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• W2897729042 abstract "Exercise is a well-documented, non-pharmaceutical intervention with the potential to impact upon the various comorbidities associated with obesity. While often considered for its contribution to cardiovascular health, endurance exercise in particular may play an important role in the reduction of the low-grade systemic inflammation that is associated with obesity and metabolic dysfunction. The increase in cytokine production associated with activated inflammatory pathways may portend disruption in lipid metabolism, thereby actively contributing to the development of atherosclerosis and other major health issues associated with a chronic inflammatory state (Ridker et al. 2000). Thus, a greater understanding of the role of early inflammatory mediators may aid in predicting inflammatory potential and capacity for deterioration. Circulating progenitor cells (CPCs) are a relatively nondescript cell group comprising endothelial progenitor cells (EPCs), mesenchymal stem cells (MSCs) and haematopoietic stem cells (HSCs), which further differentiate into haematopoietic stem/progenitor cells (HSPCs). HSPC populations, when stimulated, potentiate myeloid lineages that eventually form key inflammatory cells. In addition, CPC levels have previously been shown to be elevated in the peripheral tissues of obese individuals, thus suggesting that these cell types may represent a surrogate marker for inflammatory potential (Bellows et al. 2011). In order to determine the true effect of an endurance exercise training (EET) regimen on CPC population differentiation, Niemiro et al. (2018) studied both lean and obese individuals enrolled in a closely monitored EET protocol, in an article in a recent issue of The Journal of Physiology. This is the first study to consider the effect of a strict 6-week steady-state EET programme on CPC differentiation specifically within an obese adult population. The group conducted the study with the hypothesis that EET would decrease the quantity of HSPCs expressing inflammatory markers as well as the relative quantity of differentiated inflammatory cells in obese individuals when compared to lean individuals on the same programme. Niemiro and colleagues appear to draw from the cohort of sedentary lean (n = 17; BMI 22 ± 2.6 kg m−2) and obese individuals (n = 10; BMI 33.1 ± 6.0 kg m−2) that were previously investigated for exercise-related shifts in intestinal microbiome composition and functionality by Allen and colleagues (2018). Although the group sample sizes are notably low, it is notoriously difficult to recruit and retain participants within exercise studies due to the considerable temporal and physical commitment required of them. In line with this, the authors demonstrate excellent trial management in attaining complete compliance from all participants, thereby bolstering the power of the dataset and conclusions drawn. Participants underwent baseline testing that entailed a dual X-ray absorptiometry scan, assessment of blood progenitor cell concentrations and proportions, maximal exercise test and analysis of dietary intake. was determined during maximal exercise testing, which was performed under the widely recognized Bruce protocol. Despite the use of a standardized exercise tolerance test, the authors offered participants two modalities of exertion – cycle ergometer or treadmill – thereby introducing a largely controllable variable that has been previously demonstrated to impact upon the results of such assessments, as treadmill exercise draws from a larger group of muscles and thus allows for a greater improvement of oxygen utilization (Muscat et al. 2015). Therefore, it would be of interest to know the distribution of modality used in both groups and whether participants were instructed to select the same exercise method for the subsequent testing. Following the baseline assessments, both lean and obese participants were enlisted in a 6-week EET scheme involving three supervised 30–60 min sessions per week of incrementally increasing intensity. Upon completion of the exercise training programme, participants underwent the same battery of assessments, to allow for comparison of both the exercise and BMI × exercise effects. During baseline testing, obese participants were found to have higher percentage body fat and a significantly lower . At 40.3 ml kg−1 min−1, the lean subjects displayed ‘fair’ to ‘good’ performance during baseline testing, while the obese group demonstrated ‘very poor’ to ‘fair’ baseline at 31.5 ml kg−1 min−1. It is important to note, however, that sex was not ideally balanced between the lean and obese groups, at 47% and 70% female, respectively. This may have affected the average performance substantially, as females have inherently lower , thus potentially skewing the interpretation of the results. Finally, although the average number of granulocytes and granulocyte–macrophages was found to be higher in the obese individuals at baseline, no significant difference was observed in any blood progenitor cell concentrations or proportions between the groups. Interestingly, circulating progenitor cell concentrations have previously been shown to display sex specificity (Topel et al. 2017); this is again of relevance to the current study, due to the sex imbalances observed between the groups. In analysing diluent plate counts of peripheral blood mononuclear cells post-intervention, the authors demonstrated a significant attenuating effect of EET on both granulocytes and granulocyte–macrophage populations, independently of BMI class. Despite this, obese individuals displayed significantly higher levels of both innate immune cell types before and after EET. Interestingly, a substantial reduction was noted in both CPCs and a uniquely inflammatory-primed subset thereof, termed HSPCs. This subset undergoes differentiation towards more lymphoid or myeloid lineages depending on haematological triggers that, in turn, affect the systemic inflammatory tone. In line with these results, the authors noted a significant reduction in CPC-mobilizing ligand CXCL12 and a trend towards reduced granulocyte-colony stimulating factor in obese patients following EET. Niemiro and colleagues subsequently delved deeper into the characterization of the HSPC population by analysing the presence and rates of expression of two surface receptors, chemokine receptor 2 (CCR2) and Toll-like receptor 4 (TLR4), which are important to inflammatory regulation. While EET reduced CCR2+ HSPCs in obese individuals only, the HSPCs of both groups displayed reduced levels of expression for the receptor. To our knowledge, this was the first study to show this observation, but previous studies in humans and animals have shown the opposite, with increases in HSPC content following exercise (Marycz et al. 2016). The authors suggest that perhaps this discrepancy is a result of CPC movement from circulation into a separate pool, such as within the bone marrow, thus depleting circulating CPCs but not affecting total body CPCs. However, this is largely speculative and the phenomenon requires further research to gain a true understanding of the mechanisms. In addition, while the abundance of TLR4+ HSPCs was reduced by EET, the rate of expression was actually increased on the cell surface. This indicates that, although fewer cells with myeloid differentiation capability persisted following EET, those remaining displayed a greater propensity to respond to inflammatory stimuli, such as lipopolysaccharides. Indeed, this makes interpretation of the overall immunomodulatory effect a more challenging and complex task. Nevertheless, this may represent a promising novel pathway for future research in examining the immunomodulatory effects of EET in both healthy and diseased individuals. In an attempt to further explore relationships between the physiological and cellular datasets, the authors employed a Spearman correlation analysis to probe for associations of with the concentrations and proportions of different cell types. This analysis revealed an interesting positive correlation between cardiorespiratory fitness and HSPC proportion at baseline; however, the results of their study indicate that this 6-week intervention of EET reduces HSPCs. These results appear juxtaposed and somewhat counterintuitive at present, although the complexities of this interaction may be beyond the scope of the current clinical study. Interestingly, the data also revealed significant negative correlations between the change in and the change in both adipose tissue-derived and bone marrow-derived mesenchymal stem cell concentrations over the study. While reductions in fat mass may explain the reduced quantities of adipose tissue-derived mesenchymal stem cells observed at trial termination and the negative association with change in fitness, the reason for bone-marrow stem cell alterations is unclear at present. The present study represents an advancement in our understanding of the relationship between low-grade systemic inflammation and obesity, as well as the manner in which this can be attenuated by EET. However, the results have also raised further questions that require exploration. Future studies should aim to replicate these results in larger cohorts, as there are numerous disparities in the literature and this is the first study to show such effects with an endurance exercise intervention. Continued monitoring of these participants may also be important, as it could be of interest to determine whether these alterations in progenitor cells are maintained in the long-term or if physiological homeostatic adaptations result in a return of progenitor cells to baseline. In addition, exercise training protocols of varying intensity should be assessed to explore whether further reductions in inflammatory progenitor cells are observed, in a dose-dependent fashion. Finally, many of the discussion points around the results presented in this study are largely speculative; therefore, it may be of significant benefit to step back into the appropriate preclinical models of EET to more closely examine the physiological and cellular effects of such an intervention. The authors have no duality of interest to declare. All authors have read and approved the final version of this manuscript and agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All persons designated as authors qualify for authorship, and all those who qualify for authorship are listed. No funding was sought for this article." @default.
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• W2897729042 title "Fat or thin, exercise wins: endurance exercise training reduces inflammatory circulating progenitor cells in lean and obese adults" @default.
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