performance were found from preweight loss to postweight loss in both groups. Plasma lactate was significantly elevated after exercise in both groups, but no differences were found between groups and in response to RWL. For all these variables no differences were observed between groups. Athletes from both groups ingested high amounts of energy and carbohydrates during the recovery period after the weigh-in. CONCLUSIONS: Chronic weight cycling does not protect athletes from the negative impact of RWL on performance. The time to recover after weigh-in and the patterns of food and fluid ingestion during this period is likely to play the major role in restoring performance to baseline levels.

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Studies have been conducted in order to identify the main factors that contribute to the development of obesity. The role of genetics has also been extensively studied. However, the substantial augmentation of obesity prevalence in the last 20 years cannot be justified only by genetic alterations that, theoretically, would have occurred in such a short time. Thus, the difference in obesity prevalence in various population groups is also related to environmental factors, especially diet and the reduction of physical activity. These aspects, interacting or not with genetic factors, could explain the excess of body fat in large proportions worldwide. This article will focus on positive energy balance, high-fat diet, alteration in appetite control hormones, insulin resistance, amino acids metabolism, and the limitation of the experimental models to address this complex issue.

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BACKGROUND: Exacerbated oxidative stress is thought to be a mediator of arterial hypertension. It has been postulated that creatine (Cr) could act as an antioxidant agent preventing increased oxidative stress. The aim of this study was to investigate the effects of nine weeks of Cr or placebo supplementation on oxidative stress and cardiovascular parameters in spontaneously hypertensive rats (SHR). FINDINGS: Lipid hydroperoxidation, one important oxidative stress marker, remained unchanged in the coronary artery (Cr: 12.6 ± 1.5 vs. Pl: 12.2 ± 1.7 nmol·mg-1; p = 0.87), heart (Cr: 11.5 ± 1.8 vs. Pl: 14.6 ± 1.1 nmol·mg-1; p = 0.15), plasma (Cr: 67.7 ± 9.1 vs. Pl: 56.0 ± 3.2 nmol·mg-1; p = 0.19), plantaris (Cr: 10.0 ± 0.8 vs. Pl: 9.0 ± 0.8 nmol·mg-1; p = 0.40), and EDL muscle (Cr: 14.9 ± 1.4 vs. Pl: 17.2 ± 1.5 nmol·mg-1; p = 0.30). Additionally, Cr supplementation affected neither arterial blood pressure nor heart structure in SHR (p > 0.05). CONCLUSIONS: Using a well-known experimental model of systemic arterial hypertension, this study did not confirm the possible therapeutic effects of Cr supplementation on oxidative stress and cardiovascular dysfunction associated with arterial hypertension.