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Exosome release varies depending on the physiological state of the cell, so they could play a fundamental role in obesity, the biggest pandemic in today's societies. The beneficial effects that physical activity has both on weight and cardiovascular parameters may be mediated by exosomes released in response to exercise. Thus, we aimed (I) to study the influence of a 12-week CT intervention on exosome cargo modifications in men with obesity and (II) to determine whether changes in exosomes after the intervention were related to changes in cardiometabolic health parameters in our cohorts. An experimental, controlled design was performed in twelve (nine with valid data) adult male obese patients (mean values: 41.6 years old, 97.6 kg and 32.4 kg/m2) who were randomly divided into a control group (n = 4) and a training group (n = 5), which completed 36 sessions of CT (concurrent training) for 12 weeks. Before and after the training period, cardiometabolic health parameters were evaluated and blood samples to measure exosomes and proteins were drawn. No changes were observed in the levels of any exosomal markers and proteins; however, associations of changes between CD81 and both fat mass and weight, Flot-1 and VO2max, HSP70 and both CRP and left ventricle diastolic diameter or CD14 and leptin were found (all p ≤ 0.05). Although the current CT was not able to clearly modify the exosome cargo, a certain medium to large clinical effect was manifested considering the nature of this study. Moreover, the associations found between the promoted changes in cardiometabolic parameters and exosome-carried proteins could indicate a relationship to be considered for future treatments in patients with obesity. [ABSTRACT FROM AUTHOR]

Exercise‐released exosomes have been identified as novel players to mediate cell‐to‐cell communication in promoting systemic beneficial effects. This review aimed to systematically investigate the effects of exercise on exosome release and cargo, as well as provide an overview of their physiological implications. Among the 436 articles obtained in the database search (WOS, Scopus, and PubMed), 19 articles were included based on eligibility criteria. Results indicate that exercise promotes the release of exosomes without modification of its vesicle size. The literature has primarily shown an exercise‐driven increase in exosome markers (Alix, CD63, CD81, and Flot‐1), along with other exosome‐carried proteins, into circulation. However, exosome isolation, characterization, and phenotyping methodology, as well as timing of sample recovery following exercise can influence the analysis and interpretation of findings. Moreover, a large number of exosome‐carried microRNAs (miRNAs), including miR‐1, miR‐133a, miR‐133b, miR‐206, and miR‐486, in response to exercise are involved in the modulation of proliferation and differentiation of skeletal muscle tissue, although antigen‐presenting cells, leukocytes, endothelial cells, and platelets are the main sources of exosome release into the circulation. Collectively, with the physiological implications as evidenced by the ex vivo trials, the release of exercise‐promoted exosomes and their cargo could provide the potential therapeutic applications via the role of intercellular communication. [ABSTRACT FROM AUTHOR]

Key points An early inflammatory response and oxidative stress are implicated in the signal transduction that alters both hepatic redox status and mitochondrial function after traumatic brain injury (TBI)., Peripheral oxidative/inflammatory responses contribute to neuronal dysfunction after TBI, Exercise training alters the profile of oxidative-inflammatory status in liver and protects against acute hyperglycaemia and a cerebral inflammatory response after TBI., Approaches such as exercise training, which attenuates neuronal damage after TBI, may have therapeutic potential through modulation of responses by metabolic organs., The vulnerability of the body to oxidative/inflammatory in TBI is significantly enhanced in sedentary compared to physically active counterparts., Abstract Although systemic responses have been described after traumatic brain injury (TBI), little is known regarding potential interactions between brain and peripheral organs after neuronal injury. Accordingly, we aimed to investigate whether a peripheral oxidative/inflammatory response contributes to neuronal dysfunction after TBI, as well as the prophylactic role of exercise training. Animals were submitted to fluid percussion injury after 6 weeks of swimming training. Previous exercise training increased mRNA expression of X receptor alpha and ATP-binding cassette transporter, and decreased inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor (TNF)-α and interleukin (IL)-6 expression per se in liver. Interestingly, exercise training protected against hepatic inflammation (COX-2, iNOS, TNF-α and IL-6), oxidative stress (decreases in non-protein sulfhydryl and glutathione, as well as increases in 2′,7′-dichlorofluorescein diacetate oxidation and protein carbonyl), which altered hepatic redox status (increases in myeloperoxidase and superoxide dismutase activity, as well as inhibition of catalase activity) mitochondrial function (decreases in methyl-tetrazolium and Δψ, as well as inhibition of citrate synthase activity) and ion gradient homeostasis (inhibition of Na+,K+-ATPase activity inhibition) when analysed 24 h after TBI. Previous exercise training also protected against dysglycaemia, impaired hepatic signalling (increase in phosphorylated c-Jun NH2-terminal kinase, phosphorylated decreases in insulin receptor substrate and phosphorylated AKT expression), high levels of circulating and neuronal cytokines, the opening of the blood-brain barrier, neutrophil infiltration and Na+,K+-ATPase activity inhibition in the ipsilateral cortex after TBI. Moreover, the impairment of protein function, neurobehavioural (neuromotor dysfunction and spatial learning) disability and hippocampal cell damage in sedentary rats suggests that exercise training also modulates peripheral oxidative/inflammatory pathways in TBI, which corroborates the ever increasing evidence regarding health-related outcomes with respect to a physically active lifestyle. [ABSTRACT FROM AUTHOR]

This study investigated in older adults whether whole-body vibration (WBV) training results in significant increases of physical fitness measures without alterations in markers of inflammation. Sixteen volunteers completed a WBV programme 3 d.wk−1 during 9 weeks. The programme consisted of lower and upper-body unloaded static and dynamic exercises. Training improved significantly several tests which evaluate physical fitness, such as 30-s chair stand, arm curl or chair sit and reach test. There was a significant increase in maximal voluntary isometric contraction (MVIC) between pre- and post-training conditions. Muscle power values, reached at 20, 40 and 60% MVIC, were also significantly greater after training. However, mRNA or protein levels for C-reactive protein, interleukin-6, interleukin-1β, tumour necrosis factor-α and interleukin-10 did not significantly differ from basal values. Our data confirm the usefulness of WBV training for counteracting the loss of muscle strength associated with sarcopenia in older adults and show that WBV training could be a safe training method which induces no inflammatory effects. [ABSTRACT FROM AUTHOR]

Aging-associated inflammation is characterized by senescent cell-mediated secretion of high levels of inflammatory mediators, such as microRNA (miR)-146a. Moreover, a rise of circulating cell-free DNA (cfDNA) is also related to systemic inflammation and frailty in the elderly. Exosome-mediated cell-to-cell communication is fundamental in cellular senescence and aging. The plasma changes in exercise-promoted miR-146a-5p, cfDNA, and exosome release could be the key to facilitate intercellular communication and systemic adaptations to exercise in aging. Thirty-eight elderly subjects (28 trained and 10 controls) volunteered in an 8-week resistance training protocol. The levels of plasma miR-146a-5p, cfDNA, and exosome markers (CD9, CD14, CD63, CD81, Flotillin [Flot]-1, and VDAC1) were measured prior to and following training. Results showed no changes in plasma miR-146a-5p and cfDNA levels with training. The levels of exosome markers (Flot-1, CD9, and CD81) as well as exosome-carried proteins (CD14 and VDAC1) remained unchanged, whereas an attenuated CD63 response was found in the trained group compared to the controls. These findings might partially support the anti-inflammatory effect of resistance training in the elderly as evidenced by the diminishment of exosome CD63 protein expression, without modification of plasma miR-146a-5p and cfDNA. [ABSTRACT FROM AUTHOR]

Infrared thermography (IT) makes it possible to assess body temperature, measure changes in body heat dissipation on the surface, and relate them to body composition characteristics and anthropometric indices. The objective of this study was to increase the number of records of body areas evaluated with IT and establish the relationships of these temperatures (32 body areas) with body composition variables and anthropometric indices, such as body mass index (BMI), waist-hip ratio, waist-height ratio, in adult men divided according to their weight status. A total of 60 healthy adult men participated, divided into 2 groups: group 1 (n=30), with a body mass index (BMI) £ 24.9, age 23.2 ± 3.9 years, body mass 66.5 ± 6.5 kg, and height 170.5 ± 7.4 cm; and, group 2 (n = 30), with BMI > 24.9, age 29.4 ± 9.9 years, body mass 84.5 ± 11.9 kg, and height 172.0 ± 7.18 cm. Anthropometric and IT assessments were performed. Subjects with BMI £ 24.9 kg/m2 presented higher values of surface temperature in all areas studied, unlike subjects with BMI levels > 24.9 kg/m2, where body heat dissipation was lower. There is a close relationship between skin surface temperature and BMI, where subjects with a normal BMI showed higher heat dissipation and surface temperature values, in all evaluated areas, unlike subjects with a BMI that was above the normal limit. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the effect of eccentric exercise on the expression of the different nitric oxide synthase (NOS) isoforms in rat deep vastus lateralis muscle. Twenty-four rats were allocated to four experimental groups: rested control group, acutely exercised group after an intermittent downhill protocol for 90 min, acutely exercised group treated with pyrrolidine dithiocarbamate (100 mg/kg ip) for 24 and 1 h before the acute exercise bout, and acutely exercised group with a previous submaximal eccentric training of 8 wk. Acutely exercised rats showed increased levels of protein tyrosine nitration, NF-kappaB binding, and phospho-I kappaB alpha content. A significant increase was observed in mRNA level and protein content of neuronal NOS, inducible NOS, and endothelial NOS. The binding of NF-kappaB to the NOS isoform promoters, measured by a chromatin immunoprecipitation assay, was undetectable in rested rats, whereas it was evident in acutely exercised animals. All of these effects were partially abolished by pyrrolidine dithiocarbamate treatment and by training. In summary, our findings provide a direct link between the NF-kappaB signaling cascade and NOS expression in skeletal muscle following eccentric exercise and suggest a modulation of the expression of the three NOS isoforms by this transcription factor.

Purpose: Changes in nuclear factor kappaB (NF-kappaB) activation induced in peripheral blood mononuclear cells (PBMC) by acute eccentric exercise and by submaximal eccentric training were investigated., Methods: Eleven subjects carried out two bouts of eccentric exercise separated by 6 wk of training., Results: Soreness, vertical jump height, and plasma creatine kinase were significantly modified after the first bout. NF-kappaB activation, p50 and p65, phospho-IkappaBalpha and phospho-IKK protein level, and Mn-SOD expression increased in PBMC, whereas IkappaBalpha protein level was significantly reduced. Changes were significantly attenuated after the second exercise bout. An additional group of nine subjects carried out the two bouts of exercise without training. Effects on NF-kappaB activation were similar after the second bout compared with the first, despite a reduction in markers of muscle injury (repeated bout effect)., Conclusion: Training significantly attenuates the NF-kappaB-dependent pathway changes induced in PBMC by eccentric exercise, with no contribution from the repeated bout effect.

This study was aimed to investigate changes in blood markers of oxidative damage induced by short-term supramaximal anaerobic exercise and to determine whether oxidative stress was associated to activation of the redox-sensitive transcription factor nuclear factor-kappaB (NF-kappaB). Both a single Wingate test (WAnT) test and series of four WAnTs separated by 60 min rest intervals were carried out by eight professional cyclists. Leukocyte 8-OH-2-deoxyguanosine levels were significantly elevated 24 h after both exercise protocols. A significant decrease in blood reduced glutathione (GSH) concentration was observed immediately after and at 15, 60 and 120 min of the single WAnT, followed by a return to basal value after 24 h. This decrease was parallel to a significant increase of the oxidised/reduced glutathione (GSSG/GSH) ratio, to an activation of NF-kappaB and to a significant decrease in the protein level of its inhibitor IkappaB. GSH concentration and the GSSG/GSH ratio changed significantly for the first three of the WAnTs series and normalised thereafter. A significant activation of NF-kappaB and a decrease in the IkappaB protein level were also detected. We conclude that short-term supramaximal anaerobic exercise induces oxidative stress, as evidenced by non cumulative damage to macromolecules and changes in the glutathione status. Our data also indicate that high intensity anaerobic work gives rise to an activation of the transcription factor NF-kappaB accompanied by a degradation of IkappaB.