Oxygen reactive species (ORE) are usually produced by the body metabolism. However, ORE present the ability to remove electrons from other cellular composites, being able to cause oxidative injuries in several molecules. Such fact leads to a total loss of cellular function. Physical exercise practice increases ORE synthesis, besides promoting muscular injury and inflammation. After a physical exercise set, the recovery phase begins, where several effects positive to health are observed, including increase in resistance to new injuries induced or not by exercise, a fact which is considered an 'adaptation' process. Many studies though, have reported that this recovery is not reached by individuals who are submitted to intense and extended exercises, or even, who have high training frequency. Nutritional alternatives have been widely studied, in order to reduce the effects promoted by extenuating exercise, among which vitamin E, vitamin C, creatine and glutamine supplementation is included. This review has the aim to approach the current aspects concerning the ORE formation, the cellular injury and inflammation processes, the adaptation to the kinds of aerobic and anaerobic exercise, besides possible nutritional interventions.

Oral supplementations with GLN+ALA or DIP are effective in attenuating oxidative stress and the proinflammatory responses induced by endotoxemia in mice.

In this study, we investigated the effect of the supplementation with the dipeptide L-alanyl-L-glutamine (DIP) and a solution containing L-glutamine and L-alanine on plasma levels markers of muscle damage and levels of pro-inflammatory cytokines and glutamine metabolism in rats submitted to prolonged exercise. Rats were submitted to sessions of swim training for 6 weeks. Twenty-one days prior to euthanasia, the animals were supplemented with DIP (n = 8) (1.5 g.kg(-1)), a solution of free L-glutamine (1 g.kg(-1)) and free L-alanine (0.61 g.kg(-1)) (G&A, n = 8) or water (control (CON), n = 8). Animals were killed at rest before (R), after prolonged exercise (PE-2 h of exercise). Plasma concentrations of glutamine, glutamate, tumour necrosis factor-alpha (TNF-alpha), prostaglandin E2 (PGE2) and activity of creatine kinase (CK), lactate dehydrogenase (LDH) and muscle concentrations of glutamine and glutamate were measured. The concentrations of plasma TNF-alpha, PGE2 and the activity of CK were lower in the G&A-R and DIP-R groups, compared to the CON-R. Glutamine in plasma (p < 0.04) and soleus muscle (p < 0.001) was higher in the DIP-R and G&A-R groups relative to the CON-R group. G&A-PE and DIP-PE groups exhibited lower concentrations of plasma PGE2 (p < 0.05) and TNF-alpha (p < 0.05), and higher concentrations of glutamine and glutamate in soleus (p < 0.001) and gastrocnemius muscles (p < 0.05) relative to the CON-PE group. We concluded that supplementation with free L-glutamine and the dipeptide LL-alanyl-LL-glutamine represents an effective source of glutamine, which may attenuate inflammation biomarkers after periods of training and plasma levels of CK and the inflammatory response induced by prolonged exercise.

In this article, we discuss inflammation associated with adipose tissue dysfunction as a potential link with obesity-related insulin resistance, and how obesity-related inflammatory components, such as immune cells, cytokines/chemokines and adipocytokines, induce obesity-related pathologies.

Therapies that improve leptin sensitivity have potential as an alternative treatment approach against obesity and related comorbidities. We investigated the effects of Socs3 gene ablation in different mouse models to understand the role of SOCS3 in the regulation of leptin sensitivity, diet-induced obesity (DIO) and glucose homeostasis. Neuronal deletion of SOCS3 partially prevented DIO and improved glucose homeostasis. Inactivation of SOCS3 only in LepR-expressing cells protected against leptin resistance induced by HFD, but did not prevent DIO. However, inactivation of SOCS3 in LepR-expressing cells protected mice from diet-induced insulin resistance by increasing hypothalamic expression of Katp channel subunits and c-Fos expression in POMC neurons. In summary, the regulation of leptin signaling by SOCS3 orchestrates diet-induced changes on glycemic control. These findings help to understand the molecular mechanisms linking obesity and type 2 diabetes, and highlight the potential of SOCS3 inhibitors as a promising therapeutic approach for the treatment of diabetes.

In trained rats, oral supplementation with DIP or GLN+ALA solution increased the expression of muscle HSP70, favored muscle l-glutamine/GSH status and improved redox defenses, which attenuate markers of muscle damage, thus improving the beneficial effects of high-intensity exercise training.

Glutamine is a conditionally essential amino acid widely used in sports nutrition, especially because of its immunomodulatory role. Notwithstanding, glutamine plays several other biological functions, such as cell proliferation, energy production, glycogenesis, ammonia buffering, maintenance of the acid-base balance, among others. Thus, this amino acid began to be investigated in sports nutrition beyond its effect on the immune system, attributing to glutamine various properties, such as an anti-fatigue role. Considering that the ergogenic potential of this amino acid is still not completely known, this review aimed to address the main properties by which glutamine could delay fatigue, as well as the effects of glutamine supplementation, alone or associated with other nutrients, on fatigue markers and performance in the context of physical exercise. PubMed database was selected to examine the literature, using the keywords combination “glutamine” and “fatigue”. Fifty-five studies met the inclusion criteria and were evaluated in this integrative literature review. Most of the studies evaluated observed that glutamine supplementation improved some fatigue markers, such as increased glycogen synthesis and reduced ammonia accumulation, but this intervention did not increase physical performance. Thus, despite improving some fatigue parameters, glutamine supplementation seems to have limited effects on performance.

We evaluated the effects of chronic oral supplementation with L-glutamine and L-alanine in their free form or as the dipeptide L-alanyl-L-glutamine (DIP) on muscle damage, inflammation and cytoprotection, in rats submitted to progressive resistance exercise (RE). Wistar rats (n 8/group) were submitted to 8-week RE, which consisted of climbing a ladder with progressive loads. In the final 21 d before euthanasia, supplements were delivered in a 4 % solution in drinking water. Glutamine, creatine kinase (CK), lactate dehydrogenase (LDH), TNF-α, specific IL (IL-1β, IL-6 and IL-10) and monocyte chemoattractant protein-1 (MCP-1) levels were evaluated in plasma. The concentrations of glutamine, TNF-α, IL-6 and IL-10, as well as NF-κB activation, were determined in extensor digitorum longus (EDL) skeletal muscle. HSP70 level was assayed in EDL and peripheral blood mononuclear cells (PBMC). RE reduced glutamine concentration in plasma and EDL (P < 0·05 v. sedentary group). However, L-glutamine supplements (L-alanine plus L-glutamine (GLN + ALA) and DIP groups) restored glutamine levels in plasma (by 40 and 58 %, respectively) and muscle (by 93 and 105 %, respectively). GLN + ALA and DIP groups also exhibited increased level of HSP70 in EDL and PBMC, consistent with the reduction of NF-κB p65 activation and cytokines in EDL. Muscle protection was also indicated by attenuation in plasma levels of CK, LDH, TNF-α and IL-1β, as well as an increase in IL-6, IL-10 and MCP-1. Our study demonstrates that chronic oral L-glutamine treatment (given with L-alanine or as dipeptide) following progressive RE induces cyprotective effects mediated by HSP70-associated responses to muscle damage and inflammation.